The ability of a pathogenic virus to lie dormant within a cell (latent infection). In eukaryotes, subsequent activation and viral replication is thought to be caused by extracellular stimulation of cellular transcription factors. Latency in bacteriophage is maintained by the expression of virally encoded repressors.
The mechanism by which latent viruses, such as genetically transmitted tumor viruses (PROVIRUSES) or PROPHAGES of lysogenic bacteria, are induced to replicate and then released as infectious viruses. It may be effected by various endogenous and exogenous stimuli, including B-cell LIPOPOLYSACCHARIDES, glucocorticoid hormones, halogenated pyrimidines, IONIZING RADIATION, ultraviolet light, and superinfecting viruses.
The type species of LYMPHOCRYPTOVIRUS, subfamily GAMMAHERPESVIRINAE, infecting B-cells in humans. It is thought to be the causative agent of INFECTIOUS MONONUCLEOSIS and is strongly associated with oral hairy leukoplakia (LEUKOPLAKIA, HAIRY;), BURKITT LYMPHOMA; and other malignancies.
Nuclear antigens encoded by VIRAL GENES found in HUMAN HERPESVIRUS 4. At least six nuclear antigens have been identified.
Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses.
The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.
The semilunar-shaped ganglion containing the cells of origin of most of the sensory fibers of the trigeminal nerve. It is situated within the dural cleft on the cerebral surface of the petrous portion of the temporal bone and gives off the ophthalmic, maxillary, and part of the mandibular nerves.
A genus of the family HERPESVIRIDAE, subfamily ALPHAHERPESVIRINAE, consisting of herpes simplex-like viruses. The type species is HERPESVIRUS 1, HUMAN.
Deoxyribonucleic acid that makes up the genetic material of viruses.
Viruses whose genetic material is RNA.
Proteins found in any species of virus.
Substances elaborated by viruses that have antigenic activity.
The type species of ORTHOPOXVIRUS, related to COWPOX VIRUS, but whose true origin is unknown. It has been used as a live vaccine against SMALLPOX. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of VACCINIA VIRUS.
Proteins associated with the inner surface of the lipid bilayer of the viral envelope. These proteins have been implicated in control of viral transcription and may possibly serve as the "glue" that binds the nucleocapsid to the appropriate membrane site during viral budding from the host cell.
Established cell cultures that have the potential to propagate indefinitely.
Specific molecular components of the cell capable of recognizing and interacting with a virus, and which, after binding it, are capable of generating some signal that initiates the chain of events leading to the biological response.
A form of undifferentiated malignant LYMPHOMA usually found in central Africa, but also reported in other parts of the world. It is commonly manifested as a large osteolytic lesion in the jaw or as an abdominal mass. B-cell antigens are expressed on the immature cells that make up the tumor in virtually all cases of Burkitt lymphoma. The Epstein-Barr virus (HERPESVIRUS 4, HUMAN) has been isolated from Burkitt lymphoma cases in Africa and it is implicated as the causative agent in these cases; however, most non-African cases are EBV-negative.
Process of growing viruses in live animals, plants, or cultured cells.
The expelling of virus particles from the body. Important routes include the respiratory tract, genital tract, and intestinal tract. Virus shedding is an important means of vertical transmission (INFECTIOUS DISEASE TRANSMISSION, VERTICAL).
Virus diseases caused by the HERPESVIRIDAE.
Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.
A general term for diseases produced by viruses.
A species of POLYOMAVIRUS originally isolated from Rhesus monkey kidney tissue. It produces malignancy in human and newborn hamster kidney cell cultures.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
The assembly of VIRAL STRUCTURAL PROTEINS and nucleic acid (VIRAL DNA or VIRAL RNA) to form a VIRUS PARTICLE.
Viruses parasitic on plants higher than bacteria.
Viruses whose nucleic acid is DNA.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Viruses which lack a complete genome so that they cannot completely replicate or cannot form a protein coat. Some are host-dependent defectives, meaning they can replicate only in cell systems which provide the particular genetic function which they lack. Others, called SATELLITE VIRUSES, are able to replicate only when their genetic defect is complemented by a helper virus.
The type species of ALPHAVIRUS normally transmitted to birds by CULEX mosquitoes in Egypt, South Africa, India, Malaya, the Philippines, and Australia. It may be associated with fever in humans. Serotypes (differing by less than 17% in nucleotide sequence) include Babanki, Kyzylagach, and Ockelbo viruses.
The type species of MORBILLIVIRUS and the cause of the highly infectious human disease MEASLES, which affects mostly children.
Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.
A subtype of INFLUENZA A VIRUS with the surface proteins hemagglutinin 1 and neuraminidase 1. The H1N1 subtype was responsible for the Spanish flu pandemic of 1918.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
The type species of LYSSAVIRUS causing rabies in humans and other animals. Transmission is mostly by animal bites through saliva. The virus is neurotropic multiplying in neurons and myotubes of vertebrates.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 5 and neuraminidase 1. The H5N1 subtype, frequently referred to as the bird flu virus, is endemic in wild birds and very contagious among both domestic (POULTRY) and wild birds. It does not usually infect humans, but some cases have been reported.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 3 and neuraminidase 2. The H3N2 subtype was responsible for the Hong Kong flu pandemic of 1968.
The type species of the genus ORTHOHEPADNAVIRUS which causes human HEPATITIS B and is also apparently a causal agent in human HEPATOCELLULAR CARCINOMA. The Dane particle is an intact hepatitis virion, named after its discoverer. Non-infectious spherical and tubular particles are also seen in the serum.
A species of FLAVIVIRUS, one of the Japanese encephalitis virus group (ENCEPHALITIS VIRUSES, JAPANESE). It can infect birds and mammals. In humans, it is seen most frequently in Africa, Asia, and Europe presenting as a silent infection or undifferentiated fever (WEST NILE FEVER). The virus appeared in North America for the first time in 1999. It is transmitted mainly by CULEX spp mosquitoes which feed primarily on birds, but it can also be carried by the Asian Tiger mosquito, AEDES albopictus, which feeds mainly on mammals.
A group of viruses in the PNEUMOVIRUS genus causing respiratory infections in various mammals. Humans and cattle are most affected but infections in goats and sheep have also been reported.
Ribonucleic acid that makes up the genetic material of viruses.
The functional hereditary units of VIRUSES.
The type species of VESICULOVIRUS causing a disease symptomatically similar to FOOT-AND-MOUTH DISEASE in cattle, horses, and pigs. It may be transmitted to other species including humans, where it causes influenza-like symptoms.
The time from the onset of a stimulus until a response is observed.
Membrane glycoproteins from influenza viruses which are involved in hemagglutination, virus attachment, and envelope fusion. Fourteen distinct subtypes of HA glycoproteins and nine of NA glycoproteins have been identified from INFLUENZA A VIRUS; no subtypes have been identified for Influenza B or Influenza C viruses.
A CELL LINE derived from the kidney of the African green (vervet) monkey, (CERCOPITHECUS AETHIOPS) used primarily in virus replication studies and plaque assays.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A species of CERCOPITHECUS containing three subspecies: C. tantalus, C. pygerythrus, and C. sabeus. They are found in the forests and savannah of Africa. The African green monkey (C. pygerythrus) is the natural host of SIMIAN IMMUNODEFICIENCY VIRUS and is used in AIDS research.
Viruses that produce tumors.
Species of the genus LENTIVIRUS, subgenus primate immunodeficiency viruses (IMMUNODEFICIENCY VIRUSES, PRIMATE), that induces acquired immunodeficiency syndrome in monkeys and apes (SAIDS). The genetic organization of SIV is virtually identical to HIV.
The infective system of a virus, composed of the viral genome, a protein core, and a protein coat called a capsid, which may be naked or enclosed in a lipoprotein envelope called the peplos.
The type species of RUBULAVIRUS that causes an acute infectious disease in humans, affecting mainly children. Transmission occurs by droplet infection.
A species of RESPIROVIRUS also called hemadsorption virus 2 (HA2), which causes laryngotracheitis in humans, especially children.
Viruses which produce a mottled appearance of the leaves of plants.
Method for measuring viral infectivity and multiplication in CULTURED CELLS. Clear lysed areas or plaques develop as the VIRAL PARTICLES are released from the infected cells during incubation. With some VIRUSES, the cells are killed by a cytopathic effect; with others, the infected cells are not killed but can be detected by their hemadsorptive ability. Sometimes the plaque cells contain VIRAL ANTIGENS which can be measured by IMMUNOFLUORESCENCE.
Infections produced by oncogenic viruses. The infections caused by DNA viruses are less numerous but more diverse than those caused by the RNA oncogenic viruses.
A species in the genus HEPATOVIRUS containing one serotype and two strains: HUMAN HEPATITIS A VIRUS and Simian hepatitis A virus causing hepatitis in humans (HEPATITIS A) and primates, respectively.
Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly.
A species of ALPHAVIRUS isolated in central, eastern, and southern Africa.
The type species of SIMPLEXVIRUS causing most forms of non-genital herpes simplex in humans. Primary infection occurs mainly in infants and young children and then the virus becomes latent in the dorsal root ganglion. It then is periodically reactivated throughout life causing mostly benign conditions.
The measurement of infection-blocking titer of ANTISERA by testing a series of dilutions for a given virus-antiserum interaction end-point, which is generally the dilution at which tissue cultures inoculated with the serum-virus mixtures demonstrate cytopathology (CPE) or the dilution at which 50% of test animals injected with serum-virus mixtures show infectivity (ID50) or die (LD50).
Group of alpharetroviruses (ALPHARETROVIRUS) producing sarcomata and other tumors in chickens and other fowl and also in pigeons, ducks, and RATS.
A species of POLYOMAVIRUS, originally isolated from the brain of a patient with progressive multifocal leukoencephalopathy. The patient's initials J.C. gave the virus its name. Infection is not accompanied by any apparent illness but serious demyelinating disease can appear later, probably following reactivation of latent virus.
The binding of virus particles to receptors on the host cell surface. For enveloped viruses, the virion ligand is usually a surface glycoprotein as is the cellular receptor. For non-enveloped viruses, the virus CAPSID serves as the ligand.
A species of POLYOMAVIRUS apparently infecting over 90% of children but not clearly associated with any clinical illness in childhood. The virus remains latent in the body throughout life and can be reactivated under certain circumstances.
Viruses whose taxonomic relationships have not been established.
Insertion of viral DNA into host-cell DNA. This includes integration of phage DNA into bacterial DNA; (LYSOGENY); to form a PROPHAGE or integration of retroviral DNA into cellular DNA to form a PROVIRUS.
The type species of ALPHARETROVIRUS producing latent or manifest lymphoid leukosis in fowl.
The relationships of groups of organisms as reflected by their genetic makeup.
A family of RNA viruses causing INFLUENZA and other diseases. There are five recognized genera: INFLUENZAVIRUS A; INFLUENZAVIRUS B; INFLUENZAVIRUS C; ISAVIRUS; and THOGOTOVIRUS.
The type species of ORBIVIRUS causing a serious disease in sheep, especially lambs. It may also infect wild ruminants and other domestic animals.
Virus diseases caused by the ORTHOMYXOVIRIDAE.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. It also infects rats and newborn hamsters. It is apparently transmitted to embryos in utero and to newborns through mother's milk.
Infection with human herpesvirus 4 (HERPESVIRUS 4, HUMAN); which may facilitate the development of various lymphoproliferative disorders. These include BURKITT LYMPHOMA (African type), INFECTIOUS MONONUCLEOSIS, and oral hairy leukoplakia (LEUKOPLAKIA, HAIRY).
The type species of RESPIROVIRUS in the subfamily PARAMYXOVIRINAE. It is the murine version of HUMAN PARAINFLUENZA VIRUS 1, distinguished by host range.
The outer protein protective shell of a virus, which protects the viral nucleic acid.
The type species of the FLAVIVIRUS genus. Principal vector transmission to humans is by AEDES spp. mosquitoes.
The type species of TOBAMOVIRUS which causes mosaic disease of tobacco. Transmission occurs by mechanical inoculation.
Visible morphologic changes in cells infected with viruses. It includes shutdown of cellular RNA and protein synthesis, cell fusion, release of lysosomal enzymes, changes in cell membrane permeability, diffuse changes in intracellular structures, presence of viral inclusion bodies, and chromosomal aberrations. It excludes malignant transformation, which is CELL TRANSFORMATION, VIRAL. Viral cytopathogenic effects provide a valuable method for identifying and classifying the infecting viruses.
Elements of limited time intervals, contributing to particular results or situations.
Pneumovirus infections caused by the RESPIRATORY SYNCYTIAL VIRUSES. Humans and cattle are most affected but infections in goats and sheep have been reported.
The type species of LEPORIPOXVIRUS causing infectious myxomatosis, a severe generalized disease, in rabbits. Tumors are not always present.
Inactivation of viruses by non-immune related techniques. They include extremes of pH, HEAT treatment, ultraviolet radiation, IONIZING RADIATION; DESICCATION; ANTISEPTICS; DISINFECTANTS; organic solvents, and DETERGENTS.
A species of ORTHOPOXVIRUS that is the etiologic agent of COWPOX. It is closely related to but antigenically different from VACCINIA VIRUS.
A species of ORTHOPOXVIRUS causing infections in humans. No infections have been reported since 1977 and the virus is now believed to be virtually extinct.
The type species of PNEUMOVIRUS and an important cause of lower respiratory disease in infants and young children. It frequently presents with bronchitis and bronchopneumonia and is further characterized by fever, cough, dyspnea, wheezing, and pallor.
A species of ARENAVIRUS, part of the Old World Arenaviruses (ARENAVIRUSES, OLD WORLD), and the etiologic agent of LASSA FEVER. LASSA VIRUS is a common infective agent in humans in West Africa. Its natural host is the multimammate mouse Mastomys natalensis.
A species of ALPHAVIRUS causing an acute dengue-like fever.
The type species in the genus NOROVIRUS, first isolated in 1968 from the stools of school children in Norwalk, Ohio, who were suffering from GASTROENTERITIS. The virions are non-enveloped spherical particles containing a single protein. Multiple strains are named after the places where outbreaks have occurred.
An acute viral infection in humans involving the respiratory tract. It is marked by inflammation of the NASAL MUCOSA; the PHARYNX; and conjunctiva, and by headache and severe, often generalized, myalgia.
Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).
A collection of single-stranded RNA viruses scattered across the Bunyaviridae, Flaviviridae, and Togaviridae families whose common property is the ability to induce encephalitic conditions in infected hosts.
DNA molecules capable of autonomous replication within a host cell and into which other DNA sequences can be inserted and thus amplified. Many are derived from PLASMIDS; BACTERIOPHAGES; or VIRUSES. They are used for transporting foreign genes into recipient cells. Genetic vectors possess a functional replicator site and contain GENETIC MARKERS to facilitate their selective recognition.
Biological properties, processes, and activities of VIRUSES.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
A genus of FLAVIVIRIDAE causing parenterally-transmitted HEPATITIS C which is associated with transfusions and drug abuse. Hepatitis C virus is the type species.
Viral proteins that are components of the mature assembled VIRUS PARTICLES. They may include nucleocapsid core proteins (gag proteins), enzymes packaged within the virus particle (pol proteins), and membrane components (env proteins). These do not include the proteins encoded in the VIRAL GENOME that are produced in infected cells but which are not packaged in the mature virus particle,i.e. the so called non-structural proteins (VIRAL NONSTRUCTURAL PROTEINS).
A subgroup of the genus FLAVIVIRUS that causes encephalitis and hemorrhagic fevers and is found in eastern and western Europe and the former Soviet Union. It is transmitted by TICKS and there is an associated milk-borne transmission from viremic cattle, goats, and sheep.
A species of RESPIROVIRUS frequently isolated from small children with pharyngitis, bronchitis, and pneumonia.
A species of GAMMARETROVIRUS causing leukemia, lymphosarcoma, immune deficiency, or other degenerative diseases in cats. Several cellular oncogenes confer on FeLV the ability to induce sarcomas (see also SARCOMA VIRUSES, FELINE).
The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its VIRULENCE FACTORS.
Proteins that form the CAPSID of VIRUSES.
Production of new arrangements of DNA by various mechanisms such as assortment and segregation, CROSSING OVER; GENE CONVERSION; GENETIC TRANSFORMATION; GENETIC CONJUGATION; GENETIC TRANSDUCTION; or mixed infection of viruses.
The type species of APHTHOVIRUS, causing FOOT-AND-MOUTH DISEASE in cloven-hoofed animals. Several different serotypes exist.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
An inheritable change in cells manifested by changes in cell division and growth and alterations in cell surface properties. It is induced by infection with a transforming virus.
Specific hemagglutinin subtypes encoded by VIRUSES.
A species of ARTERIVIRUS causing reproductive and respiratory disease in pigs. The European strain is called Lelystad virus. Airborne transmission is common.
Any of the viruses that cause inflammation of the liver. They include both DNA and RNA viruses as well viruses from humans and animals.
A multistage process that includes cloning, physical mapping, subcloning, determination of the DNA SEQUENCE, and information analysis.
The type species of VARICELLOVIRUS causing CHICKENPOX (varicella) and HERPES ZOSTER (shingles) in humans.
A strain of PRIMATE T-LYMPHOTROPIC VIRUS 1 isolated from mature T4 cells in patients with T-lymphoproliferation malignancies. It causes adult T-cell leukemia (LEUKEMIA-LYMPHOMA, T-CELL, ACUTE, HTLV-I-ASSOCIATED), T-cell lymphoma (LYMPHOMA, T-CELL), and is involved in mycosis fungoides, SEZARY SYNDROME and tropical spastic paraparesis (PARAPARESIS, TROPICAL SPASTIC).
The type species of BETARETROVIRUS commonly latent in mice. It causes mammary adenocarcinoma in a genetically susceptible strain of mice when the appropriate hormonal influences operate.
Immunoglobulins produced in response to VIRAL ANTIGENS.
The interactions between a host and a pathogen, usually resulting in disease.
A suborder of PRIMATES consisting of six families: CEBIDAE (some New World monkeys), ATELIDAE (some New World monkeys), CERCOPITHECIDAE (Old World monkeys), HYLOBATIDAE (gibbons and siamangs), CALLITRICHINAE (marmosets and tamarins), and HOMINIDAE (humans and great apes).
Defective viruses which can multiply only by association with a helper virus which complements the defective gene. Satellite viruses may be associated with certain plant viruses, animal viruses, or bacteriophages. They differ from satellite RNA; (RNA, SATELLITE) in that satellite viruses encode their own coat protein.
Tumor-selective, replication competent VIRUSES that have antineoplastic effects. This is achieved by producing cytotoxicity-enhancing proteins and/or eliciting an antitumor immune response. They are genetically engineered so that they can replicate in CANCER cells but not in normal cells, and are used in ONCOLYTIC VIROTHERAPY.
The type species of PARAPOXVIRUS which causes a skin infection in natural hosts, usually young sheep. Humans may contract local skin lesions by contact. The virus apparently persists in soil.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) producing leukemia of the reticulum-cell type with massive infiltration of liver, spleen, and bone marrow. It infects DBA/2 and Swiss mice.
A group of viruses in the genus PESTIVIRUS, causing diarrhea, fever, oral ulcerations, hemorrhagic syndrome, and various necrotic lesions among cattle and other domestic animals. The two species (genotypes), BVDV-1 and BVDV-2 , exhibit antigenic and pathological differences. The historical designation, BVDV, consisted of both (then unrecognized) genotypes.
A sequence of successive nucleotide triplets that are read as CODONS specifying AMINO ACIDS and begin with an INITIATOR CODON and end with a stop codon (CODON, TERMINATOR).
The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.
A positive-stranded RNA virus species in the genus HEPEVIRUS, causing enterically-transmitted non-A, non-B hepatitis (HEPATITIS E).
The quantity of measurable virus in a body fluid. Change in viral load, measured in plasma, is sometimes used as a SURROGATE MARKER in disease progression.
An enzyme that catalyzes the hydrolysis of alpha-2,3, alpha-2,6-, and alpha-2,8-glycosidic linkages (at a decreasing rate, respectively) of terminal sialic residues in oligosaccharides, glycoproteins, glycolipids, colominic acid, and synthetic substrate. (From Enzyme Nomenclature, 1992)
Proteins found mainly in icosahedral DNA and RNA viruses. They consist of proteins directly associated with the nucleic acid inside the NUCLEOCAPSID.
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
A subfamily of HERPESVIRIDAE characterized by variable reproductive cycles. The genera include: LYMPHOCRYPTOVIRUS and RHADINOVIRUS.
The type species of DELTARETROVIRUS that causes a form of bovine lymphosarcoma (ENZOOTIC BOVINE LEUKOSIS) or persistent lymphocytosis.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
A group of replication-defective viruses, in the genus GAMMARETROVIRUS, which are capable of transforming cells, but which replicate and produce tumors only in the presence of Murine leukemia viruses (LEUKEMIA VIRUS, MURINE).
Viruses whose hosts are in the domain ARCHAEA.
INFLAMMATION of the LIVER in humans caused by HEPATITIS C VIRUS, a single-stranded RNA virus. Its incubation period is 30-90 days. Hepatitis C is transmitted primarily by contaminated blood parenterally, and is often associated with transfusion and intravenous drug abuse. However, in a significant number of cases, the source of hepatitis C infection is unknown.
A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 7 and neuraminidase 7. The H7N7 subtype produced an epidemic in 2003 which was highly pathogenic among domestic birds (POULTRY). Some infections in humans were reported.
Human immunodeficiency virus. A non-taxonomic and historical term referring to any of two species, specifically HIV-1 and/or HIV-2. Prior to 1986, this was called human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV). From 1986-1990, it was an official species called HIV. Since 1991, HIV was no longer considered an official species name; the two species were designated HIV-1 and HIV-2.
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.
The type species of the genus AVIPOXVIRUS. It is the etiologic agent of FOWLPOX.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
The study of the structure, growth, function, genetics, and reproduction of viruses, and VIRUS DISEASES.
Serologic tests in which a known quantity of antigen is added to the serum prior to the addition of a red cell suspension. Reaction result is expressed as the smallest amount of antigen which causes complete inhibition of hemagglutination.
A species of HENIPAVIRUS first identified in Australia in 1994 in HORSES and transmitted to humans. The natural host appears to be fruit bats (PTEROPUS).
Family of RNA viruses that infects birds and mammals and encodes the enzyme reverse transcriptase. The family contains seven genera: DELTARETROVIRUS; LENTIVIRUS; RETROVIRUSES TYPE B, MAMMALIAN; ALPHARETROVIRUS; GAMMARETROVIRUS; RETROVIRUSES TYPE D; and SPUMAVIRUS. A key feature of retrovirus biology is the synthesis of a DNA copy of the genome which is integrated into cellular DNA. After integration it is sometimes not expressed but maintained in a latent state (PROVIRUSES).
The type species of ARENAVIRUS, part of the Old World Arenaviruses (ARENAVIRUSES, OLD WORLD), producing a silent infection in house and laboratory mice. In humans, infection with LCMV can be inapparent, or can present with an influenza-like illness, a benign aseptic meningitis, or a severe meningoencephalomyelitis. The virus can also infect monkeys, dogs, field mice, guinea pigs, and hamsters, the latter an epidemiologically important host.
A species in the genus Bornavirus, family BORNAVIRIDAE, causing a rare and usually fatal encephalitic disease in horses and other domestic animals and possibly deer. Its name derives from the city in Saxony where the condition was first described in 1894, but the disease occurs in Europe, N. Africa, and the Near East.
A species in the ORTHOBUNYAVIRUS genus of the family BUNYAVIRIDAE. A large number of serotypes or strains exist in many parts of the world. They are transmitted by mosquitoes and infect humans in some areas.
A phenomenon in which infection by a first virus results in resistance of cells or tissues to infection by a second, unrelated virus.
The period from about 5 to 7 years to adolescence when there is an apparent cessation of psychosexual development.
A species of MORBILLIVIRUS causing distemper in dogs, wolves, foxes, raccoons, and ferrets. Pinnipeds have also been known to contract Canine distemper virus from contact with domestic dogs.
Extrachromosomal, usually CIRCULAR DNA molecules that are self-replicating and transferable from one organism to another. They are found in a variety of bacterial, archaeal, fungal, algal, and plant species. They are used in GENETIC ENGINEERING as CLONING VECTORS.
Proteins coded by the retroviral gag gene. The products are usually synthesized as protein precursors or POLYPROTEINS, which are then cleaved by viral proteases to yield the final products. Many of the final products are associated with the nucleoprotein core of the virion. gag is short for group-specific antigen.
A species of VARICELLOVIRUS producing a respiratory infection (PSEUDORABIES) in swine, its natural host. It also produces an usually fatal ENCEPHALOMYELITIS in cattle, sheep, dogs, cats, foxes, and mink.
An enzyme that synthesizes DNA on an RNA template. It is encoded by the pol gene of retroviruses and by certain retrovirus-like elements. EC
Warm-blooded VERTEBRATES possessing FEATHERS and belonging to the class Aves.
Duplex DNA sequences in eukaryotic chromosomes, corresponding to the genome of a virus, that are transmitted from one cell generation to the next without causing lysis of the host. Proviruses are often associated with neoplastic cell transformation and are key features of retrovirus biology.
Proteins, usually glycoproteins, found in the viral envelopes of a variety of viruses. They promote cell membrane fusion and thereby may function in the uptake of the virus by cells.
The presence of viruses in the blood.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
Sites on an antigen that interact with specific antibodies.
A species of MORBILLIVIRUS causing cattle plague, a disease with high mortality. Sheep, goats, pigs, and other animals of the order Artiodactyla can also be infected.
A subtype of INFLUENZA A VIRUS with the surface proteins hemagglutinin 7 and neuraminidase 9. This avian origin virus was first identified in humans in 2013.
The developmental entity of a fertilized chicken egg (ZYGOTE). The developmental process begins about 24 h before the egg is laid at the BLASTODISC, a small whitish spot on the surface of the EGG YOLK. After 21 days of incubation, the embryo is fully developed before hatching.
A defective virus, containing particles of RNA nucleoprotein in virion-like form, present in patients with acute hepatitis B and chronic hepatitis. It requires the presence of a hepadnavirus for full replication. This is the lone species in the genus Deltavirus.
An enzyme that catalyses RNA-template-directed extension of the 3'- end of an RNA strand by one nucleotide at a time, and can initiate a chain de novo. (Enzyme Nomenclature, 1992, p293)
Common name for the species Gallus gallus, the domestic fowl, in the family Phasianidae, order GALLIFORMES. It is descended from the red jungle fowl of SOUTHEAST ASIA.
A species of ORTHOPOXVIRUS causing an epidemic disease among captive primates.
The electric response evoked in the CEREBRAL CORTEX by ACOUSTIC STIMULATION or stimulation of the AUDITORY PATHWAYS.
The lone species of the genus Asfivirus. It infects domestic and wild pigs, warthogs, and bushpigs. Disease is endemic in domestic swine in many African countries and Sardinia. Soft ticks of the genus Ornithodoros are also infected and act as vectors.
Live vaccines prepared from microorganisms which have undergone physical adaptation (e.g., by radiation or temperature conditioning) or serial passage in laboratory animal hosts or infected tissue/cell cultures, in order to produce avirulent mutant strains capable of inducing protective immunity.
A genus of the family PARAMYXOVIRIDAE (subfamily PARAMYXOVIRINAE) where all the virions have both HEMAGGLUTININ and NEURAMINIDASE activities and encode a non-structural C protein. SENDAI VIRUS is the type species.
A species in the group RETICULOENDOTHELIOSIS VIRUSES, AVIAN of the genus GAMMARETROVIRUS that causes a chronic neoplastic and a more acute immunosuppressive disease in fowl.
Sudden increase in the incidence of a disease. The concept includes EPIDEMICS and PANDEMICS.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A mosquito-borne species of the PHLEBOVIRUS genus found in eastern, central, and southern Africa, producing massive hepatitis, abortion, and death in sheep, goats, cattle, and other animals. It also has caused disease in humans.
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
Semidomesticated variety of European polecat much used for hunting RODENTS and/or RABBITS and as a laboratory animal. It is in the subfamily Mustelinae, family MUSTELIDAE.
Proteins prepared by recombinant DNA technology.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
A species of LENTIVIRUS, subgenus equine lentiviruses (LENTIVIRUSES, EQUINE), causing acute and chronic infection in horses. It is transmitted mechanically by biting flies, mosquitoes, and midges, and iatrogenically through unsterilized equipment. Chronic infection often consists of acute episodes with remissions.
Genotypic differences observed among individuals in a population.
A species of CORONAVIRUS causing infections in chickens and possibly pheasants. Chicks up to four weeks old are the most severely affected.
Serological reactions in which an antiserum against one antigen reacts with a non-identical but closely related antigen.
A species of non-enveloped DNA virus in the genus ANELLOVIRUS, associated with BLOOD TRANSFUSIONS; and HEPATITIS. However, no etiological role has been found for TTV in hepatitis.
A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 5 and neuraminidase 2. The H5N2 subtype has been found to be highly pathogenic in chickens.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) isolated from spontaneous leukemia in AKR strain mice.
A species of ORTHOPOXVIRUS infecting mice and causing a disease that involves internal organs and produces characteristic skin lesions.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Antibodies produced by a single clone of cells.
A species of ALPHARETROVIRUS causing anemia in fowl.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
Electrical responses recorded from nerve, muscle, SENSORY RECEPTOR, or area of the CENTRAL NERVOUS SYSTEM following stimulation. They range from less than a microvolt to several microvolts. The evoked potential can be auditory (EVOKED POTENTIALS, AUDITORY), somatosensory (EVOKED POTENTIALS, SOMATOSENSORY), visual (EVOKED POTENTIALS, VISUAL), or motor (EVOKED POTENTIALS, MOTOR), or other modalities that have been reported.
A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 1 and neuraminidase 2. It is endemic in both human and pig populations.
The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.

The amino-terminal C/H1 domain of CREB binding protein mediates zta transcriptional activation of latent Epstein-Barr virus. (1/2054)

Latent Epstein-Barr virus (EBV) is maintained as a nucleosome-covered episome that can be transcriptionally activated by overexpression of the viral immediate-early protein, Zta. We show here that reactivation of latent EBV by Zta can be significantly enhanced by coexpression of the cellular coactivators CREB binding protein (CBP) and p300. A stable complex containing both Zta and CBP could be isolated from lytically stimulated, but not latently infected RAJI nuclear extracts. Zta-mediated viral reactivation and transcriptional activation were both significantly inhibited by coexpression of the E1A 12S protein but not by an N-terminal deletion mutation of E1A (E1ADelta2-36), which fails to bind CBP. Zta bound directly to two related cysteine- and histidine-rich domains of CBP, referred to as C/H1 and C/H3. These domains both interacted specifically with the transcriptional activation domain of Zta in an electrophoretic mobility shift assay. Interestingly, we found that the C/H3 domain was a potent dominant negative inhibitor of Zta transcriptional activation function. In contrast, an amino-terminal fragment containing the C/H1 domain was sufficient for coactivation of Zta transcription and viral reactivation function. Thus, CBP can stimulate the transcription of latent EBV in a histone acetyltransferase-independent manner mediated by the CBP amino-terminal C/H1-containing domain. We propose that CBP may regulate aspects of EBV latency and reactivation by integrating cellular signals mediated by competitive interactions between C/H1, C/H3, and the Zta activation domain.  (+info)

Epstein-barr virus regulates c-MYC, apoptosis, and tumorigenicity in Burkitt lymphoma. (2/2054)

Loss of the Epstein-Barr virus (EBV) genome from Akata Burkitt lymphoma (BL) cells is coincident with a loss of malignant phenotype, despite the fact that Akata and other EBV-positive BL cells express a restricted set of EBV gene products (type I latency) that are not known to overtly affect cell growth. Here we demonstrate that reestablishment of type I latency in EBV-negative Akata cells restores tumorigenicity and that tumorigenic potential correlates with an increased resistance to apoptosis under growth-limiting conditions. The antiapoptotic effect of EBV was associated with a higher level of Bcl-2 expression and an EBV-dependent decrease in steady-state levels of c-MYC protein. Although the EBV EBNA-1 protein is expressed in all EBV-associated tumors and is reported to have oncogenic potential, enforced expression of EBNA-1 alone in EBV-negative Akata cells failed to restore tumorigenicity or EBV-dependent down-regulation of c-MYC. These data provide direct evidence that EBV contributes to the tumorigenic potential of Burkitt lymphoma and suggest a novel model whereby a restricted latency program of EBV promotes B-cell survival, and thus virus persistence within an immune host, by selectively targeting the expression of c-MYC.  (+info)

Anti-rheumatic compound aurothioglucose inhibits tumor necrosis factor-alpha-induced HIV-1 replication in latently infected OM10.1 and Ach2 cells. (3/2054)

NF-kappaB is a potent cellular activator of HIV-1 gene expression. Down-regulation of NF-kappaB activation is known to inhibit HIV replication from the latently infected cells. Gold compounds have been effectively used for many decades in the treatment of rheumatoid arthritis. We previously reported that gold compounds, especially aurothioglucose (AuTG) containing monovalent gold ion, inhibited the DNA-binding of NF-kappaB in vitro. In this report we have examined the efficacy of the gold compound AuTG as an inhibitor of HIV replication in latently infected OM10.1 and Ach2 cells. Tumor necrosis factor (TNF)-alpha-induced HIV-1 replication in OM10.1 or Ach2 cells was significantly inhibited by non-cytotoxic doses of AuTG (>10 microM in OM10.1 cells and >25 F.M in Ach2 cells), while 25 microM of the counter-anion thioglucose (TG) or gold compound containing divalent gold ion, HAuCl3, had no effect. The effect of AuTG on NF-kappaB-dependent gene expression was confirmed by a transient CAT assay. Specific staining as well as electron microscopic examinations revealed the accumulation of metal gold in the cells, supporting our previous hypothesis that gold ions could block NF-kappaB-DNA binding by a redox mechanism. These observations indicate that the monovalent gold compound AuTG is a potentially useful drug for the treatment of patients infected with HIV.  (+info)

EBP2, a human protein that interacts with sequences of the Epstein-Barr virus nuclear antigen 1 important for plasmid maintenance. (4/2054)

The replication and stable maintenance of latent Epstein-Barr virus (EBV) DNA episomes in human cells requires only one viral protein, Epstein-Barr nuclear antigen 1 (EBNA1). To gain insight into the mechanisms by which EBNA1 functions, we used a yeast two-hybrid screen to detect human proteins that interact with EBNA1. We describe here the isolation of a protein, EBP2 (EBNA1 binding protein 2), that specifically interacts with EBNA1. EBP2 was also shown to bind to DNA-bound EBNA1 in a one-hybrid system, and the EBP2-EBNA1 interaction was confirmed by coimmunoprecipitation from insect cells expressing these two proteins. EBP2 is a 35-kDa protein that is conserved in a variety of organisms and is predicted to form coiled-coil interactions. We have mapped the region of EBNA1 that binds EBP2 and generated internal deletion mutants of EBNA1 that are deficient in EBP2 interactions. Functional analyses of these EBNA1 mutants show that the ability to bind EBP2 correlates with the ability of EBNA1 to support the long-term maintenance in human cells of a plasmid containing the EBV origin, oriP. An EBNA1 mutant lacking amino acids 325 to 376 was defective for EBP2 binding and long-term oriP plasmid maintenance but supported the transient replication of oriP plasmids at wild-type levels. Thus, our results suggest that the EBNA1-EBP2 interaction is important for the stable segregation of EBV episomes during cell division but not for the replication of the episomes.  (+info)

Genetic evidence that EBNA-1 is needed for efficient, stable latent infection by Epstein-Barr virus. (5/2054)

Replication and maintenance of the 170-kb circular chromosome of Epstein-Barr virus (EBV) during latent infection are generally believed to depend upon a single viral gene product, the nuclear protein EBNA-1. EBNA-1 binds to two clusters of sites at oriP, an 1, 800-bp sequence on the EBV genome which can support replication and maintenance of artificial plasmids introduced into cell lines that contain EBNA-1. To investigate the importance of EBNA-1 to latent infection by EBV, we introduced a frameshift mutation into the EBNA-1 gene of EBV by recombination along with a flanking selectable marker. EBV genomes carrying the frameshift mutation could be isolated readily after superinfecting EBV-positive cell lines, but not if recombinant virus was used to infect EBV-negative B-cell lines or to immortalize peripheral blood B cells. EBV mutants lacking almost all of internal repeat 3, which encode a repetitive glycine and alanine domain of EBNA-1, were generated in the same way and found to immortalize B cells normally. An EBNA-1-deficient mutant of EBV was isolated and found to be incapable of establishing a latent infection of the cell line BL30 at a detectable frequency, indicating that the mutant was less than 1% as efficient as an isogenic, EBNA-1-positive strain in this assay. The data indicate that EBNA-1 is required for efficient and stable latent infection by EBV under the conditions tested. Evidence from other studies now indicates that autonomous maintenance of the EBV chromosome during latent infection does not depend on the replication initiation function of oriP. It is therefore likely that the viral chromosome maintenance (segregation) function of oriP and EBNA-1 is what is required.  (+info)

Expression of EBNA-1 mRNA is regulated by cell cycle during Epstein-Barr virus type I latency. (6/2054)

Expression of EBNA-1 protein is required for the establishment and maintenance of the Epstein-Barr virus (EBV) genome during latent infection. During type I latency, the BamHI Q promoter (Qp) gives rise to EBNA-1 expression. The dominant regulatory mechanism for Qp appears to be mediated through the Q locus, located immediately downstream of the transcription start site. Binding of EBNA-1 to the Q locus represses Qp constitutive activity, and repression has been reported to be overcome by an E2F family member that binds to the Q locus and displaces EBNA-1 (N. S. Sung, J. Wilson, M. Davenport, N. D. Sista, and J. S. Pagano, Mol. Cell. Biol. 14:7144-7152, 1994). These data suggest that the final outcome of Qp activity is reciprocally controlled by EBNA-1 and E2F. Since E2F activity is cell cycle regulated, Qp activity and EBNA-1 expression are predicted to be regulated in a cell cycle-dependent manner. Proliferation of the type I latently infected cell line, Akata, was synchronized with the use of the G2/M blocking agent nocodazole. From 65 to 75% of cells could be made to peak in S phase without evidence of viral reactivation. Following release from G2/M block, EBNA-1 mRNA levels declined as the synchronized cells entered the G1 phase of the cell cycle. As cells proceeded into S phase, EBNA-1 mRNA levels increased parallel to the peak in cell numbers in S phase. However, EBNA-1 protein levels showed no detectable change during the cell cycle, most likely due to the protein's long half-life as estimated by inhibition of protein synthesis by cycloheximide. Finally, in Qp luciferase reporter assays, the activity of Qp was shown to be regulated by cell cycle and to be dependent on the E2F sites within the Q locus. These findings demonstrate that transcriptional activity of Qp is cell cycle regulated and indicated that E2F serves as the stimulus for this regulation.  (+info)

Macrophages are the major reservoir of latent murine gammaherpesvirus 68 in peritoneal cells. (7/2054)

B cells have previously been identified as the major hematopoietic cell type harboring latent gammaherpesvirus 68 (gammaHV68) (N. P. Sunil-Chandra, S. Efstathiou, and A. A. Nash, J. Gen. Virol. 73:3275-3279, 1992). However, we have shown that gammaHV68 efficiently establishes latency in B-cell-deficient mice (K. E. Weck, M. L. Barkon, L. I. Yoo, S. H. Speck, and H. W. Virgin, J. Virol. 70:6775-6780, 1996), demonstrating that B cells are not required for gammaHV68 latency. To understand this dichotomy, we determined whether hematopoietic cell types, in addition to B cells, carry latent gammaHV68. We observed a high frequency of cells that reactivate latent gammaHV68 in peritoneal exudate cells (PECs) derived from both B-cell-deficient and normal C57BL/6 mice. PECs were composed primarily of macrophages in B-cell-deficient mice and of macrophages plus B cells in normal C57BL/6 mice. To determine which cells in PECs from C57BL/6 mice carry latent gammaHV68, we developed a limiting-dilution PCR assay to quantitate the frequency of cells carrying the gammaHV68 genome in fluorescence-activated cell sorter-purified cell populations. We also quantitated the contribution of individual cell populations to the total frequency of cells carrying latent gammaHV68. At early times after infection, the frequency of PECs that reactivated gammaHV68 correlated very closely with the frequency of PECs carrying the gammaHV68 genome, validating measurement of the frequency of viral-genome-positive cells as a measure of latency in this cell population. F4/80-positive macrophage-enriched, lymphocyte-depleted PECs harbored most of the gammaHV68 genome and efficiently reactivated gammaHV68, while CD19-positive, B-cell-enriched PECs harbored about a 10-fold lower frequency of gammaHV68 genome-positive cells. CD4-positive, T-cell-enriched PECs contained only a very low frequency of gammaHV68 genome-positive cells, consistent with previous analyses indicating that T cells are not a reservoir for gammaHV68 latency (N. P. Sunil-Chandra, S. Efstathiou, and A. A. Nash, J. Gen. Virol. 73:3275-3279, 1992). Since macrophages are bone marrow derived, we determined whether elicitation of a large inflammatory response in the peritoneum would recruit additional latent cells into the peritoneum. Thioglycolate inoculation increased the total number of PECs by about 20-fold but did not affect the frequency of cells that reactivate gammaHV68, consistent with a bone marrow reservoir for latent gammaHV68. These experiments demonstrate gammaHV68 latency in two different hematopoietic cell types, F4/80-positive macrophages and CD19-positive B cells, and argue for a bone marrow reservoir for latent gammaHV68.  (+info)

Role for gamma interferon in control of herpes simplex virus type 1 reactivation. (8/2054)

Observation of chronic inflammatory cells and associated high-level gamma interferon (IFN-gamma) production in ganglia during herpes simplex type 1 (HSV-1) latent infection in mice (E. M. Cantin, D. R. Hinton, J. Chen, and H. Openshaw, J. Virol. 69:4898-4905, 1995) prompted studies to determine a role of IFN-gamma in maintaining latency. Mice lacking IFN-gamma (GKO mice) or the IFN-gamma receptor (RGKO mice) were inoculated with HSV-1, and the course of the infection was compared with that in IFN-gamma-competent mice with the same genetic background (129/Sv//Ev mice). A time course study showed no significant difference in trigeminal ganglionic viral titers or the timing of establishment of latency. Spontaneous reactivation resulting in infectious virus in the ganglion did not occur during latency in any of the mice. However, 24 h after the application of hyperthermic stress to mice, HSV-1 antigens were detected in multiple neurons in the null mutant mice but in only a single neuron in the 129/Sv//Ev control mice. Mononuclear inflammatory cells clustered tightly around these reactivating neurons, and by 48 h, immunostaining was present in satellite cells as well. The incidence of hyperthermia-induced reactivation as determined by recovery of infectious virus from ganglia was significantly higher in the null mutant than in control mice: 11% in 129/Sv//Ev controls, 50% in GKO mice (P = 0.0002), and 33% in RGKO mice (P = 0.03). We concluded that IFN-gamma is not involved in the induction of reactivation but rather contributes to rapid suppression of HSV once it is reactivated.  (+info)

After replication at sites of initial inoculation, herpes simplex virus type 1 and 2 (HSV-1 and HSV-2) establish lifelong latent infections of the sensory and autonomic neurons of the ganglia serving those sites. Periodically, the virus reactivates from these neurons, and travels centripetally along the neuronal axon to cause recurrent epithelial infection. The major clinically observed difference between infections with herpes simplex virus type 1 and type 2 is the anatomic site specificity of recurrence. HSV-1 reactivates most efficiently and frequently from trigeminal ganglia, causing recurrent ocular and oral-facial lesions, while HSV-2 reactivates primarily from sacral ganglia causing recurrent genital lesions. An intertypic recombinant virus was constructed and evaluated in animal models of recurrent ocular and genital herpes. Substitution of a 2.8-kbp region from the HSV-1 latency-associated transcript (LAT) for native HSV-2 sequences caused HSV-2 to reactivate with an HSV-1 phenotype in ...
Antibodies for proteins involved in establishment of integrated proviral latency pathways, according to their Panther/Gene Ontology Classification
Viruses that infect the nervous system may cause acute, chronic or latent infections. Despite the so-called immunoprivileged status of the nervous system, immunosurveillance plays an important role in the fate of viral infection of the brain. Herpes simplex virus 1 (HSV-1) persists in the nervous system for the life of the host with periodic stress induced reactivation that produces progeny viruses. Prevention of reactivation requires a complex interplay between virus neurons, and immune response. New evidence supports the view that CD8+T cells employing both lytic granule- and IFN-gamma-dependent effectors are essential in setting up and maintaining HSV-1 latency. HSV-1 infection of the nervous system can be seen as a parasitic invasion which leaves the individual at risk for subsequent reactivation and disease. The recent observation that herpes virus latency may confer protection against experimental bacterial infection suggests that unexpected symbiosis may exist between latent viruses and the
Despite successful control of HIV replication in patients receiving HAART, the prolonged life span and slow rate of decay of latently infected CD4+ T cells provide a long-lasting cellular reservoir for HIV (8, 10, 15, 45). Indeed, independent projections estimate the time required to fully eliminate HIV in patients on completely suppressive HAART alone to be 10 to 60 years (9, 15, 16, 52). Latently infected resting memory CD4+ T cells contain integrated DNA provirus yet are transcriptionally inactive and may therefore escape both immune recognition and the antiviral effects of HAART regimes which affect only viral RNA species (10). Since current therapies for HIV are ineffective in eradicating latently infected cell populations, control of these populations depends on the interplay of cellular half-life and the ability to suppress viral replication in order to prevent repopulation of the latent reservoir (25). The importance of this reservoir (17) is underscored by observations of viral rebound ...
In response to numerous signals, latent herpesvirus genomes abruptly switch their developmental program, aborting stable host-cell colonization in favor of productive viral replication that ultimately destroys the cell. To achieve a rapid gene expression transition, newly minted capped, polyadenylated viral mRNAs must engage and reprogram the cellular translational apparatus. While transcriptional responses of viral genomes undergoing lytic reactivation have been amply documented, roles for cellular translational control pathways in enabling the latent-lytic switch have not been described. Using PEL-derived B-cells naturally infected with KSHV as a model, we define efficient reactivation conditions and demonstrate that reactivation substantially changes the protein synthesis profile. New polypeptide synthesis correlates with 4E-BP1 translational repressor inactivation, nuclear PABP accumulation, eIF4F assembly, and phosphorylation of the cap-binding protein eIF4E by Mnk1. Significantly, ...
HIV Latency Project, part of the genomics of gene regulation project at the University of Massachusetts Medical School, Our goal is to develop precise nucleases that will permit the targeted inactivation of latent HIV-1 provirus in patients.
CTD kinases are critical for the elongation of HIV transcription and co-transcriptional processing of viral transcripts. They function after chromatin remodelin...
The state of latency occurs when a microbes persistence in a host produces host damage without perturbing homeostasis sufficiently to cause clinical symptoms or disease. The mechanisms contributing to latency are diverse and depend on the nature of both the microbe and the host. Latency has advantages for both host and microbe. The host avoids progressive damage caused by interaction with the microbe that may translate into disease, and the microbe secures a stable niche in which to survive. Latency is clinically important because some latent microbes can be transmitted to other hosts, and it is associated with a risk for recrudescent microbial growth and development of disease. In addition, it can predispose the host to other diseases, such as malignancies. Hence, latency is a temporally unstable state with an eventual outcome that mainly depends on host immunity. Latency is an integral part of the pathogenic strategies of microbes that require human (and/or mammalian) hosts, including ...
High -Fidelity Latency Measurements in Low -Latency Networks. Ramana Rao Kompella Myungjin Lee (Purdue), Nick Duffield (AT&T Labs - Research). Low Latency Applications. Many important data center applications require low end-to-end latencies ( microseconds ) Slideshow 2187781 by nike
Luna Innovations (LUNA) surged in morning trading Tuesday off the strength of Rada Electronic Industries (RADA), which reported second-quarter earnings Monday.
Researchers at the University of Pittsburgh have come up with a more cost- and time-effective test that detects hidden HIV more accurately.
Hi this is Luna our cozy cat. She is born the 30th of August and with us since the 1st of Decemb… Jeroen van Hoeven needs your support for Help Luna Fight FIP
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I dont know If this topic was picked before, but giving a look at old threads something came to my mind. We all know this game is ruled by TEs, and luna is
HIV cure researchers seek out markers that would allow the specific targeting of cells harboring latent HIV. Enter a new candidate: interferon-induced ...
Human cytomegalovirus (HCMV) is a frequent cause of major disease following primary infection or reactivation from latency in immunocompromised patients. Infection of non-permissive mononuclear cells is used for analyses of HCMV latency in vitro. Using this approach, it is shown here that repression of lytic gene expression following experimental infection of CD34+ cells, a site of HCMV latency in vivo, correlates with recruitment of repressive chromatin around the major immediate-early promoter (MIEP). Furthermore, long-term culture of CD34+ cells results in carriage of viral genomes in which the MIEP remains associated with transcriptionally repressive chromatin. Finally, specific differentiation of long-term cultures of infected CD34+ cells to mature dendritic cells results in acetylation of histones bound to the MIEP, concomitant loss of heterochromatin protein 1 and the reactivation of HCMV. These data are consistent with ex vivo analyses of latency and may provide a model for further analyses of
Viruses that establish lifelong latent infections must ensure that the viral genome is maintained within the latently infected cell throughout the life of the host, yet at the same time must also be capable of avoiding elimination by the immune surveillance system. Gammaherpesviruses, which include the human viruses Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus, establish latent infections in lymphocytes. Infection of this dynamic host-cell population requires that the viruses have appropriate strategies for enabling the viral genome to persist while these cells go through rounds of mitosis, but at the same time must avoid detection by host CD8+ cytotoxic T lymphocytes (CTLs). The majority of gammaherpesviruses studied have been found to encode a specific protein that is critical for maintenance of the viral genome within latently infected cells. This protein is termed the genome maintenance protein (GMP). Due to its vital role in long-term latency, this offers the immune system a
Resting CD4 cells (or other cells) that are infected with HIV but not actively producing HIV. Latent HIV reservoirs are established during the earliest stage of HIV infection. Although antiretroviral therapy (ART) can reduce the level of HIV in the blood to an undetectable level, latent reservoirs of HIV continue to survive. When a latently infected cell is reactivated, the cell begins to produce HIV again. Although ART can suppress HIV levels, ART cannot eliminate latent HIV reservoirs. For this reason, ART cannot cure HIV infection.
Despite antiretroviral therapy (ART) which halts HIV-1 replication and reduces plasma viral load to clinically undetectable levels, viral rebound inevitably occurs once ART is interrupted. HIV-1-infected cells can undergo clonal expansion, and these clonally expanded cells increase over time. Over 50% of latent reservoirs are maintained through clonal expansion. The clonally expanding HIV-1-infected cells, both in the blood and in the lymphoid tissues, contribute to viral rebound. The major drivers of clonal expansion of HIV-1-infected cells include antigen-driven proliferation, homeostatic proliferation and HIV-1 integration site-dependent proliferation. Here, we reviewed how viral, immunologic and genomic factors contribute to clonal expansion of HIV-1-infected cells, and how clonal expansion shapes the HIV-1 latent reservoir. Antigen-specific CD4+ T cells specific for different pathogens have different clonal expansion dynamics, depending on antigen exposure, cytokine profiles and exhaustion
Novirin hits the online market and becomes available on April 21, 2014. Both Novirin and Gene-Eden-VIR help the immune system target latent viruses, and reduce symptoms of latent viral infections with the Herpes (HSV), Human Papillomavirus (HPV), Hepatitis B and C (HBV and HCV), the Epstein Barr Virus (EBV), and the Human Cytomegalovirus (CMV) viruses. Individuals who suffer from an infection with one or more of these viruses can order Novirin at, and Gene-Eden-VIR at, ...
Alphaherpesviruses. HSV-1, HSV-2, and VZV establish latency in nonreplicating cells (neurons), where the viral genome circularizes to form an episome. These viruses express only a few RNA transcripts, none of which are translated during latency. Since neurons do not divide, it is not necessary to express a viral protein to tether the viral genome to chromosomes during cell division of latently infected cells.. The primary HSV-1 latency-associated transcript (LAT) is an approximately 8.3-kb long noncoding RNA that is spliced to form stable 2.0 and 1.5 introns with lariat structures (9). The LAT has a neuron-specific enhancer that promotes its expression in the nucleus of latently infected cells. Multiple functions have been attributed to LAT in regulation of viral latency. The two LAT introns are expressed antisense to the HSV ICP0 immediate-early gene. Deleting the LAT from HSV reduces the frequency of reactivation (10, 11), and replacing the HSV-2 LAT with the HSV-1 LAT results in HSV-2 with a ...
Background: Efforts to disrupt the establishment and maintenance of the latent reservoir have focused on the shock-and-kill therapeutic approach to reverse HIV latency from CD4+ T cells with subsequent killing of the infected cells. The X-linked inhibitor of apoptosis protein (XIAP) is up regulated in latently infected cell lines. In this study, we investigated whether this molecular signature existed in primary latently-infected resting central memory CD4+ T cells and whether this could be used to selectively target and kill latent HIV harboring cells.. Methods: CCL19-treated naïve CD4+ T cells isolated from HIV-uninfected donors were infected with HIV then expanded in the presence of IL2 for 12 d. Memory CD4+ T cells were then isolated and cultured in the presence of IL7 for a further 20 d then analyzed by flow cytometry. HIV integration was analyzed by Alu-LTR qPCR. Expression of XIAP was assessed using Western blotting. HIV p24 antigen was quantified by ELISA. Long-lived, resting memory ...
The major barrier to a HIV-1 cure is the persistence of latent genomes despite treatment with antiretrovirals. To investigate host factors which promote HIV-1 latency, we conducted a genome-wide functional knockout screen using CRISPR-Cas9 in a HIV-1 latency cell line model. This screen identified I …
View Notes - 1385953320_755__Lecture%252B31_HIV%252Blatency%252Band%252Bcure (1) from MBB 322 at Simon Fraser. Lecture 31: Dec 2 HIV latency and eradica6on Integra6on is an essen6al
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The presence of endogenous oncornavirus and herpesvirus in guinea pigs has been established. The oncornavirus apparently is present in all guinea pigs but is expressed only under certain conditions. Expression of the latent herpesvirus is generally age and strain dependent as is the development of spontaneous guinea pig leukemia. Following special laboratory manipulation, expression of both virus types was accomplished in vitro. Studies of the role played by these two virus types in the development of neoplastic disease in guinea pigs revealed that, in the presence of the endogenous oncornavirus, a superinfection with herpesvirus led to the development of self-limited lymphoproliferative changes. Together with the studies reported by other investigators, it appears that interaction between the DNA and RNA viruses may play an important role in the natural occurrence of viral oncogenesis. Guinea pigs provide an intriguing animal model for the study of herpesvirus and oncornavirus interaction both ...
The experiments outlined in this study present evidence for an intracellular compartment in macrophages into which HIV‐1 virions assemble and in which virions retain infectivity for extended intervals. Although infectious virions were sequestered intracellularly at low levels, these results have important implications regarding reservoirs for viral persistence. Because of the efficiency of viral dissemination in trans and the replicative capacity of the virus, low levels of intracellular infectious virus may ignite viral replication upon transmission to lymphocytes (Carr et al, 1999). By analogy, DCs can capture extracellular virions and, even though at undetectable levels, captured virions can initiate a vigorous infection upon dissemination to lymphocytes (Cameron et al, 1992). Furthermore, rare latent proviruses ignite efficient replication upon reactivation from latency (Kieffer et al, 2004). While such mechanisms may have a minor contributing role to cumulative virus burden in highly ...
Exchange servers should generally have database write latencies under 20 ms, with spikes (maximum values) under 50 ms. However, it is not always possible to keep write latencies in this range when synchronous replication is in use. Database write latency issues often do not become apparent to the end user until the database cache is full and cannot be written to. When using synchronous replication, the Performance Monitor Database Page Fault Stalls/sec counter is a better indicator of whether the client is being affected by write latency than the PhysicalDisk\Average Disk sec/Write counter. On a production server, the value of the Database Page Fault Stalls/sec counter should always be zero, because a database page fault stall indicates that the database cache is full. A full database cache means that Exchange is unable to place items in cache until pages are committed to disk. Moreover, on most storage subsystems, read latencies are affected by write latencies. These read latencies may not be ...
In a new study published in Nature today, Dan H. Barouch, MD, PhD, Director of the Center for Virology and Vaccine Research at BIDMC, and colleagues demonstrate that administering broadly neutralizing antibodies (bNAb) designed to target HIV in combination with agents that stimulate the innate immune system delayed viral rebound following discontinuation of ART in monkeys. The findings suggest that this two-pronged approach represents a potential strategy for targeting the viral reservoir.
Although highly active retroviral therapy (HAART) dramatically reduces viral load and restores CD4 T-cell counts in HIV-infected individuals, its success is ham...
Latent viruses replicate on a small scale even when they are not reactivated. This is something overlooked by many in the medical field today. As stated by Dr. Hanan Polansky, the latent EBV virus microcompetes with human genes for limited genetic resources, and as a result, can drive the human genes to malfunction, and cause disease ...
Gil Tene explains latency and how it relates to service and response times, measuring latency, common misconceptions about latency, what to do when a systems latency cant meet SLAs, and much more.
I write about whats new in virology from the molecular biology point of view, covering topics such as human papiloma virus, hepatitis C, herpes simplex, and other viruses, especially those occurring in the body in a latent state. Read more ...
This MATLAB function returns filtered state probabilities FS from conducting optimal conditional inference of the probabilities of the operative latent states in the regime-switching data Y.
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This is something thats come up often as I talk to people about my Honours project. Why cant we cure HIV? Its been around since the 50s, although it was only identified in 1983. Whats going on? Early on during infection, HIV establishes something called the latent reservoir. Whats that? That is the reason we…
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FINZI INFECTION LATENT LIFELONG MECHANISM PDF - Thus, latent infection of resting CD4+ T cells provides a mechanism for lifelong persistence of HIV-1, even in patients on effective anti-retroviral
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The latency-associated nuclear antigen (LANA) of Kaposis sarcoma-associated herpesvirus functions as an origin-binding protein (OBP) and transcriptional regulator. LANA binds the terminal repeats via the C-terminal DNA-binding domain (DBD) to support latent DNA replication. To date, the structure of LANA has not been solved. Sequence alignments among OBPs of gammaherpesviruses have revealed that the C terminus of LANA is structurally related to EBNA1, the OBP of Epstein-Barr virus. Based on secondary structure predictions for LANA(DBD) and published structures of EBNA1(DBD), this study used bioinformatics tools to model a putative structure for LANA(DBD) bound to DNA. To validate the predicted model, 38 mutants targeting the most conserved motifs, namely three alpha-helices and a conserved proline loop, were constructed and functionally tested. In agreement with data for EBNA1, residues in helices 1 and 2 mainly contributed to sequence-specific DNA binding and replication activity, whilst ...
The life cycle of Kaposis sarcoma-associated herpesvirus (KSHV) consists of two phases, latent and lytic. The virus establishes latency as a strategy for avoiding host immune surveillance and fusing symbiotically with the host for lifetime persistent infection. However, latency can be disrupted and KSHV is reactivated for entry into the lytic replication. Viral lytic replication is crucial for efficient dissemination from its long-term reservoir to the sites of disease and for the spread of the virus to new hosts. The balance of these two phases in the KSHV life cycle is important for both the virus and the host and control of the switch between these two phases is extremely complex. Various environmental factors such as oxidative stress, hypoxia, and certain chemicals have been shown to switch KSHV from latency to lytic reactivation. Immunosuppression, unbalanced inflammatory cytokines, and other viral co-infections also lead to the reactivation of KSHV. This review article summarizes the current
The novelty of our comprehensive study is the demonstration for the first time that a proinflammatory lipid metabolite, such as PGE2 and its receptors, plays a crucial role in herpes virus latency. Previous reports have indicated the role of Ca2+ in KSHV lytic cycle (17-20). In contrast, our studies showing the downregulation of LANA-1 expression by EP1 receptor antagonist, the blockage of supernatant-induced [Ca2+]i signal by EP1 antagonist, and the downregulation of PGE2-induced LANA-1 promoter activity by calcium chelators are the first demonstration of a role for [Ca2+]i in KSHV latency program. Unlike calcium, previous reports have shown the role of Src, PI3K, PKCζ/λ, and NF-κB in KSHV latency program (21-23). However, the novelty of our study is that the data linking PGE2/EP receptors with KSHV LANA-1 expression and LANA-1 promoter through PGE2 via Src, PI3K, PKCζ/λ, and NF-κB signal induction provides a new framework to understand the host mechanisms used by KSHV to induce these ...
Human cytomegalovirus (HCMV) latency is typically harmless but reactivation can be largely detrimental to immune compromised hosts. We modeled latency and reactivation using a traceable HCMV laboratory strain expressing the Gaussia luciferase reporter gene (HCMV/GLuc) in order to interrogate the viral modulatory effects on the human adaptive immunity. Humanized mice with long-term (more than 17 weeks) steady human T and B cell immune reconstitutions were infected with HCMV/GLuc and 7 weeks later were further treated with granulocyte-colony stimulating factor (G-CSF) to induce viral reactivations. Whole body bio-luminescence imaging analyses clearly differentiated mice with latent viral infections vs. reactivations. Foci of vigorous viral reactivations were detectable in liver, lymph nodes and salivary glands. The number of viral genome copies in various tissues increased upon reactivations and were detectable in sorted human CD14+, CD169+, and CD34+ cells. Compared with non-infected controls, ...
Major human pathologies are caused by nuclear replicative viruses establishing life-long latent infection in their host. During latency the genomes of these viruses are intimately interacting with the cell nucleus environment. A hallmark of herpes simplex virus type 1 (HSV-1) latency establishment is the shutdown of lytic genes expression and the concomitant induction of the latency associated (LAT) transcripts. Although the setting up and the maintenance of the latent genetic program is most likely dependent on a subtle interplay between viral and nuclear factors, this remains uninvestigated. Combining the use of in situ fluorescent-based approaches and high-resolution microscopic analysis, we show that HSV-1 genomes adopt specific nuclear patterns in sensory neurons of latently infected mice (28 days post-inoculation, d.p.i.). Latent HSV-1 genomes display two major patterns, called Single and Multiple, which associate with centromeres, and with promyelocytic leukemia nuclear bodies ...
Chick embryo tissues maintained for from 11 to 28 days in Hanks balanced salt solution lost their capacity to support the multiplication of psittacosis virus.
TY - JOUR. T1 - Barriers for HIV Cure. T2 - The Latent Reservoir. AU - Castro-Gonzalez, Sergio. AU - Colomer-Lluch, Marta. AU - Serra-Moreno, Ruth. N1 - Publisher Copyright: © Copyright 2018, Mary Ann Liebert, Inc., publishers 2018.. PY - 2018/9. Y1 - 2018/9. N2 - Thirty-five years after the identification of HIV-1 as the causative agent of AIDS, we are still in search of vaccines and treatments to eradicate this devastating infectious disease. Progress has been made in understanding the molecular pathogenesis of this infection, which has been crucial for the development of the current therapy regimens. However, despite their efficacy at limiting active viral replication, these drugs are unable to purge the latent reservoir: a pool of cells that harbor transcriptionally inactive, but replication-competent HIV-1 proviruses, and that represent the main barrier to eradicate HIV-1 from affected individuals. In this review, we discuss advances in the field that have allowed a better understanding of ...
In this paper we have verified a key tenet of the GC model of EBV persistence by showing for the first time that EBV-infected cells expressing the default latency transcription program are physically located in GCs and express functional markers, homing receptors, and the phenotypic markers of GC cells. These experiments further demonstrate that EBV can reside latently within GC cells in vivo without imposing the growth latency transcription program and the lymphoblastoid form of latency. What distinguishes infected GC cells in vivo is expression of the viral default latency transcription program which, unlike the growth latency program, appears to be fully consistent with retention of GC function. Since direct infection of GC cells in vitro (43) or in vivo (26) produces the growth latency program and obliterates the GC phenotype, it follows that the latently infected GC cells we have described in vivo cannot arise through direct infection and must be derived by another mechanism, i.e., ...
Throughout the process of virus-host coevolution, herpesviruses have developed an array of immunomodulatory mechanisms to avoid detection and destruction by the hosts immune system. Although loss of immune control can lead to herpesvirus reactivation from latency and result in serious disease (2, 3, 4), delayed primary infection with herpesviruses in affluent societies (1, 2) coincides with higher incidence of allergic disorders (32), which in contrast indicates a beneficial role for these viruses.. In connection with this, our group has previously reported an inverse association between EBV seropositivity and IgE sensitization in 2-year-old children (25). Recent observations from our laboratory did not provide support for a Th1-biased cytokine profile in EBV SP children (26), which could have explained the protection against the allergic phenotype (32, 33). However, latent herpesvirus infections in mice result in potentiated innate activity and increased systemic IFN-γ levels (29). To ...
Reason for review Renewed interest provides emerged to handle the latent reservoir of HIV to attain a cure. remove latently contaminated cells is as well primitive to attain a treat without a lot of preliminary research to elucidate a few of these areas. Overview A resurgence appealing in latent an infection and its own treatment promises improvement in Mctp1 addressing the task of a remedy, although realistically this will demand a prolonged amount of investigation in lots of areas. and continues to be. With only one 1 within a million Compact disc4+ T cells latently contaminated around, many reports of can only just be conducted with cell culture choices latency. Will a latency model within a proliferating cell series using a molecular build reveal a latent provirus within a principal Compact disc4+ lymphocyte thats not turned on or dividing? Few models of latency have been developed in main human CD4+ lymphocytes using infectious HIV-1. Do these models, in which main CD4 lymphocytes can only ...
Types of Cytomegalovirus Latency Cell culture choices possess reinforced the part from the cellular differentiation state in the maintenance of CMV latency-reactivation balance. Recent years have seen a focus on the role of the cellular environment in dictating outcome. Only a small proportion (10?4 to 10?5) of total bone marrow-derived myelomonocytic cells naturally support CMV latency (4); thus, these models are critical to provide clues into natural persistence and latency (5C10). Precursors of DCs harbor latent infection, and once terminally differentiated into mature antigen-presenting cells, they support reactivation and viral persistent replication (11, 12). Furthermore, the differentiation pathways that lead to reactivation depend on the inflammatory environment and also likely stimulate the adaptive T-cell response to viral infection. The virus confronts the host by constraining and corralling the potency of the blockquote course=pullquote The key areas of the stand-off between human ...
Overcoming HIV latency - induction of HIV in CD4+ T cells that lay dormant throughout the body - is a major step toward creating a cure for HIV. For the first time, scientists at UNC-Chapel Hill, Emory University, and Qura Therapeutics - a partnership between UNC and ViiV Healthcare - have shown that a new approach can expose latent HIV to attack in two different animal model systems with little or no toxicity. Researchers Reverse HIV Latency, Important Scientific Step Toward Cure - Read More… ...
Still, much more work needs to be done before this work could be applied to AIDS patients. Curing patients of HIV infection is a very difficult task as it requires eliminating all latent reservoirs. While the researchers show that they can detect successful cutting of the latent provirus in various cell types, they do not show evidence that their therapy removes all proviruses or that their delivery system can target all cells that may be harboring the latent HIV reservoirs. It will likely be very difficult for the researchers method to eliminate 100% of the virus, and testing the ability of their delivery method to target all infected cells will be particularly difficult as mouse models of HIV may not harbor the same types of reservoirs present in humans. Still, the research represents an important step forward in developing CRISPR technology into a potential cure for HIV ...
Every day Verisign processes upwards of 100 billion authoritative DNS requests for .COM and .NET from all corners of the earth. The vast majority of these requests are via the UDP protocol. Because UDP is connectionless, it is impossible to passively estimate the latency of the UDP-based requests. A very small percentage of these requests though, are over TCP, thus providing the means to estimate the latency of specific requests and paths for a subset of the hosts that interact with Verisigns network infrastructure.. In this work, we combine this relatively small number of datapoints from TCP (on the order of a few hundred million per day) with the much larger dataset of all DNS requests. Our focus is the process of data analysis of real world, imperfect data at very large scale with the goals of understanding network latency at an unprecedented magnitude, identifying large volume, high latency clients and improving their latency. We discuss the techniques we used for data selection and ...
Spina CA, Anderson J, Archin NM, Bosque A, Chan J, Famiglietti M, Greene WC, Kashuba A, Lewin SR, Margolis DM, Mau M, Ruelas D, Saleh S, Shirakawa K, Siliciano RF, Singhania A, Soto PC, Terry VH, Verdin E, Woelk C, Wooden S, Xing S, Planelles V
The persistence of latently human immunodeficiency virus-1 (HIV-1) infected cellular reservoirs in resting CD4+ T cells is a major obstacle to HIV-1 eradication. The detailed mechanism of HIV-1 latency remains unclear. We investigated histones and th
Researchers at the University of North Carolina identified a better dosing strategy for a drug that exposes HIV hiding inside the bodys viral reservoir, ...
Figure 7 - Layer 3 RFC 3918 2-to-46 multicast 49.9% load test. Weve heard some vendors try to emphasize the two source multicast test to point out a supposed weakness of the Nexus 3548. Its important to understand that any switch from any vendor would exhibit an increase in latency with this test in both synchronous and asynchronous mode.. Last, weve seen customers encounter higher than expected latency when performing 100% line rate testing using a traffic generator. In these cases, weve found clocking differences between the traffic generator and the switch causes the issue - the internal system clock of the traffic generator and the switch are not always in sync. The difference between these clocks could be + or -100 PPM per the 10 Gigabit Ethernet standard. In cases where the traffic generator port is clocked slightly higher than the switch, at 100% line rate traffic will be buffered at the egress port, introducing latency. In the opposite case, when the switch is clocked slightly higher ...
While a cure for HIV remains elusive, new research suggests that eliminating HIV from the reservoirs where the virus persists is possible.
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Background: Interferon-α (IFN-α) treatment suppresses HIV-1 viremia and reduces the size of the HIV-1 latent reservoir. Therefore, investigation of the molecular and immunologic effects of IFN-α may provide insights that contribute to the development of ...
Background: Interferon-α (IFN-α) treatment suppresses HIV-1 viremia and reduces the size of the HIV-1 latent reservoir. Therefore, investigation of the molecular and immunologic effects of IFN-α may provide insights that contribute to the development of ...
Xylon today announced a reference design for a real-time video rotation for an arbitrary angle, which can be dynamically changed in sub-degree steps. The video rotation works with a video output latency that can be as low as one frame time.
Trial Team members review FOREO LUNA 3. Read the reviews to find out how our Trial Team rated this multi-tasking skincare tool....
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Scientists at the Gladstone Institutes discovered that an enzyme called SMYD2 could be a new therapeutic target for flushing out the HIV that hides in infected individuals. Overcoming this latent virus remains the most significant ...
A team of researchers from the University of California, Davis (UC Davis), recently tested if idiopathic headshaking in horses could be similar to a condition in humans--trigeminal nerve pain caused by the reactivation of a latent virus.
Replication of HIV within the CNS continues to be a hot topic, because it represents a viral reservoir that can complicate treatment, as well as control and prevention efforts.
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"Virus latency". ViralZone. Swiss Institute of Bioinformatics. Retrieved 15 June 2020. Keen EC (January 2015). "A century of ... As all viruses in the realm are double-stranded DNA (dsDNA) viruses, the realm belongs to Group I: dsDNA viruses of Baltimore ... fold MCP viruses, and the suffix -virae, which is the suffix used for virus kingdoms. All viruses in Duplodnaviria contain a ... While viruses in Duplodnaviria make use of the HK97 fold for their major capsid proteins, the major capsid proteins of viruses ...
Regardless of this, the virus enters a latency phase and the infected individual becomes a lifetime asymptomatic carrier of EBV ... Houldcroft CJ, Kellam P (March 2015). "Host genetics of Epstein-Barr virus infection, latency and disease". Reviews in Medical ... It seems likely that the virus acts similarly to cause IVNK/TL. IVNK/TL may differ from the other types of NK- and T-cell ... Since infection with this virus is rarely seen in IVBCL, this form of IVL is not typically regarded as one of the Epstein-Barr ...
Hurley EA, Thorley-Lawson DA (December 1988). "B cell activation and the establishment of Epstein-Barr virus latency". The ...
CS1 maint: discouraged parameter (link) Persaud, Deborah (2003). "Latency in human immunodeficiency virus type 1 infection: No ... Persaud and her research team found that viremia persists in children with plasma virus remaining at a level under the limit of ... In 2003, she stated about the Human Immunodeficiency Virus (HIV)- type1 included in the subtypes of HIV. For the HIV patient, ... In 2009, her research team focused on the ongoing human immunodeficiency virus type 1 (HIV-1). From this research, it was ...
In contrast to the herpes simplex virus, the latency of VZV is poorly understood. The virus has never been successfully ... Mitchell BM, Bloom DC, Cohrs RJ, Gilden DH, Kennedy PG (2003). "Herpes simplex virus-1 and varicella-zoster virus latency in ... Varicella zoster virus is not the same as herpes simplex virus; however, they belong to the same family of viruses. The ... Virus-specific proteins continue to be made by the infected cells during the latent period, so true latency, as opposed to ...
Amon, Wolfgang; Farrell, Paul J. (2005-05-01). "Reactivation of Epstein-Barr virus from latency". Reviews in Medical Virology. ... Simian immunodeficiency virus (SIV), a virus similar to HIV, is capable of infecting primates. The Epstein-Barr virus (EBV) is ... When the virus is able to use the cell to replicate its genetic information, the virus can spread infection throughout the body ... If a host cell expresses the complementary surface receptor for the virus, then the virus can attach and enter the cell. If a ...
Bet hedging has been used to explain the latency of Herpes viruses. The Varicella Zoster Virus, for instance, causes chickenpox ... Stumpf, Michael P. H.; Laidlaw, Zoe; Jansen, Vincent A. A. (2002). "Herpes Viruses Hedge Their Bets". Proceedings of the ...
... establish latency (site where virus lies dormant until reactivated) in leukocytes. This is different from ... "Virus Taxonomy: 2019 Release". International Committee on Taxonomy of Viruses. Retrieved 9 May 2020. Adams ... The virus exits the host cell by nuclear egress, and budding. Mammals serve as the natural host. Transmission routes are ... Both human herpesvirus 6B (HHV-6B) and human herpesvirus 7 (HHV-7), as well as other viruses, can cause a skin condition in ...
... inhibitors may modulate the latency of some viruses, resulting in reactivation. This has been shown to ... Arbuckle JH, Medveczky PG (Aug 2011). "The molecular biology of human herpesvirus-6 latency and telomere integration". Microbes ...
Zhang L, Pagano JS (October 1997). "IRF-7, a new interferon regulatory factor associated with Epstein-Barr virus latency". ... IRF7 has been shown to play a role in the transcriptional activation of virus-inducible cellular genes, including the type I ... Smith EJ, Marié I, Prakash A, García-Sastre A, Levy DE (March 2001). "IRF3 and IRF7 phosphorylation in virus-infected cells ... Lin R, Noyce RS, Collins SE, Everett RD, Mossman KL (February 2004). "The herpes simplex virus ICP0 RING finger domain inhibits ...
HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated ... For the virus that causes herpes simplex, see Herpes simplex virus. For all types of herpes viruses, see Herpesviridae. ... "Helping You With Herpes - Herpes Viruses Association". Herpes Viruses Association. Archived from the original on 2015-07-26. ... Laboratory tests include culture of the virus, direct fluorescent antibody (DFA) studies to detect virus, skin biopsy, and ...
"Signal Transduction and Transcription Factor Modification during Reactivation of Epstein-Barr Virus from Latency". Journal of ...
The RNA transcript is produced by the virus and accumulates in host cells during latent infection; it is known as Latency ... encoded by the DNA of herpes viruses. It is produced by herpes viruses during the earliest stage of infection, when the virus ... "Pseudorabies virus EPO is functionally homologous to varicella-zoster virus ORF61 protein and herpes simplex virus type 1 ICPO ... Ou Y, Davis KA, Traina-Dorge V, Gray WL (August 2007). "Simian varicella virus expresses a latency-associated transcript that ...
However, some viruses have evolved to twist this process to their own advantage by establishing latency. Latent proviral DNA ... Jung YJ, Choi H, Kim H, Lee SK (August 2014). "MicroRNA miR-BART20-5p stabilizes Epstein-Barr virus latency by directly ... Generally, the long-term latency of a mammalian virus is a dynamic interaction between it and the host cell's antiviral ... During latency, most viral genes are silenced, and infected individuals are asymptomatic. More importantly, during latency, ...
Even though they are not essential for lytic phases of the virus, these latency genes are important for promoting chronic ... Genes characteristic of this concept are those that control latency in some viruses like herpes. Murine gamma herpesvirus 68 ( ... Viruses also have notable virulence factors. Experimental research, for example, often focuses on creating environments that ... Virulence factors are molecules produced by bacteria, viruses, fungi, and protozoa that add to their effectiveness and enable ...
... in the maintenance of Epstein-Barr virus latency". The Journal of Biological Chemistry. 286 (25): 22007-16. doi:10.1074/jbc. ... JDP2 inhibits the promoter of the Epstein-Barr virus (EBV) immediate early gene BZLF1 for the regulation of the latent-lytic ...
The virus then enters a latency phase in which infected individuals become lifetime asymptomatic carriers of the virus in a set ... Epstein-Barr virus-positive plasmablastic lymphoma. The virus in infected plasmablastic cells appears to be in its latency I ... Lymphoma Epstein-Barr virus-associated lymphoproliferative diseases Chen BJ, Chuang SS (March 2020). "Lymphoid Neoplasms With ... The malignant plasmablasts in more than half the cases of PBL are infected with a potentially cancer-causing virus, Epstein ...
... beginning with the polyoma virus. They were able to culture this virus and examine its latency, resulting in another classic ... Vogt, M.; Dulbecco, R. (1960). "VIRUS-CELL INTERACTION WITH A TUMOR-PRODUCING VIRUS". Proc. Natl. Acad. Sci. U.S.A. 46 (3): 365 ... They were the first to successfully grow the virus in vitro and were able to plaque purify it, an essential step for subsequent ... They continued their work on tumor-causing viruses. However, their interests diverged, and in 1973, Vogt was appointed as a ...
Xing L, Kieff E (September 2007). "Epstein-Barr virus BHRF1 micro- and stable RNAs during latency III and after induction of ... The mir-BHRF1-3 microRNA precursor found in Human herpesvirus 4 (Epstein-Barr virus). In Epstein-Barr virus, mir-BHRF1-3 is ... with two other microRNAs also found in the Epstein-Barr virus genome. BHRF-3 has been shown to be expressed in latency-III ... "Identification of virus-encoded microRNAs". Science. 304 (5671): 734-6. doi:10.1126/science.1096781. PMID 15118162. Feederle R ...
... s have been recognized as regulators of viral latency processes in human immunodeficiency virus (HIV) infections. ... Also binds to a specific Brome Mosaic Virus, which is a plant-infecting RNA virus. TruD is able to modify a variety of RNA, and ... 1 transcription and escape from latency". EMBO Reports. 17 (10): 1441-1451. doi:10.15252/embr.201642682. ISSN 1469-221X. PMC ...
Xing L, Kieff E (September 2007). "Epstein-Barr virus BHRF1 micro- and stable RNAs during latency III and after induction of ... with two other microRNAs also found in the Epstein-Barr virus genome. BHRF-1-2 has been shown to be expressed in latency-III ... In Epstein-Barr virus, mir-BHRF1-2 is found in the 3' UTR of the BHRF1 (Bam HI fragment H rightward open reading frame 1) gene ... The mir-BHRF1-2 microRNA precursor found in human herpesvirus 4 (Epstein-Barr virus), cercopithicine herpesvirus 15 and ...
Only one other virus, Marek's disease virus, is known to achieve latency in this fashion. This phenomenon is possible as a ... HHV-6 has also been demonstrated to transactivate Epstein-Barr virus. Humans acquire the virus at an early age, some as early ... Electron microscopy revealed a novel virus that they named Human B-Lymphotrophic Virus (HBLV). Shortly after its discovery, ... Shiley, Kevin; Blumberg, Emily (2010). "Herpes Viruses in Transplant Recipients: HSV, VZV, Human Herpes Viruses, and EBV". ...
HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated ... Herpes simplex is a double-stranded DNA virus. Herpes simplex virus is divided into two types. However, each may cause ... Laboratory tests include culture of the virus, direct fluorescent antibody (DFA) studies to detect virus, skin biopsy, and ... "Helping You With Herpes - Herpes Viruses Association". Herpes Viruses Association. Archived from the original on 2015-07-26. ...
Cliffe, A. R.; Garber, D. A.; Knipe, D. M. (2009). "Transcription of the Herpes Simplex Virus Latency-Associated Transcript ... His work has shown that replication-defective viruses can serve as a genital herpes vaccine and as a vaccine vector-one of ... Da Costa, X. J.; Jones, C. A.; Knipe, D. M. (1999). "Immunization against genital herpes with a vaccine virus that has defects ... Wang, Q.-Y.; Zhou, C.; Johnson, K. E.; Colgrove, R. C.; Coen, D. M.; Knipe, D. M. (2005). "Herpesviral latency-associated ...
The longest period of detectable virus has been 11 days and Zika virus does not appear to establish latency. Later on, serology ... "Zika Virus". CDC. 5 November 2014. Retrieved 20 June 2019. "Symptoms, Diagnosis, & Treatment of Zika Virus". Zika Virus Home. ... Zika virus has been isolated from semen samples, with one person having 100,000 times more virus in semen than blood or urine, ... Zika virus is a mosquito-borne flavivirus closely related to the dengue and yellow fever viruses. While mosquitoes are the ...
"Famciclovir and valaciclovir differ in the prevention of herpes simplex virus type 1 latency in mice: a quantitative study". ... Use of famciclovir in this manner has been shown to reduce the amount of latent virus in the neural ganglia compared to no ... Neither drug affected latency if treatment was delayed for several months. Penciclovir Valaciclovir "Famciclovir". Merriam- ... Thackray AM, Field HJ (October 2000). "The effects of antiviral therapy on the distribution of herpes simplex virus type 1 to ...
"A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation". The Journal of General ... Healing (day 9-14): New skin begins to form underneath the scab as the virus retreats into latency. A series of scabs will form ... The virus moves from the mouth to remain latent in the central nervous system. In approximately one-third of people, the virus ... The cause is usually herpes simplex virus type 1 (HSV-1) and occasionally herpes simplex virus type 2 (HSV-2). The infection is ...
Weinberger and his lab are looking for ways to target the latency reservoir of viruses as a form of treatment. Weinberger's ... He is credited with discovering the HIV virus latency circuit, which provided the first experimental evidence that stochastic ... "Evolvable 'Resistance-Proof' Therapies". Cite journal requires ,journal= (help) "To Fight a Virus, Get a Virus: Military Bets ... between viruses and treatment: viruses evolve, vaccines do not. TIPs also have the capacity to transmit along viral ...
The virus then enters a latency phase in which the infected individual becomes a lifetime asymptomatic carrier of the virus. ... The neoplastic B-cells in these spaces carry the EBV virus in stage III latency (see EBV latency infections) and therefore ... Draborg A, Izarzugaza JM, Houen G (July 2016). "How compelling are the data for Epstein-Barr virus being a trigger for systemic ... Li ZX, Zeng S, Wu HX, Zhou Y (February 2019). "The risk of systemic lupus erythematosus associated with Epstein-Barr virus ...
The virus then enters a latency phase in which the infected individual becomes a lifetime asymptomatic carrier of the virus. ... One individual who had a FA-DLBCL removed from a subdural hematoma developed an Epstein-Barr virus-associated diffuse large B- ... Both diseases appear driven by EBV-infected (latency stage III), large, activated B-cells and develop in spaces known or ... FA-DLBCL is an Epstein-Barr virus-associated lymphoproliferative disease (EBV+ LPD), i.e. disease in which lymphocytes infected ...
Local replicas are also sometimes maintained for use while connected to the network in order to reduce network latency. ... This class includes server and client backup software, anti-spam and anti-virus products, and e-discovery and archiving systems ... Examples include spam and anti-virus products (e.g. Spam Sentinel), server administration and monitoring tools (e.g. RPRWyatt's ... to avoid virus propagation through Notes/Domino environments. Administrators can centrally control whether each mailbox user ...
Novel HIV-1-encoded microRNA have been found to enhance the production of the virus as well as activating HIV-1 latency by ... The TATA-binding protein (TBP) could also be targeted by viruses as a means of viral transcription.[6] ... MicroRNAs also play a role in replicating viruses such as HIV-1.[44] ...
Pawan JL (1959). "Rabies in the vampire bat of Trinidad, with special reference to the clinical course and the latency of ... David D, Yakobson B, Rotenberg D, Dveres N, Davidson I, Stram Y (2002). "Rabies virus detection by RT-PCR in decomposed ... "Transmission of rabies virus from an organ donor to four transplant recipients" (PDF). N Engl J Med. 352 (11): 1103-11. doi ...
... herpes simplex virus 1 (HSV-1) - herpes simplex virus 2 (HSV-2) - herpes varicella zoster virus (VZV) - herpes viruses - highly ... clinical latency - clinical practice guidelines - clinical trial - - cloning - CMS - CMV - CNS - co- ... human papilloma virus (HPV) - human T cell lymphotropic virus type I (HTLV-I) - human T cell lymphotropic virus type II (HTLV- ... human immunodeficiency virus type 1 (HIV-1) - human immunodeficiency virus type 2 (HIV-2) - human leukocyte antigens (HLA) - ...
Such viruses are either single stranded RNA (e.g. HIV) or double stranded DNA (e.g. Hepatitis B virus) viruses. ... Genus Betaretrovirus; type species: Mouse mammary tumour virus. *Genus Gammaretrovirus; type species: Murine leukemia virus; ... "Virus Taxonomy: 2018b Release" (html). International Committee on Taxonomy of Viruses (ICTV). March 2019. Retrieved 16 March ... Group VII viruses[edit]. Both families in Group VII have DNA genomes contained within the invading virus particles. The DNA ...
... computing/151498-researchers-create-fiber-network-that-operates-at-99-7-speed-of-light-smashes-speed-and-latency-records ...
The latency sites of APV-1 is similar to other herpesviruses. Vaccination for duck viral enteritis is now routine in the United ... Virus particles can be shed by the latent host in shared water or through direct contact (horizontal transmission), ... The clinical signs of DVE "vary with virulence of virus strain, species, sex, and immune system status" of the host. Due to the ... DVH-1 replicates in the mucus membranes of bird's esophagus and cloaca, the two primary entrances of the virus. The means of ...
In influenza viruses[edit]. In the influenza virus, the two relevant antigens are the surface proteins, hemagglutinin and ... Antigenic drift occurs in both influenza A and influenza B viruses.. The immune system recognizes viruses when antigens on the ... All influenza viruses experience some form of antigenic drift, but it is most pronounced in the influenza A virus. ... As in all RNA viruses, mutations in influenza occur frequently because the virus' RNA polymerase has no proofreading mechanism ...
A new virus has been described in fish - White sucker hepatitis B virus.[3] This is the first hepadnavirus described from fish ... "Virus Taxonomy: 2014 Release". Retrieved 15 June 2015.. *^ Hahn CM, Iwanowicz LR, Cornman RS, Conway CM, Winton JR, Blazer VS ( ... "Deciphering the Origin and Evolution of Hepatitis B Viruses by Means of a Family of Non-enveloped Fish Viruses". Cell Host & ... Endogenous hepatitis B virus genomes have been described in crocodilian, snake and turtle genomes.[7] This suggests that these ...
Like the other herpesviruses (Epstein Barr virus, varicella zoster virus, etc.), HHV-6 establishes lifelong latency and can ... Newly Found Herpes Virus Is Called Major Cause of Illness in Young, New York Times HHV-6 Foundation DermNet viral/roseola Virus ... The virus exits the host cell by nuclear egress, and budding. Humans serve as the natural host. Transmission routes are direct ... Human herpesvirus 6 (HHV-6) is a set of two closely related herpes viruses known as HHV-6A and HHV-6B that infect nearly all ...
Some viruses once acquired never leave the body. A typical example is the herpes virus, which tends to hide in nerves and ... "Herpesviruses: latency and reactivation - viral strategies and host response". Journal of Oral Microbiology. 5: 22766. doi ... Viruses are also usually identified using alternatives to growth in culture or animals. Some viruses may be grown in ... Pathogenic viruses. Pathogenic bacteria Pathophysiology[edit]. There is a general chain of events that applies to infections.[ ...
It may make sense to separate read latency and write latency (especially for non-volatile memory[8]) and in case of sequential ... "This Speck of DNA Contains a Movie, a Computer Virus, and an Amazon Gift Card". The Atlantic. Archived from the original on 3 ... Latency (access time) ~15ms (swift) ~150ms (moderate) None (instant) None (instant) Lack of random access (very slow) ... Latency. The time it takes to access a particular location in storage. The relevant unit of measurement is typically nanosecond ...
... such as miRNAs expressed by the herpes virus that may act as heterochromatin organization triggers to mediate viral latency.[94 ... Some viruses have evolved mechanisms for suppressing the RNAi response in their host cells, particularly for plant viruses.[81] ... influenza virus,[147][148][149][150] respiratory syncytial virus (RSV),[150] SARS coronavirus (SARS-CoV),[150] adenovirus[150] ... Ebola-virus infection I Recruiting Tekmira Pharmaceutical NCT01518881 ALN-RSV01 RSV nucleocapsid Naked siRNA Respiratory ...
Some viruses also exhibit a dormant phase, called viral latency, in which the virus hides in the body in an inactive state. For ... The latency period is the time between infection and the ability of the disease to spread to another person, which may precede ... The micro-organisms that cause these diseases are known as pathogens and include varieties of bacteria, viruses, protozoa and ... example, varicella zoster virus causes chickenpox in the acute phase; after recovery from chickenpox, the virus may remain ...
Some diseases have multiple possible latency periods, in which case the reproduction number for the disease overall is the sum ... Infectious Disease Modeling: Measles Virus. *Model-Builder: Interactive (GUI-based) software to build, simulate, and analyze ...
Incubation of the virus may range from 2-9 weeks.[14] Death often occurs within 4-5 days of infection of the virus.[13] There ... Pawan, J.L. (1936b). "Rabies in the Vampire Bat of Trinidad with Special Reference to the Clinical Course and the Latency of ... Beamer PD, Mohr CO, Barr TR (1960). "Resistance of the opossum to rabies virus". Am. J. Vet. Res. 21: 507-10. PMID 13797881.. ... Baynard, Ashley C. et al. (2011). "Bats and Lyssaviruses." In: Advances in VIRUS RESEARCH VOLUME 79. Research Advances in ...
This is to keep the virus in circulation thereby exposing the population to the virus at an early age, when it is less harmful ... or after a latency period of many years.[29] ... "Understanding Viruses (2nd ed.). Jones & Bartlett. p. 459. ISBN ... After a chickenpox infection, the virus remains dormant in the body's nerve tissues. The immune system keeps the virus at bay, ... Wharton M (1996). "The epidemiology of varicella-zoster virus infections". Infect Dis Clin North Am. 10 (3): 571-81. doi: ...
An initial link to the Epstein-Barr virus saw the illness acquire the name "chronic Epstein-Barr virus syndrome".[1]:29[80] ... increased sleep latency, decreased slow wave sleep, and abnormal heart rate response to tilt table tests suggesting a role of ... "Absence of xenotropic murine leukaemia virus-related virus in UK patients with chronic fatigue syndrome". Retrovirology. 7 (1 ... "Prevalence of xenotropic murine leukaemia virus-related virus in patients with chronic fatigue syndrome in the Netherlands: ...
They are classified as group II viruses in the Baltimore classification of viruses. Parvoviruses are among the smallest viruses ... which only work with a helper virus such as adenovirus. Other viruses that can infect without helper viruses are called as ... The Parvoviridae family has two subfamilies; the Parvovirinae (vertebrate viruses) and the Densovirinae (invertebrate viruses ... Autonomous Parvoviruses do not require a helper virus like dependoviruses. The virus B19 was discovered in blood serum and ...
During latency, the virus genome depends on the host replication machinery and replicates as closed circular episome ("plasmid ... Infection with this virus is thought to be lifelong, but a healthy immune system will keep the virus in check. Many people ... When the virus enters into lytic replication, thousands of virus particles can be made from a single cell, which usually ... When the virus reactivates into lytic replication, it is believed that the virus genome is replicated as a continuous linear ...
response to virus. • immunoglobulin mediated immune response. • establishment of viral latency. • cytokine-mediated signaling ... Zhang L, Pagano JS (1997). «IRF-7, a new interferon regulatory factor associated with Epstein-Barr virus latency». Mol. Cell. ... Smith EJ, Marié I, Prakash A, García-Sastre A, Levy DE (2001). «IRF3 and IRF7 phosphorylation in virus-infected cells does not ... Lin R, Noyce RS, Collins SE, Everett RD, Mossman KL (2004). «The Herpes Simplex Virus ICP0 RING Finger Domain Inhibits IRF3- ...
... viral latency and reservoirs], Retrovirology 2009, 6:51 doi:10.1186/1742-4690-6-51, veebiversioon (vaadatud 8.07.2014),small ... sectitle Hypothesis of snake and insect venoms against Human Immunodeficiency Virus: a review], AIDS Res. Ter. 2009, 6:25, ...
... so have lower mating latencies, meaning that they are able to reproduce more quickly. This decreased mating latency leads to a ... "Drosophila as a genetic model for studying pathogenic human viruses". Virology. 423 (1): 1-5. doi:10.1016/j.virol.2011.11.016 ...
The within-host dynamics of HIV infection include the spread of the virus in vivo, the establishment of latency, the effects of ... 9, 35 In active infection, HIV pro virus is active and HIV virus particles are actively replicated; and the infected cells ... while the virus is in a person's body but before the virus has established itself. In both cases, the drugs would be the same ... Virus characteristics[edit]. See also: Structure and genome of HIV and Subtypes of HIV ...
A mature virus particle measures about 170 nanometres (1,700 Å) in diameter. The genome of HHV-7 is very similar to that of HHV ... Katsafanas, GC; Schirmer, EC; Wyatt, LS; Frenkel, N (1996). "In vitro activation of human herpesviruses 6 and 7 from latency" ( ... Both HHV-6B and HHV-7, as well as other viruses, can cause a skin condition in infants known as exanthema subitum, although HHV ... Atedzoe, BN; Menezes, J; D'Addario, M; Xu, J; Ongradi, J; Ahmad, A (1999). "Modulatory effects of human herpes virus-7 on ...
This is in contrast to viral latency, a form of dormancy in which the virus does not replicate. An example of latency is HIV ... During latency, an infection is subclinical. With respect to viral infections, in incubation the virus is replicating.[2] ... In some diseases, as depicted in this diagram, the latency period is shorter than the incubation period. After the latency ... While latent or latency period may be synonymous, a distinction is sometimes made between incubation period, the period between ...
Lamb RA, Horvath CM (August 1991). "Diversity of coding strategies in influenza viruses". Trends in Genetics. 7 (8): 261-66. ... However high costs, extremely slow read and write times (memory latency), and insufficient reliability has prevented its ... This enzyme system acts at least in part as a molecular immune system protecting bacteria from infection by viruses.[22] ... In bacteria, this overlap may be involved in the regulation of gene transcription,[36] while in viruses, overlapping genes ...
Role in transmission of influenza viruses from non-human animals to people[edit]. Influenza A viruses are found in many ... It could occur with primate viruses and may be a factor for the appearance of new viruses in the human species such as HIV. Due ... Antigenic shift is the process by which two or more different strains of a virus, or strains of two or more different viruses, ... but the process is also known to occur with other viruses, such as visna virus in sheep.[1] Antigenic shift is a specific case ...
The fourth is the latency stage, which occurs from age five until puberty. During the latency stage, the child's sexual ... infectious disease agents such as the rubella virus and the toxoplasmosis parasite, maternal malnutrition, maternal emotional ...
The mice that had a latent infection of the virus had an increased resistance to the bacteria, but those with a non-latent ... 17 May 2007). "Herpesvirus latency confers symbiotic protection from bacterial infection". Nature. 447 (7142): 326-9. doi: ... al., IN (23 November 2006). "Three Indonesian Clusters of H5N1 Virus Infection in 2005". New England Journal of Medicine. 355 ( ... However, infection with human herpes simplex virus type-1, a member of the alphaherpesvirinae subfamily, did not provide ...
Virus latency (or viral latency) is the ability of a pathogenic virus to lie dormant (latent) within a cell, denoted as the ... Virus latency is not to be confused with clinical latency during the incubation period when a virus is not dormant. Episomal ... Herpes virus include chicken-pox virus and herpes simplex viruses (HSV-1, HSV-2), all of which establish episomal latency in ... HIV latency allows the virus to largely avoid the immune system. Like other viruses that go latent, it does not typically cause ...
... but only to the strain of virus that has the same antigenic composition as the original infecting virus. Certain of these ... influenza viruses, rhinoviruses, herpesviruses, and adenoviruses but less frequently to measles and chickenpox viruses. In ... Such viruses probably reside inside cells, where they are protected from antibodies that cannot penetrate ... Latency: Inapparent infections (those that do not cause specific signs and symptoms) often result after exposure to ...
Herpes simplex virus latency-associated transcript is a stable intron. M J Farrell, A T Dobson, and L T Feldman ... Herpes simplex virus latency-associated transcript is a stable intron Message Subject (Your Name) has sent you a message from ... The latency-associated transcript (LAT) is the major viral transcript detected by in situ hybridization of mouse and human ... simplex virus type 1 immediate-early gene that encodes a transactivating protein that may facilitate re-activation of the virus ...
Articles on viral structure, function, and genetics will be considered, as well as articles focusing on virus-host interactions ... and clinical studies on viruses and viral diseases. ... 3. Latency and Reactivation from Latency. Latency can be ... The virus can be reactivated from latency following an appropriate stimulus, however, and reactivation causes lytic virus ... S. Efstathiou and C. M. Preston, "Towards an understanding of the molecular basis of herpes simplex virus latency," Virus ...
Articles on viral structure, function, and genetics will be considered, as well as articles focusing on virus-host interactions ... and clinical studies on viruses and viral diseases. ... Herpes Simplex Virus Latency: The DNA Repair-Centered Pathway. ... Lytic infections occur in a broad range of cells while latency is highly specific for neurons. Although latency suggests itself ... Repair is suggested to be involved in both HSV1 entry into latency and reactivation from it. Here I describe the basic features ...
HIV-1 establishes latent infection in resting CD4+ T cells and findings indicate that latency can also be established in the ... These cells are relatively more resistant to apoptosis induced by HIV-1, thus are important stable hideouts of the virus. Much ... In this review we will describe our current understanding of the mechanism of latency in monocyte/macrophage lineage and how ... Human immunodeficiency virus type 1 (HIV-1) targets CD4+ T cells and cells of the monocyte/macrophage lineage. HIV pathogenesis ...
... a genetic switch that causes latent HIV inside cells to begin to replicate can be manipulated to completely eradicate the virus ... New way of controlling HIV latency to completely eradicate the virus. *Download PDF Copy ... But even in people where the virus is undetectable, it doesnt mean its completely absent. The HIV virus can hide in cells in ... When activated, it initiates a takeover of the cells machinery to churn out new copies of the HIV virus, which eventually ...
Latency Associated Nuclear Antigen (LANA) is among the most abundantly expressed proteins during latency and is required for ... like other human herpes viruses, establishes a biphasic life cycle referred to as dormant or latent, and productive or lytic ... Uppal, T.; Banerjee, S.; Sun, Z.; Verma, S.C.; Robertson, E.S. KSHV LANA-The Master Regulator of KSHV Latency. Viruses 2014, 6 ... Latency Associated Nuclear Antigen (LANA) is among the most abundantly expressed proteins during latency and is required for ...
Anatomical context of Virus Latency. *The BZLF1 protein of Epstein-Barr virus (EBV) is a key immediate-early protein which has ... Vaccination with gp150 (a homologue of gp350 of Epstein-Barr virus) results in a reduction in splenomegaly and virus latency ... Chemical compound and disease context of Virus Latency. *N-linked oligosaccharides on herpes simplex virus glycoprotein gD are ... N-linked oligosaccharides on herpes simplex virus glycoprotein gD are not essential for establishment of viral latency or ...
... reactivation from latency occurs resulting in virus transmission and recurrent disease. During latency, the latency-associated ... Towards an understanding of the herpes simplex virus type 1 latency-reactivation cycle.. Perng GC1, Jones C. ... Towards an Understanding of the Herpes Simplex Virus Type 1 Latency-Reactivation Cycle ... Towards an Understanding of the Herpes Simplex Virus Type 1 Latency-Reactivation Cycle ...
Groundbreaking discovery challenges the conventional theory that infected host cells control latency and could open the door to ... Viral latency is one of the premier challenges in developing a cure for HIV. Latency causes the virus to go into hibernation, ... "HIV latency is not an accident: It is a survival tactic employed by the virus." Medical News Today. MediLexicon, Intl., 3 Mar. ... "Latency has been seen as an accident, a lucky break for HIV that allows the virus to avoid eradication by modern drug therapies ...
A novel form of Epstein-Barr virus latency in normal B cells in vivo.. Miyashita EM1, Yang B, Lam KM, Crawford DH, Thorley- ... We further show that the virus in these cells is latent, but readily reactivated to produce infectious immortalizing virus; ... We have developed a PCR assay that can detect a single Epstein-Barr virus (EBV) genome in the presence of 10(6) uninfected ...
Virus-Induced Neuronal Apoptosis Blocked by the Herpes Simplex Virus Latency-Associated Transcript ... Virus-Induced Neuronal Apoptosis Blocked by the Herpes Simplex Virus Latency-Associated Transcript ... Virus-Induced Neuronal Apoptosis Blocked by the Herpes Simplex Virus Latency-Associated Transcript ... Virus-Induced Neuronal Apoptosis Blocked by the Herpes Simplex Virus Latency-Associated Transcript ...
Herpes simplex virus type 1 latency-associated transcript mRNAImported. ,p>Information which has been imported from another ... tr,Q69079,Q69079_HHV1 Herpes simplex virus type 1 latency-associated transcript mRNA OS=Human herpesvirus 1 OX=10298 PE=2 SV=1 ... help/virus_host target=_top>More...,/a>,/p>Virus hosti. Homo sapiens (Human) [TaxID: 9606]. ... Human herpesvirus 1 (HHV-1) (Human herpes simplex virus 1)Imported. Automatic assertion inferred from database entriesi ...
In this review, we discuss our current knowledge about host and viral factors involved in the establishment of SVV latency and ... In this review, we discuss our current knowledge about host and viral factors involved in the establishment of SVV latency and ... Following primary infection, VZV establishes latency in the sensory ganglia and can reactivate to cause herpes zoster, more ... Following primary infection, VZV establishes latency in the sensory ganglia and can reactivate to cause herpes zoster, more ...
Epstein-Barr virus with heterogeneous DNA disrupts latency. Message Subject (Your Name) has forwarded a page to you from ... Epstein-Barr virus with heterogeneous DNA disrupts latency.. G Miller, M Rabson, L Heston ... we show that the genome of the activated virus resembles that of the virus which was endogenous to X50-7 cells. This result ... virus lacks heterogeneous DNA (het-) and EAI+ virus contains heterogeneous DNA (het+), we suggested that spontaneous viral ...
Investigation of Herpes Simplex Virus Latency in a Tissue Culture System. D R S Jamieson, J M Rhodes ... Investigation of Herpes Simplex Virus Latency in a Tissue Culture System Message Subject (Your Name) has forwarded a page to ...
Herpes simplex virus and varicella-zoster virus establish latency in sensory neurons, persisting in these long-lived cells by ... Latency in Human Immunodeficiency Virus Type 1 Infection: No Easy Answers. Deborah Persaud, Yan Zhou, Janet M. Siliciano, ... Latency in Human Immunodeficiency Virus Type 1 Infection: No Easy Answers. Deborah Persaud, Yan Zhou, Janet M. Siliciano, ... Latency in Human Immunodeficiency Virus Type 1 Infection: No Easy Answers. Deborah Persaud, Yan Zhou, Janet M. Siliciano, ...
The molecular basis of herpes simplex virus (HSV) latency has been investigated by analysis of a latent interaction between HSV ... Russell, Jackie (1989) Herpes Simplex Virus Latency in Cultured Cells. PhD thesis, University of Glasgow. ... An in vitro latency system for HSV, based on previous work by E. Notarianni and C. M. Preston, has been characterised, in which ... During the latter incubation period no virus was usually detectable and the HSV was considered to be in a latent state. HSV ...
... which keeps these viruses under control for life. Far less is known about how these viruses influence B-cell responses. ... which keeps these viruses under control for life. Far less is known about how these viruses influence B-cell responses. ... Both viruses have a significant impact on the immune system, especially through mediating the establishment of cellular ... Both viruses have a significant impact on the immune system, especially through mediating the establishment of cellular ...
PubMed journal article Epstein-barr virus latency in B cells leads to epigenetic repression and CpG methylation of the tumour ... In human B cells infected with Epstein-Barr virus (EBV), latency-associated virus gene products inhibit expression of the pro- ... VL - 5 IS - 6 N2 - In human B cells infected with Epstein-Barr virus (EBV), latency-associated virus gene products inhibit ... Epstein-barr virus latency in B cells leads to epigenetic repression and CpG methylation of the tumour suppressor gene Bim.. ...
2) To explain the neuronal latency of herpes simplex virus. (3) To explain the reason for the specificity in the sites of ... Pathogenesis and life cycle of herpes simplex virus infection-stages of primary, latency and recurrence ... Marina Lazar Chandy, Shanavas, Mb, Khan, Sc, and Suresh, K. Vd, "Pathogenesis and life cycle of herpes simplex virus infection- ... Results and conclusion: Herpes simplex virus is a highly contagious human pathogen that has widespread infections in the oro- ...
Switching Viral Latency to Viral Lysis: A Novel Therapeutic Approach for Epstein-Barr Virus-associated Neoplasia. Marina I. ... Switching Viral Latency to Viral Lysis: A Novel Therapeutic Approach for Epstein-Barr Virus-associated Neoplasia ... Switching Viral Latency to Viral Lysis: A Novel Therapeutic Approach for Epstein-Barr Virus-associated Neoplasia ... Switching Viral Latency to Viral Lysis: A Novel Therapeutic Approach for Epstein-Barr Virus-associated Neoplasia ...
This may reflect the tropism of the virus. The similarities between HIV-1 and FIV replication and latency support the notion of ... Chan, Chi Ngai (2013) Cell signalling and feline immunodeficiency virus growth and latency. PhD thesis, University of Glasgow. ... This intimate relationship between the viruses and their respective hosts plays crucial roles in the pathogenesis of each virus ... Next the activation status of susceptible CD4+ T cells was manipulated to study FIV latency and it was shown that by removing ...
The hallmark of KSHV interaction in human host, like in other herpes viruses, is the establishment of lifelong latency with ... Piracy of Prostaglandin E2/EP Receptor-Mediated Signaling by Kaposis Sarcoma-Associated Herpes Virus (HHV-8) for Latency Gene ... Piracy of Prostaglandin E2/EP Receptor-Mediated Signaling by Kaposis Sarcoma-Associated Herpes Virus (HHV-8) for Latency Gene ... Piracy of Prostaglandin E2/EP Receptor-Mediated Signaling by Kaposis Sarcoma-Associated Herpes Virus (HHV-8) for Latency Gene ...
Regulation of Human T-Lymphotropic Virus Type I Latency and Reactivation by HBZ and Rex Download PDF České info ... Regulation of Human T-Lymphotropic Virus Type I Latency and Reactivation by HBZ and Rex ... Elucidating mechanisms underlying HTLV-1 latency and reactivation can facilitate virus control to prevent progression to ... Elucidating mechanisms underlying HTLV-1 latency and reactivation can facilitate virus control to prevent progression to ...
Polymorphic proteins encoded within BZLF1 of defective and standard Epstein-Barr viruses disrupt latency ... Our previous work had shown that the 2.7-kilobase-pair WZhet piece of rearranged Epstein-Barr virus DNA from a defective virus ... Our previous work had shown that the 2.7-kilobase-pair WZhet piece of rearranged Epstein-Barr virus DNA from a defective virus ... Polymorphic proteins encoded within BZLF1 of defective and standard Epstein-Barr viruses disrupt latency. Journal of virology ...
Virus enters through the mucous membranes of orofacial region and reach the TG where it resides and take control of its ... SARS-Corona Virus-2 May Initially Infect Brainstem through Trigeminal Ganglion-Latency May Be Present-A New Perspective Riffat ... How to cite: Mehboob, R.; Ahmad, F.J. SARS-Corona Virus-2 May Initially Infect Brainstem through Trigeminal Ganglion-Latency ... Mehboob, R.; Ahmad, F.J. SARS-Corona Virus-2 May Initially Infect Brainstem through Trigeminal Ganglion-Latency May Be Present- ...
Latent uDNA was activated to de novo virus production by latency reversing agents that also activated latent integrated ... Results: Here, we characterize in primary resting CD4 T cells the dynamics of integrated and unintegrated virus expression, ... Similar to what has recently been demonstrated for latent integrated proviruses, one or two applications of latency reversing ... Experimental models of HIV-1 latency employing directly infected resting CD4 T cells should calibrate the contribution of ...
... Published on: March 2, 2016. Author: the CVR science blog editors In this episode ... Categories: DNA virus, Meet the expert, podcast, prevention and treatment Tags: antivirals, cell biology, HCMV, herpes viruses ... Like other herpes viruses (a diverse group of large DNA viruses), HCMV can cause a chronic, life-long infection, establishing ... scicomm from the MRC-University of Glasgow Centre for Virus Research. Navigation Menu. *Home ...
  • Periodically, reactivation from latency occurs resulting in virus transmission and recurrent disease. (
  • Occasional reactivation from latency into virus replicative cycles at oropharyngeal sites promotes the shedding and transmission of EBV ( 1 , 2 ). (
  • In small animal models of infection, expression of the first 1.5 kb of LAT coding sequences is necessary and sufficient for wild-type reactivation from latency. (
  • The ability of LAT to inhibit apoptosis is important for reactivation from latency. (
  • Human cytomegalovirus (HCMV) is a frequent cause of major disease following primary infection or reactivation from latency in immunocompromised patients. (
  • Murata, T 2014, ' Regulation of Epstein-Barr virus reactivation from latency ', Microbiology and Immunology , vol. 58, no. 6, pp. 307-317. (
  • Therefore, in strains that require thymidine kinase for reactivation from latency, low levels of enzyme synthesized via a ribosomal frameshift can suffice. (
  • Expression of the first 1.5 kb of the latency-associated transcript (LAT) that is encoded by herpes simplex virus type 1 (HSV-1) is sufficient for wild-type (wt) levels of reactivation from latency in small animal models. (
  • In addition, systems based on the use of clinical samples allow us to study HIV-1 reactivation from latency, but not how latency is established. (
  • In cases of inapparent infection, long-lasting immunity develops, but only to the strain of virus that has the same antigenic composition as the original infecting virus. (
  • Certain of these viruses persist in the tissues of the host after the initial infection despite the presence of circulating antibodies to it in the blood and tissues. (
  • Latency is the phase in certain viruses' life cycles in which, after initial infection, proliferation of virus particles ceases. (
  • One example is herpes virus family, Herpesviridae, all of which establish latent infection. (
  • Both proviral and episomal latency may require maintenance for continued infection and fidelity of viral genes. (
  • While viral latency exhibits no active viral shedding nor causes any pathologies or symptoms, the virus is still able to reactivate via external activators (sunlight, stress, etc) to cause an acute infection. (
  • Lytic infection refers to the situation in which the virus replicates in a host cell and causes its lysis, releasing hundreds to thousands of progeny virions. (
  • In a lytic infection the virus is exposed to components of the immune response that have the potential to clear the virus from the host. (
  • As a result, the virus can survive an otherwise effective immune response and be reactivated later to spread its infection in a less hostile immunological environment [ 4 ]. (
  • Progeny virus from this initial infection is able to traffic to sensory neurons in the trigeminal ganglion where a latent infection is produced. (
  • Virus reactivated from latently infected neurons migrates back to the site of the initial infection in the oral epithelium producing a second lytic infection. (
  • HIV-1 establishes latent infection in resting CD4 + T cells and findings indicate that latency can also be established in the cells of monocyte/macrophage lineage. (
  • Infection by herpes simplex virus type 1 (HSV-1) can cause clinical symptoms in the peripheral and central nervous system. (
  • LAT expression is important for the latency-reactivation cycle in animal models, in part, because it inhibits apoptosis, viral gene expression, and productive infection. (
  • What's more, the researchers suggest that latency is a naturally selected tactic employed by the virus to increase infection rates. (
  • This new data indicate that latency is far from an accident--it is encoded in the virus's circuitry and is an evolutionarily advantageous strategy, likely increasing the odds of infection by a substantial amount. (
  • Latent infections with periodic reactivation are a common outcome after acute infection with many viruses. (
  • After primary infection of the eye, herpes simplex virus-type 1 (HSV-1) establishes a lifelong latent infection in neurons of the trigeminal ganglia (TGs), with sporadic periods of reactivation and recurrent disease. (
  • Following primary infection, VZV establishes latency in the sensory ganglia and can reactivate to cause herpes zoster, more commonly known as shingles, which causes significant morbidity and sometimes mortality in the elderly. (
  • As an alternative, infection of rhesus macaques with the homologous simian varicella virus (SVV) recapitulates the hallmarks of VZV infection and thus constitutes a robust animal model to provide critical insights into VZV pathogenesis and the host antiviral response. (
  • In this model, SVV infection results in the development of varicella during primary infection, generation of an adaptive immune response, establishment of latency in the sensory ganglia and viral reactivation upon immune suppression. (
  • For some viruses, long-term persistence in the host depends on the establishment of latency, a reversibly nonproductive state of infection. (
  • This is in sharp contrast to human immunodeficiency virus type 1 (HIV-1) infection. (
  • Here it is argued that HIV-1 latency renders the infection intrinsically incurable by antiretroviral therapy alone. (
  • They are unique since they persist after primary infection in a clinically silent state known as latency. (
  • Two herpesviruses often contracted during childhood are Epstein-Barr virus (EBV), which establishes latent infection in the memory B-cell (MBC) compartment ( 1 , 2 ), and Cytomegalovirus (CMV), which has a number of latency targets including CD34 + and CD33 + hematopoietic cells ( 3 , 4 ). (
  • COX-2 inhibition significantly abrogated expression of the major KSHV latent gene latency-associated nuclear antigen-1 (LANA-1) during de novo KSHV infection of fibroblast (HFF) and endothelial (HMVEC-d) cells, and exogenous PGE2 reversed this downregulation ( 5 ). (
  • However, longitudinal studies of HTLV-1 carriers indicate that the patterns of proviral DNA integration in PBMCs continue to evolve over time [5] , suggesting that de novo infection of naïve cells occurs constantly in virus carriers (see [4] for a review). (
  • They use this method to understand infection by human cytomegalovirus (HCMV - also known as human herpes virus 5) with an overall aim of discovering novel antiviral targets, which are required urgently. (
  • Like other herpes viruses (a diverse group of large DNA viruses), HCMV can cause a chronic, life-long infection, establishing latency within cells throughout your body very easily. (
  • Initial infection is associated with a lack of disease with your immune system controlling the virus very well. (
  • Despite ongoing research, no vaccines are licensed to date against HCMV and our currently licensed antivirals , which include the famous Ganciclovir, are inhibitors of DNA polymerases (including that of HCMV), only affect actively replicating HCMV (not a latent infection), are associated with toxic side-effects and some HCMV viruses are resistant to them. (
  • Host genetics is also important in infectious disease, however there have been no large-scale efforts towards understanding the contribution that human genetic variation plays in primary EBV infection and latency. (
  • Existing highly active antiretroviral therapy (HAART) effectively controls viral replication in human immunodeficiency virus type 1 (HIV-1) infected individuals but cannot completely eradicate the infection, at least in part due to the persistence of latently infected cells. (
  • One strategy that is being actively pursued to eliminate the latent aspect of HIV-1 infection involves therapies combining latency antagonists with HAART. (
  • Quantitation of viral genomes in spleens of infected animals revealed a reduced amount of {Delta}IE1 virus produced during acute infection, suggesting a role for IE1 as a regulator in establishing a chronic or persistent infection, rather than in more directly influencing the latency or reactivation processes. (
  • Antiviral drugs have been defined that inhibit the lytic infection cycle, but there are no approaches that target the latent virus. (
  • To test hypotheses for possible mechanisms by which the HSV latency-associated transcript reduces lytic gene expression during acute infection and during latent infection of trigeminal ganglia: a. (
  • We have exciting unpublished results that ICP0 mutant viruses have a different chromatin profile on their genome during latent infection. (
  • We will test the hypothesis that LAT forms duplex RNA with ICP0 transcripts to recruit histone modifying enzymes by mutating the ICP0 promoter or mutating the ICP0 translational initiation site and by constructing LAT and ICP0 double mutant viruses to determine their combinatorial effects on latent infection, and viral chromatin. (
  • Herpes simplex viruses cause considerable genital, ocular and nervous system disease, and genital herpes increases the risk of HIV infection. (
  • There are drugs that target the active growth of herpes simplex virus but none that target the latent infection. (
  • The EBNA1 protein of Epstein-Barr virus (EBV) contributes in multiple ways to the latent mode of EBV infection that leads to lifelong infection. (
  • Importantly, HCMV, like all herpes viruses, establishes a lifelong latent infection of the host--one major site of latency being the undifferentiated haematopoietic progenitor cells resident in the bone marrow. (
  • Infection of non-permissive mononuclear cells is used for analyses of HCMV latency in vitro. (
  • Using this approach, it is shown here that repression of lytic gene expression following experimental infection of CD34+ cells, a site of HCMV latency in vivo, correlates with recruitment of repressive chromatin around the major immediate-early promoter (MIEP). (
  • Incubation of SV40 tumor cell cultures with herpes simplex virus type 2 (HSV 2) at 40°C resulted in rapidly growing cells which survived the infection and lacked both virus cytopathology and synthesis of detectable infectious virus. (
  • The Epstein-Barr virus (EBV) BamHI Q promoter (Qp) is the only promoter used for the transcription of Epstein-Barr virus nuclear antigen 1 (EBNA-1) mRNA in cells in the most restricted (type I) latent infection state. (
  • These latency types are present at specific stages of infection and are also characteristic of different tumor types, but their generation is not fully understood. (
  • The two book volumes on EBV summarize the first 50 years of research on this tumor virus, starting with historical perspectives on discovery, oncogenicity and immune control, reviewing the role that the virus plays in the various associated diseases and concluding with a discussion on how the immune system keeps persistent EBV infection under control in healthy EBV carriers and can be used to treat EBV associated diseases. (
  • The vaccine materials and methods for their construction are exemplified with the virus that causes chickenpox and whose latent infection results in shingles, a condition that affects up to an estimated 1 million people per year in the United States alone. (
  • In this phase the host will show little to no signs of virus infection. (
  • This contrasts other genes normally found in lytic infection that are not associated with acetylated H3K9 histones during latency. (
  • Herpes simplex virus (HSV) infection is a highly prevalent condition responsible for significant morbidity and occasional mortality each year. (
  • Once EBV's initial lytic infection is brought under control, EBV latency persists in the individual's B cells for the rest of their life. (
  • We show that fundamental properties of the Epstein-Barr virus involvement in latent infection, with implications for tumor biology, can be modelled and understood mathematically. (
  • Epstein-Barr virus (EBV) primary infection usually occurs early in childhood until teens, and then persists through-out life as latent infection in a fraction of B-lymphocytes in more than 90% of adults. (
  • Herpes simplex is a viral infection caused by the herpes simplex virus . (
  • [1] After infection, the viruses are transported along sensory nerves to the nerve cell bodies, where they reside lifelong . (
  • [1] Testing the blood for antibodies against the virus can confirm a previous infection but will be negative in new infections. (
  • 5. The Process of Infection: I. Attachment of Viruses and the Entry of Their Genomes into the Target Cell. (
  • Conclusions: These studies demonstrate that contributions by unintegrated genomes to HIV-1 gene expression, virus production, latency and immune responses are inherent properties of the direct infection of resting CD4 T cells. (
  • Analysis of HIV integration sites from induced and non-induced latently infected populations reveals the role of genomic localization and chromatin context in the fate of HIV-1 infection and the reversal of viral latency. (
  • To investigate the possibility of extraneuronal latency during ocular HSV infection, corneal specimens from 18 patients with quiescent herpes simplex keratitis (HSK) were obtained at the time of keratoplasty. (
  • These results demonstrate that the HSV genome was retained, at least in part, in human corneas during quiescent HSV infection, giving further support to the concept of corneal extraneuronal latency. (
  • After ocular herpes simplex virus type 1 (HSV-1) infection, the virus travels up axons and establishes a lifelong latent infection in neurons of the trigeminal ganglia. (
  • Moreover, latent virus can re-enter the replication cycle by reactivation and return to peripheral tissues to start recurrent infection. (
  • This ability to escape host immune surveillance during latent infection and to spread during reactivation is a viral survival strategy and the fundamental reason why no drug can completely eradicate the virus at present. (
  • The transfer of CD8+T cells increased survival in the acute infection, but their engraftment seemed less needed for latency than that of CD4+T cells. (
  • Minagawa, H & Yanagi, Y 2000, ' Latent herpes simplex virus-1 infection in SCID mice transferred with immune CD4+T cells: A new model for latency ', Archives of Virology , vol. 145, no. 11, pp. 2259-2272. (
  • Yanagi, Y. / Latent herpes simplex virus-1 infection in SCID mice transferred with immune CD4+T cells : A new model for latency . (
  • LAT-deletion-mutant virus strains have reducedreactivation phenotypes in small animal models of infection, demonstrating that LAT plays an important role in the latency-reactivation cycle of HSV-1. (
  • These findings may be indicative of an abortive infection in which transcription is limited to the immediate-early genes, or the result of a very low level persistent infection, or a transient reactivation of latent virus. (
  • However, HIV-1 also establishes a status of nonproductive infection known as viral latency. (
  • However, no drug can cure infection so far, because various cell types continue to carry the virus in a latent, i.e. quiescent, state. (
  • An examination of patients infected with hepatitis C virus (HCV) demonstrated that Ag-specific Th17 cells are induced during infection and that these cells are regulated by IL-10 and TGF-β. (
  • Cutaneous vesicles characteristic of herpes simplex virus infection. (
  • The virus travels from the site of infection in the skin or mucosa to the sensory dorsal root and remains latent until a recurrent outbreak. (
  • However, zoonotic infection with B virus in humans usually results in fatal encephalomyelitis or severe neurologic impairment. (
  • Approximately 40 cases of zoonotic B-virus infection have been reported. (
  • The first documented case of human B-virus infection occurred in 1932 when a researcher (patient W.B.) was bitten on the hand by an apparently healthy rhesus macaque ( Macaca mulatta ) and died of progressive encephalomyelitis 15 days later. (
  • A major hurdle to curing people of HIV infection is the way the virus hides in a reservoir composed primarily of dormant immune cells. (
  • Using mathematical models based on patient data, the researchers found that latency benefitted the virus overall, resulting in higher infection rates. (
  • The latency-associated transcript (LAT) is the major viral transcript detected by in situ hybridization of mouse and human sensory ganglia latently infected with herpes simplex virus type 1. (
  • During latency, the latency-associated transcript (LAT) is abundantly expressed. (
  • The latency-associated transcript ( LAT ) gene is required for wild-type reactivation of herpes simplex virus (HSV). (
  • The herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) is abundantly expressed in latently infected sensory neurons. (
  • Herpes simplex virus type 1 latency-associated transcript expression protects trigeminal ganglion neurons from apoptosis. (
  • Each copy of the R L region encodes the latency-associated transcript (LAT), the long-short spanning transcript (L/ST), infected cell protein 0 (ICP0), and infected cell protein 34.5 (ICP34.5) (Fig. 1A ). (
  • Latency is maintained in a variety of ways, one of which is the latency-associated transcript, or LAT. (
  • Two pairs of oligonucleotides from the region of the HSV thymidine kinase (TK) gene and the latency-associated transcript (LAT) gene were used as primers in the PCR amplification. (
  • The latency-associated transcript (LAT) is essential for the wild-type herpes simplex virus type 1 (HSV-1) high-reactivation phenotype since LAT - mutants have a low-reactivation phenotype. (
  • A gene capable of blocking apoptosis can substitute for the herpes simplex virus type 1 latency-associated transcript gene and restore wild-type reactivation levels. (
  • LAT (latency-associated transcript), the only known viral gene abundantly transcribed during HSV-1 neuronal latency, is required for high levels of reactivation. (
  • abstract = "Infectivity of feline immunodeficiency virus (FIV) in feline and human lymphoblastoid cell lines was examined using homogeneous populations of FIV derived from infectious molecular clones of strains TM2 and Petaluma, and two recombinant chimeric clones carrying gag, pol, vif and ORF-A from the heterologous virus. (
  • abstract = "In C.B-17 severe combined immunodeficiency (SCID) mice, corneal challenge with herpes simplex virus-1 (HSV-1) KOS strain usually leads to fatal encephalitis. (
  • The virus can reactivate and begin producing large amounts of viral progeny (the lytic part of the viral life cycle) without the host becoming reinfected by new outside virus, and stays within the host indefinitely. (
  • Epstein-Barr virus lytic reactivation (which can be due to chemotherapy or radiation) can result in genome instability and cancer. (
  • Like all herpesviruses, herpes simplex virus 1 (HSV1) is able to produce lytic or latent infections depending on the host cell type. (
  • Lytic infections occur in a broad range of cells while latency is highly specific for neurons. (
  • The virus can be reactivated from latency following an appropriate stimulus, however, and reactivation causes lytic virus replication [ 1 - 3 ]. (
  • Herpes simplex virus (HSV1) resembles other herpesviruses in its ability to cause both lytic and latent infections [ 1 , 5 ]. (
  • I begin with a brief summary of HSV1 lytic replication and the basic features of latency. (
  • Kaposi's sarcoma associated herpesvirus (KSHV), like other human herpes viruses, establishes a biphasic life cycle referred to as dormant or latent, and productive or lytic phases. (
  • One possibility is that a block in viral gene expression occurs at a very early stage in the viral cycle, either as the direct cause or as a consequence of establishment of latency, and that the block can be released by the Vmw110 gene product, thereby allowing HSV to continue into the lytic cycle. (
  • This system takes advantage of the transactivating properties of EBNA-1, a latency protein expressed in all EBV-containing cells, to drive the expression of Zta , a gene sufficient for inducing the EBV lytic cycle. (
  • Although, the role of COX-2 and PGE2 in herpes viral lytic cycle is shown, their role in viral latency has been observed only in KSHV. (
  • During periods of immunosuppression, the virus may 'reactivate' , initiating 'lytic' replication, which can damage your cells. (
  • In the lytic phase the virus is able to spread to other hosts due to open sores and other such mechanisms. (
  • During the latent phase, researchers have found more methylated chromatin in the lytic genes and less acetylated chromatin, whereas in the LAT region there is less methylation and more acetylation found during latency. (
  • These viruses have their lytic phase in mucoepithelial cells and are latent in neuronal cells. (
  • Epstein-Barr virus latency type and spontaneous reactivation predict lytic induction levels. (
  • The genetic information of herpesviruses and adenoviruses can be integrated into the genome of the host cell, but it is believed that these viruses frequently, and the measles virus invariably, reside in cells in the form of extrachromosomal genes (genes not integrated in chromosomes). (
  • In this latency type, viral genes are stabilized, floating in the cytoplasm or nucleus as distinct objects, either as linear or lariat structures. (
  • Latency is generally maintained by viral genes expressed primarily during latency. (
  • Expression of these latency-associated genes may function to keep the viral genome from being digested by cellular ribozymes or being found out by the immune system. (
  • The virus DNA is present in the latently infected cell nucleus, but there is little DNA replication and only minimal expression of virus-encoded genes. (
  • 50 years since the discovery of EBV and its identification as a human oncogenic virus, a glimpse of the future is shown by the first whole-genome and whole-exome studies, revealing new human genes at the heart of the host-EBV interaction. (
  • A viral function represses accumulation of transcripts from productive-cycle genes in mouse ganglia latently infected with herpes simplex virus. (
  • However, it is becoming increasingly clear that a distinct subset of viral genes is also expressed during latency. (
  • The mechanism that controls this is very complex because expression of viral proteins during latency is decreased a great deal, meaning that the virus must have transcription of its genes repressed. (
  • The virus is about 122-180 nm in diameter and is composed of a double helix of deoxyribonucleic acid (DNA) which contains about 172,000 base pairs and 85 genes . (
  • During latency EBV genes are expressed in four programs, denoted latency 0, I, II and III. (
  • In latency III all 12 latency genes are expressed, including six nuclear proteins, EBNA-1-6, three membrane proteins (LMP-1, LMP-2A and LMP-2B), BART and two small non-translated RNAs (EBER 1 & 2). (
  • This virus did not reactivate, confirming that mutations in other genes that would influence reactivation had not arisen. (
  • Previous studies demonstrated that the anti-apoptosis functions of LAT are important for regulating the latency-reactivation cycle because three different anti-apoptosis genes can substitute for LAT. (
  • Cytomegalovirus (CMV) establishes latency in myeloid progenitor cells, and is reactivated by inflammation. (
  • Whether or how HTLV-1 establishes latency and reactivates is unclear. (
  • HIV-1 establishes latency primarily by infecting activated CD4 + T cells that later return to quiescence as memory cells. (
  • HIV-1 establishes latency by exploiting the cellular events of CD4 + T cell blast transformation, clonal expansion, and clonal contraction that lead to the formation of immunological memory (for a comprehensive review, see Refs. (
  • Although latency suggests itself as an attractive target for novel anti-HSV1 therapies, progress in their development has been slowed due in part to a lack of agreement about the basic biochemical mechanisms involved. (
  • The pathway to identification of the desired inhibitors would be easier, however, if investigators had a clear understanding of the molecular mechanisms involved in latency. (
  • We need to better understand the mechanisms that regulate HIV latency so we can identify new opportunities for intervention and develop better drugs that can either lock viral particles in a latent state, or kill latent cells, or both,' Liang said. (
  • Elucidating mechanisms underlying HTLV-1 latency and reactivation can facilitate virus control to prevent progression to disease. (
  • In this review, we will discuss the mechanisms that control the expression of these latency-associated transcripts and illustrate that regulation of these latency-associated promoters is also subject to chromatin mediated regulation and that the instructive observations previously reported regarding the negative regulation of the MIEP during latency are paralleled in the regulation of latent gene expression. (
  • These data are consistent with ex vivo analyses of latency and may provide a model for further analyses of the mechanisms involved during latency and reactivation. (
  • 15. Mechanisms in Virus Latency. (
  • Although there are many studies on latency and reactivation of HSV, and much progress has been made, many specific mechanisms of the process remain obscure or even controversial due to the complexity of this process and the limitations of research models. (
  • Of particular interest in our laboratory, has been the mechanisms of control of latent virus. (
  • Thus, this system may allow us to study the biology of HIV-1 latency, as well as the mechanisms of CD4 + T cell death following HIV-1 reactivation. (
  • This system may help shed light into the mechanisms of HIV-1 latency and lead to identify new therapeutic strategies. (
  • LAT may enhance the establishment or maintenance of latency ( 5-8 ), thereby increasing the pool of latently infected neurons, which in turn results in increased levels of spontaneous and/or induced reactivation ( 9 ). (
  • In this review, we discuss our current knowledge about host and viral factors involved in the establishment of SVV latency and reactivation as well as the important role played by T cells in SVV pathogenesis and antiviral immunity. (
  • Both viruses have a significant impact on the immune system, especially through mediating the establishment of cellular immunity, which keeps these viruses under control for life. (
  • Crucially, the establishment of latency is concomitant with the recruitment of cellular enzymes that promote extensive methylation of histones bound to the major immediate early promoter. (
  • Our previous study suggested a role for COX-2 in the establishment and maintenance of KSHV latency. (
  • Evidence suggests that the latent VZV genome may express transcripts unlike those of closely related herpesviruses, and some evidence suggests an unusual site for the establishment of VZV latency. (
  • This review summarizes our current understanding of events that may contribute to establishment and maintenance of VZV latency and reactivation from it. (
  • The Epstein-Barr virus (EBV) is a human gamma-herpesvirus that is implicated in various types of proliferative diseases. (
  • Herpes viruses are often herpes simplex virus 1 and herpes simplex virus 2 meant in general but the herpesvirus group includes eight different human pathogenic herpesviruses (HHV). (
  • The Epstein-Barr virus ( EBV ), formally called Human gammaherpesvirus 4 , is one of the nine known human herpesvirus types in the herpes family , and is one of the most common viruses in humans. (
  • CMV is a member of the herpesvirus family, which includes herpes simplex virus types 1 and 2, varicella-zoster virus, and Epstein-Barr virus. (
  • Varicella zoster virus (VZV) is the herpesvirus which causes the childhood disease varicella, also known as chickenpox, and the adult disease herpes zoster, also known as shingles. (
  • Cercopithecine herpesvirus 1 (B virus), an alphaherpesvirus endemic in Asian macaques, is closely related to herpes simplex virus (HSV). (
  • Of the 35 herpesviruses identified in nonhuman primates, only Cercopithecine herpesvirus 1 (B virus) is known to be pathogenic for humans. (
  • Electron micrograph studies of B virus show a typical herpesvirus structure ( 6 ), including an electron dense core with viral DNA inside an icosapentahedral capsid surrounded by an amorphous tegument protein layer and a lipid envelope studded with viral glycoproteins. (
  • In this review, an update of viral factors that are expressed during latency and their potential roles in regulating the latency-reactivation cycle is discussed. (
  • Such viruses probably reside inside cells, where they are protected from antibodies that cannot penetrate the cell membrane. (
  • A rare, but invariably fatal, disease of the nervous system is subacute sclerosing panencephalitis (SSPE), which is a progressive degenerative condition caused by measles virus (a paramyxovirus) lying dormant in brain cells for many years and then reactivated, usually in adolescence. (
  • The Gammaherpesvirinae subfamily is associated with episomal latency established in cells of the immune system, such as B-cells in the case of Epstein-Barr virus. (
  • Some of the proteins expressed by these viruses have co-evolved with host cells to play important roles in normal processes. (
  • The pathway is particularly attractive because it is able to account for important features of the latent response, including the specificity for neurons, the specificity for neurons of the peripheral compared to the central nervous system, the high rate of genetic recombination in HSV1-infected cells, and the genetic identity of infecting and reactivated virus. (
  • In latency, however, infected cells are less readily recognized by the immune system because of the low level of virus gene expression. (
  • Human immunodeficiency virus type 1 (HIV-1) targets CD4 + T cells and cells of the monocyte/macrophage lineage. (
  • HIV pathogenesis is characterized by the depletion of T lymphocytes and by the presence of a population of cells in which latency has been established called the HIV-1 reservoir. (
  • These cells are relatively more resistant to apoptosis induced by HIV-1, thus are important stable hideouts of the virus. (
  • In this review we will describe our current understanding of the mechanism of latency in monocyte/macrophage lineage and how such cells can be specifically eliminated from the infected host. (
  • A new study suggests that a genetic switch that causes latent HIV inside cells to begin to replicate can be manipulated to completely eradicate the virus from the human body. (
  • When activated, it initiates a takeover of the cell's machinery to churn out new copies of the HIV virus, which eventually burst from the cell and infect neighboring cells. (
  • HIV-specific immune effector cells kill cells infected with HIV, but only when the cells are being used to produce more of the virus, meaning that the Tat gene circuit is switched on. (
  • By targeting the Tat gene circuit with drugs or small molecules to activate it, we would be able to cause latently-infected cells to start producing more virus, and then they can be destroyed by the immune system,' said Jie Liang, the Richard and Loan Hill Professor of Bioengineering in the University of Illinois at Chicago College of Engineering and a lead author of the paper. (
  • The HIV virus can hide in cells in an inactivated state, meaning it isn't actively replicating. (
  • It is extremely difficult to flush latently-infected cells out of their latency,' Liang said. (
  • Using different models and algorithms, we were able to accurately map a 'probability landscape' of the cellular reactions that can impact Tat gene circuit reactivation, and our results suggest new ways of targeting latent cells that may lead to the eradication of the HIV virus from a host,' Liang said. (
  • Latency Associated Nuclear Antigen (LANA) is among the most abundantly expressed proteins during latency and is required for various nuclear functions including the recruitment of cellular machineries for viral DNA replication and segregation of the replicated genomes to daughter cells. (
  • New research from the Gladstone Institutes for the first time provides strong evidence that HIV latency is controlled not by infected host cells, but by the virus itself. (
  • However, a pair of articles published in the journal Cell turn this model on its head, proposing that the virus itself--not the body's immune cells--controls when HIV is in the latent or active state. (
  • To demonstrate this, the researchers first showed that the virus remains highly active as infected cells transition to rest, suggesting the two processes are independent. (
  • A novel form of Epstein-Barr virus latency in normal B cells in vivo. (
  • We have developed a PCR assay that can detect a single Epstein-Barr virus (EBV) genome in the presence of 10(6) uninfected cells. (
  • This represents a novel form of latency in normal B cells. (
  • A rare variant spontaneously releases virus which is capable of inducing early antigen in Raji cells (EAI+). (
  • By use of restriction endonuclease polymorphisms unique to both the superinfecting and endogenous genomes, we show that the genome of the activated virus resembles that of the virus which was endogenous to X50-7 cells. (
  • Herpes simplex virus and varicella-zoster virus establish latency in sensory neurons, persisting in these long-lived cells by using a limited program of gene expression ( 10 ). (
  • The immune system exerts some control over viral replication, as demonstrated by increases in viremia with acute experimental depletion of CD8 + T cells in the simian immunodeficiency virus model ( 24 , 48 ). (
  • The molecular basis of herpes simplex virus (HSV) latency has been investigated by analysis of a latent interaction between HSV and cells in culture. (
  • An in vitro latency system for HSV, based on previous work by E. Notarianni and C. M. Preston, has been characterised, in which incubation at a supraoptimal temperature converts HSV to a latent state within tissue culture cells. (
  • In human B cells infected with Epstein-Barr virus (EBV), latency-associated virus gene products inhibit expression of the pro-apoptotic Bcl-2-family member Bim and enhance cell survival. (
  • Importantly, cytosine hypermethylation in the 5'-long terminal repeat (LTR) U3 and R regions was associated with true latency in the lymphoma-derived B-cell line L267 but not with defective latency in YR2 cells. (
  • This antagonistic relationship between ICP0 and the host IFN response may be relevant in regulating whether the HSV-1 genome is expressed, or silenced, in virus-infected cells in vivo . (
  • BACKGROUND: The persistence of latently human immunodeficiency virus-1 (HIV-1) infected cellular reservoirs in resting CD4+ T cells is a major obstacle to HIV-1 eradication. (
  • We investigated histones and their post-translational modification associated with HIV-1 latency in novel HIV-1 latently infected cell lines established previously, NCHA cells. (
  • METHODS: To examine histones and their modification linked with HIV-1 latency, the expression profiles for core histone proteins and histone deacetylases (HDACs) in NCHA cells were characterized by RT-PCR, ELISA, and western blot. (
  • CONCLUSIONS: Our results suggest that tri-methylation of histone H3K27 and H2A ubiquitylation via polycomb group protein may play a crucial role in epigenetic silencing accounting for HIV-1 latency in NCHA cells. (
  • Finally, the expression of IRF-7 is consistently high in type III latency cells and almost undetectable in type I latency, corresponding to the activity of endogenous Qp in these latency states and the ability of the IRF- 7 proteins to repress Qp-reporter constructs. (
  • In this study, we analyzed the role of T cells in the regulation of EBV viral latency by using humanized NOD/SCID/IL2Rγ -/- mice. (
  • Quantitative PCR analysis of promoter activities specific for the different EBV latency types confirmed that in addition to type III cells, type IIa and type I cells were present in the spleen. (
  • These results indicate that CD4 + T cells are necessary for the generation/maintenance of cells with latency I/IIa in the humanized mice. (
  • Adverse cellular conditions, such as nutrient starvation, inhibit networks controlling MCV replication protein turnover and signal the virus to spread to uninfected cells or to a new host. (
  • EBV infects both B cells and epithelial cells and is able to undergo latency in both of these cells. (
  • Viruses lacking the gp42 portion are able to bind to human B cells, but unable to infect. (
  • In infected cells the virus can adopt several different latency programs, affecting the cells' behaviour. (
  • Experimental results indicate that a specific genetic switch between viral latency programs, reprograms human B-cells between proliferative and resting states. (
  • Indeed, the ability of the virus to transiently induce proliferation of latently infected B-lymphocytes results in an increased pool of infected cells. (
  • If this switch gets out of balance, more proliferation leads to a higher load of virus-infected cells and hypothetically increases the risk for lymphoma development. (
  • Featuring an all new art program in full color, the new edition has been updated throughout, and reorganized into thematic sections on the fundamental nature of viruses, their growth in cells, their interactions with the host organism and their role as agents of human disease. (
  • 13. Interactions Between Animal Viruses and Cells. (
  • Results: Here, we characterize in primary resting CD4 T cells the dynamics of integrated and unintegrated virus expression, genome persistence and sensitivity to latency reversing agents. (
  • Experimental models of HIV-1 latency employing directly infected resting CD4 T cells should calibrate the contribution of unintegrated HIV-1. (
  • Building on previous work (Zanini et al, 2015), deep-sequencing is used to show that HIV persistence during suppressive antiretroviral therapy, the main hurdle for HIV cure, is due to homeostatic proliferation and longevity of infected cells rather than ongoing virus replication. (
  • Telomerase-immortalized human umbilical vein endothelial cells supporting KSHV stable latency (TIVE-LTC) expressed elevated levels of functional COX-2 and microsomal PGE2 synthase (m-PGES), and secreted the predominant eicosanoid inflammatory metabolite PGE2. (
  • FIV from the clones with the env region of the Petaluma strain was shown to infect and establish provirus in a human lymphoid cell line (MOLT-4), although the FIV-infected cells did not produce any infectious viruses. (
  • By treatment of the infected MOLT-4 cells with a phorbol ester, infectious virus was rescued. (
  • These results strongly suggest that latency of the virus in MOLT-4 cells is due to a failure in transcription. (
  • Using Epstein-Barr virus (EBV) transformation of primary B cells, we have studied the ability of an oncogenic virus to alter the mRNA isoform profile of its host. (
  • Some latently infected SCID mice had anti-HSV antibodies while others did not, indicating that the engraftment of antibody-producing B cells was not required for latency. (
  • Cells stably transfected with LAT or trigeminal ganglionic neurons of mice infected with a LAT expressing virus appeared to express the L2 or L8 ORF. (
  • In this study, we attempted to model HIV-1 latency using human primary CD4 + T cells infected in vitro with HIV-1 after activation with Ag-loaded dendritic cells and then brought back to quiescence through a resting phase in the presence of IL-7. (
  • In their resting state, HIV-1-infected cells do not actively replicate the virus, which remains dormant for extended periods of time ( 16 , 17 ). (
  • Currently, the study of HIV-1 latency relies primarily on clinical samples and chronically infected cell lines, which present severe limitations such as the very low frequency of latently infected cells in the former and the lack of physiological relevance of the latter (for a review see Ref. 8 ). (
  • So far, no experimental model has existed to study HIV latency in these cells. (
  • Conversely, it was also possible to inhibit the reactivation of the virus by treating the cells with certain compounds. (
  • Thus silencing the virus in brain cells is an important goal. (
  • We identified one LRA combination that displayed synergistic latency reversal and low cytotoxicity in a cell model of HIV and in CD4 + T cells from virologically suppressed patients. (
  • But the medications do not actually rid the body of the virus, which has the ability to elude medications by lying dormant in cells called CD4+ T cells, which signal another type of T cell, the CD8, to destroy HIV-infected cells. (
  • Destroying the reservoir cells could rid some or all of the HIV virus from people who are infected. (
  • It is generally believed that HIV does not replicate in these cells because the virus depends on active cellular machinery to do so. (
  • Now, two new papers by NIAID grantees propose that the virus itself-not cells-controls whether HIV is replicating, and that periods of latency paradoxically give the virus a survival advantage. (
  • The similarities between HIV-1 and FIV replication and latency support the notion of using FIV and the cat as a model for HIV-1 latency in the development of novel therapeutic measures to eradicate hidden HIV-1 from the host. (
  • The fact that the proteasome positively influences both HIV-1 replication and latency makes it a unique drug target whose inhibition has the potential to elicit dual antiviral effects. (
  • Deletion of the rat cytomegalovirus immediate-early 1 gene results in a virus capable of establishing latency, but with lower levels of acute virus replication and latency that compromise reactivation efficiency. (
  • In the case of herpes simplex (HSV), the virus has been shown to fuse with DNA in neurons, such as nerve ganglia or neurons, and HSV reactivates upon even minor chromatin loosening with stress, although the chromatin compacts (becomes latent) upon oxygen and nutrient deprivation. (
  • LAT leads to chromatin changes by serving as a precursor to an miRNA that reduces ICP0 expression through studies of miRNA mutant viruses. (
  • As such, the repressive chromatin structure formed at the major immediate early promoter (MIEP) elicits inhibition of IE gene expression and is a major factor involved in maintenance of HCMV latency. (
  • Instead, it appears that the main way that expression of viral transcripts is maintained at a lower level during latency is through chromatin structure. (
  • Occupancy of chromatin organizers in the Epstein-Barr virus genome. (
  • A provirus is a virus genome that is integrated into the DNA of a host cell. (
  • However, viruses that integrate into the host cell's genome can stay there as long as the cell lives. (
  • These viruses have incorporated into the human genome in the distant past, and are now transmitted through reproduction. (
  • However, superinfection with d11403 failed to reactivate latent HSV-2 as a consequence of a deletion in the region of the genome encoding Vmw110, strongly suggesting that Vmw110, which is known to regulate gene expression by trans-activation, is required for reactivation in the in vitro latency system. (
  • This study describes a viral latency mechanism based on phosphorylation-regulated viral replication protein stability that may underlie chronic viral infections for some small genome DNA and RNA viruses. (
  • Viral latency, in which a virus genome does not replicate independently of the host cell genome and produces no infectious particles, is required for long-term virus persistence. (
  • Virus activation is not mediated by viral gene transactivation, given that these mutations do not increase late gene transcription in the absence of genome replication. (
  • Genome Replication in RNA Viruses. (
  • 2) In experiments using reverse transcriptase PCR, we were able to detect immediate-early I transcripts at a level roughly 10-fold higher than that of viral genome, indicating that a significant fraction of latent virus is transcriptionally active. (
  • The B-virus genome is only partially sequenced, but thus far, is colinear with that of HSV ( 5 ). (
  • Our laboratory studies the genome organization of human viruses associated with cancer. (
  • To define the HSV gene products involved in latency, the behaviour of various temperature-sensitive (ts), insertion (in) and deletion (dl) mutants of HSV in the in vitro latency system was examined. (
  • The physical nature of the HSV DNA in the in vitro latency system described has been determined. (
  • The researchers showed that various substances, including the cytokine TNF-alpha, can reactivate the inactive virus. (
  • Once a person becomes infected, the virus remains latent and may reactivate occasionally. (
  • A proposed strategy to cure HIV uses latency-reversing agents (LRAs) to reactivate latent proviruses for purging HIV reservoirs. (
  • Inapparent infections (those that do not cause specific signs and symptoms) often result after exposure to picornaviruses , influenza viruses, rhinoviruses , herpesviruses , and adenoviruses but less frequently to measles and chickenpox viruses. (
  • On the other hand, a study in mice suggests that latency with EBV or CMV equivalents can be beneficial for the carrier by mediating increased protection against subsequent bacterial infections, potentially through the action of elevated systemic cytokines ( 9 ). (
  • IFN-sensitive ICP0 - viruses are avirulent, establish long-term latent infections, and induce an adaptive immune response that is highly protective against lethal challenge with HSV-1. (
  • There is no known latency mechanism for chronic small DNA virus infections. (
  • Famciclovir (FCV) is efficacious in the treatment of acute herpes zoster and recurrent genital infections but has not been used to treat ocular herpes simplex virus (HSV) infections. (
  • Among the common CNS infections faced by neurologists, HIV and other viral infections of the brain (particularly herpes simplex virus and measles) can cause either subacute or chronic debilitating neurological syndromes that offer particular challenges for diagnosis and treatment. (
  • When a person with HIV stops treatment, the virus emerges and replicates in the body, weakening the immune system and raising the likelihood of opportunistic infections or cancers that can sicken or kill the patient. (
  • Providing an integrated account of the subject across different host systems, with an emphasis on human and animal viruses, this book covers the field of virology from molecular biology to disease processes using a unique systems approach. (
  • Provides integrated account of virology across different host systems, with an emphasis on human and animal viruses. (
  • The Institute of Virology (VIRO) investigates viruses that chronically infect humans and can cause life-threatening diseases. (
  • HIV-1 is able to persist within its cellular host by entering a reversible dormant state, termed latency, which provides protection from the immune system and antiviral pharmaceuticals. (
  • His main research interests are influenza viruses, HIV, and antiviral immunology. (
  • Herpes simplex virus thymidine kinase is important for reactivation of virus from its latent state and is a target for the antiviral drug acyclovir. (
  • Antiviral therapies can keep the virus from multiplying. (
  • 70% before the availability of antiviral therapy makes this virus a serious zoonotic threat. (
  • Knowledge of the clinical signs and risk factors for human B-virus disease allows early initiation of antiviral therapy and prevents severe disease or death. (
  • Treatment with antiviral medication may decrease the death rate, but rapid diagnosis and initiation of therapy are essential in controlling the spread of the virus in the central nervous system and limiting neurologic sequelae. (
  • Virus latency (or viral latency) is the ability of a pathogenic virus to lie dormant (latent) within a cell, denoted as the lysogenic part of the viral life cycle. (
  • Virus latency is not to be confused with clinical latency during the incubation period when a virus is not dormant. (
  • One of the most notable functions of this virus family is their ability to enter a latent phase and lay dormant within animals for extended periods of time. (
  • Shingles, also called herpes zoster or zoster, occurs when the virus that once gave someone chickenpox reawakens after lying dormant in nerve tissue. (
  • The scientists' approach sends an agent to "wake up" the dormant virus, causing it to begin replicating so that either the immune system or the virus itself would kill the cell harboring HIV. (
  • To fully display function of RING proteins in WSSV, here we focus on WSSV403, another viral E3 candidate, which is potentially involved in the regulation of WSSV latency. (
  • The identification of a functional viral ISRE and association of IRF-7 with type III latency may be relevant to the mechanism of regulation of Qp. (
  • We build a physico-chemical model to investigate quantitatively the dynamical properties of the promoter regulation and experimentally examine protein level variations between the two latency programs. (
  • Gene Expression and its Regulation in RNA Viruses. (
  • Epstein-Barr virus (EBV) and cytomegalovirus (CMV) are ubiquitous and persistent herpesviruses commonly acquired during childhood. (
  • 1) My laboratory is engaged in studies of viral latency using murine cytomegalovirus, a member of the family of beta-Herpes viruses. (
  • This intimate relationship between the viruses and their respective hosts plays crucial roles in the pathogenesis of each virus. (
  • However, insights into features of the molecular events of VZV latency have been gleaned from its pathogenesis and from recent advances in molecular probing of human and animal ganglia. (
  • Herpes virus include chicken-pox virus and herpes simplex viruses (HSV-1, HSV-2), all of which establish episomal latency in neurons and leave linear genetic material floating in the cytoplasm. (
  • Herpes simplex viruses cause considerable morbidity and mortality. (
  • The herpes simplex viruses comprise 2 distinct types of DNA viruses: herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2). (
  • There is no simple explanation for why latent viruses, such as those in the family Herpesviridae , that are present in the tissues of most adult humans can be activated to cause disease in some people but not in others. (
  • Varicella zoster virus (VZV) is a neurotropic alphaherpesvirus and the causative agent of varicella (chickenpox) in humans. (
  • Human Herpes Viruses, also known as HHVs, are part of a family of DNA viruses that cause several diseases in humans. (
  • However, the mechanistic aspects of how COX-2/PGE2 mediates KSHV latent gene expression is not known and the role of EP receptors is unexplored in herpes virus biology. (
  • Gene Expression in DNA Viruses and Reverse-Transcribing Viruses. (
  • Experimental wounding of developing bees increases relative immune gene expression and deformed wing virus titers. (
  • By cloning the HR-1 Burkitt lymphoma line, we previously uncovered two distinct biological variants of nontransforming Epstein-Barr virus (EBV). (
  • The primary site of HSV-1 latency is sensory neurons within trigeminal ganglia. (
  • Herpes simplex virus (HSV) latency in sensory ganglion neurons is well documented, but the existence of extraneuronal corneal latency is less well defined. (
  • HIV latency allows the virus to largely avoid the immune system. (
  • Bovine leukemia virus (BLV) proviral latency represents a viral strategy to escape the host immune system and allow tumor development. (
  • AIDS, transmissible disease of the immune system caused by the human immunodeficiency virus (HIV). (
  • 12. The Immune System and Virus Neutralization. (
  • The last 750 bases of LAT are complementary to infected-cell polypeptide 0, a herpes simplex virus type 1 immediate-early gene that encodes a transactivating protein that may facilitate re-activation of the virus from the latent state. (
  • Next, with the help of computer modeling, the scientists identified the protein Tat as the crucial mechanism in the virus that controls its on/off switch. (
  • Two mutants of HSV type 1 (HSV-1) used in these studies, tsK and inl 411, do not synthesise active immediate early (IE) polypeptide Vmw175 and are blocked at a very early stage of the virus replication cycle, and a third mutant of HSV-1, d11403, does not produce IE polypeptide Vmw110, but otherwise exhibits a pattern of protein synthesis indistinguishable from that of wt HSV-1. (
  • Epstein-Barr virus EBNA1 protein regulates viral latency throu. (
  • Epstein-Barr virus EBNA1 protein regulates viral latency through effects on let-7 microRNA and dicer. (
  • The herpes simplex virus type 1 (HSV-1) ICP0 protein is an E3 ubiquitin ligase, which is encoded within the HSV-1 latency-associated locus. (
  • Protein-mediated viral latency through cellular SCF E3 ligase targeting of viral replication proteins is a unique form of latency that may promote chronic viral persistence for some small DNA and RNA viruses. (
  • and (iii) dLAT-EGFP, a control virus identical to dLAT-cpIAP except that it contained the enhanced green fluorescent protein open reading frame (ORF) in place of the cpIAP ORF, thereby controlling for expression of a random foreign gene instead of the cpIAP gene. (
  • Presently using a recombinant virus containing the gene for green fluorescent protein we will attempt to localize the cellular reservoir latent virus by confocal microscopy. (
  • Through computer modeling, the scientists identified the HIV protein Tat as the controller of the virus' on/off switch and found that manipulating Tat levels consistently changed the state of the virus. (
  • Latent uDNA was activated to de novo virus production by latency reversing agents that also activated latent integrated proviruses, including PKC activators, histone deacetylase inhibitors and P-TEFb agonists. (
  • Similar to what has recently been demonstrated for latent integrated proviruses, one or two applications of latency reversing agents failed to activate all latent unintegrated genomes. (
  • Herpes simplex virus and varicella-zoster virus can be reactivated from latency, but during intervals between reactivation, there is little ongoing virus replication. (
  • Varicella Zoster Virus (VZV) is a member of the alpha subfamily of herpesviruses and is responsible for the human diseases of the chicken pox and shingles. (
  • Episomal latency is more vulnerable to ribozymes or host foreign gene degradation than proviral latency (see below). (
  • Unfortunately, HIV in proviral latency is nearly impossible to target with antiretroviral drugs. (
  • Altogether, these findings suggest that site-specific DNA methylation of the BLV promoter represses viral transcription by directly inhibiting transcription factor binding, thereby contributing to true proviral latency. (
  • A remarkable fact concerning the latency of EBV is that different patterns of expression exist while it is latent, known as latency programs. (
  • Epstein-Barr virus induces global changes in cellular mRNA isoform usage that are important for the maintenance of latency. (
  • Hepatitis , for example, is a subacute or chronic disease, with a long latent period, that is caused by at least five viruses with different properties. (
  • Virus Latency Causes Cattle Disease? (
  • Therefore, ICP0 - viruses appear to possess the desired safety and efficacy profile of a live vaccine against herpetic disease. (
  • The Epstein-Barr virus is widespread in all human populations and is strongly associated with human disease, ranging from infectious mononucleosis to cancer. (
  • There is a new chapter on Human Viral Disease and rapidly developing areas, such as the use of viruses as gene therapy vectors, have been included. (
  • Updated throughout, including a new chapter on human viral disease and new material on the use of viruses as gene therapy vectors. (
  • Re-emergence from latency occurs in approximately one fifth of the population, usually during their elderly years or when their immune status is compromised, resulting in the painful and debilitating disease known as herpes zoster, or shingles. (
  • Most macaques carry B virus without overt signs of disease. (
  • Neither group was able to produce disease in rhesus macaques, presumably because the monkeys were already naturally infected with what Sabin's group named B virus (after patient W.B. (
  • With little fanfare on July 13, Florida officials released the findings of a Centers for Disease Control (CDC) study conducted recently in the Key West area revealing that about 10 percent, or 1,000 people, of the coastal town's population are infected with the dengue fever virus. (
  • Dengue fever is a virus-based disease spread by the bites of mosquitoes. (
  • We have chosen to examine viruses as our systems of interest not only because of relevance to human disease, but also because viral genomes, unlike human chromosomes, are genetically tractable and well annotated. (
  • The Weekes lab , focuses on identifying and characterising human proteins that can restrict the ability of viruses such as HCMV to replicate . (
  • Although not essential for persistence, latency has clinical importance as a mechanism of HIV-1 persistence in individuals treated with antiretroviral drugs. (
  • The detailed mechanism of HIV-1 latency remains unclear. (
  • Herpes simplex virus 1 (HSV-1) and 2 (HSV-2) are the human herpesviruses that cause recurrent cold sores and genital herpes. (
  • These two viruses are the cause of oral and genital herpes. (
  • With the model we identify two stable latency programs, corresponding to a resting and proliferating cell. (
  • Latency thus represents the principal form of persistence. (
  • The persistence of HIV-1 is therefore not dependent on latency. (
  • Viral latency is required for long-term persistence and allows viruses to evade host immune surveillance. (
  • Episomal latency refers to the use of genetic episomes during latency. (
  • The viruses have one or more genetic mutations that allow for continued replication but that inhibit latency. (
  • In light of this, it may be important to not only treat patients with both latency activators and HAART simultaneously, but to ensure their concurrent delivery to the same tissue and cellular compartments. (
  • However, Qp is inactive in type III latency, with the use of the yeast one- hybrid system, a new cellular gene has been identified that encodes proteins which bind to sequence in Qp. (
  • Zhang, L & Pagano, JS 1997, ' IRF-7, a new interferon regulatory factor associated with Epstein-Barr virus latency ', Molecular and cellular biology , vol. 17, no. 10, pp. 5748-5757. (
  • The lack of a valid cellular model to study HIV-1 latency has hindered advances in the understanding of its biology. (
  • We demonstrate that let-7 miRNAs inhibit the reactivation of latent EBV, providing an explanation for our previous observation that EBNA1 promotes latency. (
  • Although some viruses multiply slowly, this is not always the explanation for the chronicity or the slow progression of the diseases caused by these viruses. (
  • 21. Vaccines and Antivirals: The Prevention and Treatment of Virus Diseases. (
  • Herpes simplex virus (HSV), including HSV-1 and HSV-2, is an important pathogen that can cause many diseases. (
  • Molecular studies identify new diagnostic and therapeutic concepts to prevent and treat these viral diseases or to prevent the formation of virus-induced tumors. (
  • These distinct diseases are separated by a lengthy period of latency, often lasting decades, in which the virus resides within the ganglia of the host. (
  • People infected with the HIV virus can live relatively normal lives with exceedingly low or even undetectable viral loads thanks to powerful antiretroviral therapies that work to suppress viral replication. (
  • Latency causes the virus to go into hibernation, enabling it to escape eradication by currently available antiretroviral therapies. (
  • Latency allows HIV-1 to evade immune responses and to persist during antiretroviral therapy, which represents an important problem in clinical practice. (
  • Our study suggests that there may be means of activating latent virus in the body while the patient is on antiretroviral drugs to prevent the virus from spreading, and that this may eliminate at least some of the latent reservoir. (
  • An example of such a gene product is the latency associated transcripts (LAT) in herpes simplex virus, which interfere with apoptosis by downregulating a number of host factors, including major histocompatibility complex (MHC) and inhibiting the apoptotic pathway. (
  • For all types of herpes viruses, see Herpesviridae . (
  • During latency, a single viral gene-the LAT gene-is abundantly transcribed ( 1 , 2 ). (
  • Further studies using immunohistochemistry indicate that this viral gene is active during latency although not exclusively and therefore not likely to be a regulatory gene for latency. (