Viruses whose genetic material is RNA.
A large family of RNA helicases that share a common protein motif with the single letter amino acid sequence D-E-A-D (Asp-Glu-Ala-Asp). In addition to RNA helicase activity, members of the DEAD-box family participate in other aspects of RNA metabolism and regulation of RNA function.
One of the type I interferons produced by fibroblasts in response to stimulation by live or inactivated virus or by double-stranded RNA. It is a cytokine with antiviral, antiproliferative, and immunomodulating activity.
Ribonucleic acid that makes up the genetic material of 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 capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.
Established cell cultures that have the potential to propagate indefinitely.
Proteins found in any species of virus.
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.
A polynucleotide consisting essentially of chains with a repeating backbone of phosphate and ribose units to which nitrogenous bases are attached. RNA is unique among biological macromolecules in that it can encode genetic information, serve as an abundant structural component of cells, and also possesses catalytic activity. (Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
Deoxyribonucleic acid that makes up the genetic material of viruses.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
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.
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.
The complete genetic complement contained in a DNA or RNA molecule in a virus.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses.
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 general term for diseases produced by 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.
Viruses parasitic on plants higher than bacteria.
The assembly of VIRAL STRUCTURAL PROTEINS and nucleic acid (VIRAL DNA or VIRAL RNA) to form a VIRUS PARTICLE.
RNA consisting of two strands as opposed to the more prevalent single-stranded RNA. Most of the double-stranded segments are formed from transcription of DNA by intramolecular base-pairing of inverted complementary sequences separated by a single-stranded loop. Some double-stranded segments of RNA are normal in all organisms.
Process of growing viruses in live animals, plants, or cultured cells.
Viruses whose nucleic acid is DNA.
The interactions between a host and a pathogen, usually resulting in disease.
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.
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.
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.
The functional hereditary units of VIRUSES.
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)
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.
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.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
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.
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.
The ultimate exclusion of nonsense sequences or intervening sequences (introns) before the final RNA transcript is sent to the cytoplasm.
Substances elaborated by viruses that have antigenic activity.
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).
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.
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.
Virus diseases caused by the ORTHOMYXOVIRIDAE.
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.
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.
A genus of FLAVIVIRIDAE causing parenterally-transmitted HEPATITIS C which is associated with transfusions and drug abuse. Hepatitis C virus is the type species.
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 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.
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.
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.
The spatial arrangement of the atoms of a nucleic acid or polynucleotide that results in its characteristic 3-dimensional shape.
A process that changes the nucleotide sequence of mRNA from that of the DNA template encoding it. Some major classes of RNA editing are as follows: 1, the conversion of cytosine to uracil in mRNA; 2, the addition of variable number of guanines at pre-determined sites; and 3, the addition and deletion of uracils, templated by guide-RNAs (RNA, GUIDE).
Proteins encoded by a VIRAL GENOME that are produced in the organisms they infect, but not packaged into the VIRUS PARTICLES. Some of these proteins may play roles within the infected cell during VIRUS REPLICATION or act in regulation of virus replication or VIRUS ASSEMBLY.
Immunoglobulins produced in response to VIRAL ANTIGENS.
The type species of MORBILLIVIRUS and the cause of the highly infectious human disease MEASLES, which affects mostly children.
A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.
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.
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.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Enzymes that catalyze DNA template-directed extension of the 3'-end of an RNA strand one nucleotide at a time. They can initiate a chain de novo. In eukaryotes, three forms of the enzyme have been distinguished on the basis of sensitivity to alpha-amanitin, and the type of RNA synthesized. (From Enzyme Nomenclature, 1992).
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.
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.
Pneumovirus infections caused by the RESPIRATORY SYNCYTIAL VIRUSES. Humans and cattle are most affected but infections in goats and sheep have been reported.
Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).
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.
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.
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 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.
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.
A species of POLYOMAVIRUS originally isolated from Rhesus monkey kidney tissue. It produces malignancy in human and newborn hamster kidney cell cultures.
A single-stranded DNA-binding protein that is found in EUKARYOTIC CELLS. It is required for DNA REPLICATION; DNA REPAIR; and GENETIC RECOMBINATION.
The outer protein protective shell of a virus, which protects the viral nucleic acid.
A family of proteins that promote unwinding of RNA during splicing and translation.
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.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
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.
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 most abundant form of RNA. Together with proteins, it forms the ribosomes, playing a structural role and also a role in ribosomal binding of mRNA and tRNAs. Individual chains are conventionally designated by their sedimentation coefficients. In eukaryotes, four large chains exist, synthesized in the nucleolus and constituting about 50% of the ribosome. (Dorland, 28th ed)
Any DNA sequence capable of independent replication or a molecule that possesses a REPLICATION ORIGIN and which is therefore potentially capable of being replicated in a suitable cell. (Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
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.
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.
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.
The relationships of groups of organisms as reflected by their genetic makeup.
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.
Ribonucleic acid in bacteria having regulatory and catalytic roles as well as involvement in protein synthesis.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
The type species of the genus INFLUENZAVIRUS A that causes influenza and other diseases in humans and animals. Antigenic variation occurs frequently between strains, allowing classification into subtypes and variants. Transmission is usually by aerosol (human and most non-aquatic hosts) or waterborne (ducks). Infected birds shed the virus in their saliva, nasal secretions, and feces.
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.
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.
The presence of viruses in the blood.
The type species of RESPIROVIRUS in the subfamily PARAMYXOVIRINAE. It is the murine version of HUMAN PARAINFLUENZA VIRUS 1, distinguished by host range.
Proteins that form the CAPSID of VIRUSES.
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.
Elements of limited time intervals, contributing to particular results or situations.
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.
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).
Viruses which produce a mottled appearance of the leaves of plants.
A species of the genus FLAVIVIRUS which causes an acute febrile and sometimes hemorrhagic disease in man. Dengue is mosquito-borne and four serotypes are known.
A genus of the family HERPESVIRIDAE, subfamily ALPHAHERPESVIRINAE, consisting of herpes simplex-like viruses. The type species is HERPESVIRUS 1, HUMAN.
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.
Diamond MS, Zachariah M, Harris E. Mycophenolic acid inhibits dengue virus infection by preventing replication of viral RNA. ... 在美國食品藥品監督管理局(FDA)已發出警告,指接受黴酚酸酯和黴酚酸的患者受機會性感染的風險有所增加,例如激活潛在的病毒感染,如帶狀皰疹、其他單純皰疹感染、鉅細胞
"Mycophenolic acid inhibits dengue virus infection by preventing replication of viral RNA". Virology. 304 (2): 211-21. doi: ... such as activation of latent viral infections, including shingles, other herpes infections, cytomegalovirus, and BK virus ... A combination of mycophenolate and ribavirin has been found to stop infection by and replication of dengue virus in vitro. It ... This is a viral infection known as progressive multifocal leukoencephalopathy; it attacks the brain and is usually fatal. ...
Tract-Binding Protein and Its Binding to Viral RNA during Japanese Encephalitis Virus Infection Inhibits Virus Replication". ... Known for his studies in the fields of RNA virus replication and vaccine development, Vrati is an elected fellow of the ... molecular mechanisms of virus replication, assembly, egress as well as the clinical development of an oral rotavirus vaccine. ... "Viral Vaccines in India: An Overview". Proceedings of the National Academy of Sciences, India Section B: Biological Sciences. ...
... a positive sense RNA virus) infection model. HnRNPA1 has been found redistributed in the cytoplasmic site of viral replication ... and negative sense RNA viruses are multiple stages post-infection. The proteins role in viral life cycles varies depending on ... In the case of Hepatitis C virus (HCV), a positive sense RNA virus, hnRNPA1 interacts with a crucial region near the 3' end of ... In some, it promotes viral replication while in others, it abrogates it. hnRNPA1's anti-viral effect is present in human T-cell ...
RNA2 (2.9 kb) encodes the 2a protein (94 kDa), the RNA-dependent RNA polymerase, responsible for replication of the viral ... 3a and coat protein are essential for systemic infection in plants but not RNA replication. Lucas, R. W.; Larson, S. B.; ... Brome mosaic virus (BMV) is a small (28 nm, 86S), positive-stranded, icosahedral RNA plant virus belonging to the genus ... "Effects of deletions in the N-terminal basic arm of brome mosaic virus coat protein on RNA packaging and systemic infection". ...
List of viruses Viral replication Positive/negative-sense Animal viruses Double-stranded RNA viruses Retrovirus DNA viruses ... Purified RNA of a positive-sense virus can directly cause infection though it may be less infectious than the whole virus ... ve RNA ancestor and the -ve RNA viruses from within the dsRNA viruses. The closest relation to the -ve stranded RNA viruses is ... There are three distinct groups of RNA viruses depending on their genome and mode of replication: Double-stranded RNA viruses ( ...
The first proteins to be expressed after infection serve genome replication functions; they recruit the positive-strand viral ... All positive-strand RNA virus genomes encode RNA-dependent RNA polymerase a viral protein that synthesizes RNA from an RNA ... Positive-strand RNA viruses encode an RNA-dependent RNA polymerase (RdRp) which is used during replication of the genome to ... The ability of the RNA-dependent RNA polymerase of these viruses to switch RNA templates suggests a copy choice model of RNA ...
A3G combats HIV infection by interacting with and mutating the virus' RNA. The mutations genetically damage the virus protein ... RNA editing APOBEC3G Viral infectivity factor Michael Wentzel (12 January 2004). "UR Invests in Anti-HIV Startup". Rochester ... Interfering with ViF's ability to bind to A3G can effectively block HIV replication. OyaGen is researching several compounds ... The company is also researching drugs that protect A3G from Viral infectivity factor (ViF). ViF is a protein created by HIV ...
These people may carry high quantities of a protein called APOBEC3G that disrupts viral replication in cells. APOBEC3G, or "A3 ... This process involves the virus transcribing its singe-stranded RNA genome into double-stranded DNA that is incorporated into ... A3 usually stops dormant viruses in the human genome, called endogenous retroviruses, from reawakening and causing infections. ... Long-term nonprogressors typically have viral loads under 10,000 copies RNA/ml blood, do not take antiretrovirals, and have ...
UTR is the viral protein VPg which aids in viral entry and replication. 2A and 3C are viral proteinases which aid in the ... 3D is the RNA-dependent RNA polymerase (RdRP). 2B, 2C, and 3A are core viral proteins. The genome also codes for 4 capsid ... Coxsackie B4 virus is able to infect the brain and spinal cord and cause inflammation. Infection due to Coxsackie B viruses can ... CB4 virus has caused transplacental infections in mice. Infection in the first couple weeks of gestation has been shown to be ...
... are produced during high multiplicity of infection and contain cis-acting sequences which are required for viral replication. ... The Infectious bronchitis virus D-RNA is an RNA element known as defective RNA or D-RNA. This element is thought to be ... The helper virus identifies and responds to signals within the IBV D-RNA that are responsible for replication and packaging of ... essential for viral replication and efficient packaging of avian infectious bronchitis virus (IBV) particles. Coronavirus D-RNA ...
... how host range of a virus can be altered and to identify cellular proteins necessary for replication of the viral RNA. ... Though not susceptible to poliovirus infection, murine cells do allow for efficient replication of poliovirus RNA introduced ... An element present within the virus RNA was hypothesized to govern viral tropism which tissues the virus infected. Newborn mice ... The aim of his laboratory is to understand replication and pathogenesis of small RNA animal viruses Picornaviruses. The life ...
... which comprise a large and diverse family of RNA viruses that make a DNA copy of their RNA genome after infection of a host ... An essential step in the replication cycle of HIV-1 and other retroviruses is the integration of this viral DNA into the host ... The RNA genome of progeny virions and the template for translation of viral proteins are made when the integrated viral DNA is ... viral proteins, and host proteins. The viral proteins include integrase, nucleocapsid, matrix, viral protein R (Vpr), and ...
... early genes are transcribed in the cytoplasm by viral RNA polymerase. Early expression begins at 30 minutes post-infection. ... Replication follows the DNA strand displacement model. Dna templated transcription is the method of transcription. The virus ... Hare fibroma virus Myxoma virus Rabbit fibroma virus Squirrel fibroma virus Viruses in Leporipoxvirus are enveloped, with brick ... Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment of the viral proteins to host ...
... early genes are transcribed in the cytoplasm by viral RNA polymerase. Early expression begins at 30 minutes post-infection. ... Replication follows the DNA strand displacement model. DNA-templated transcription is the method of transcription. The virus ... Camelpox virus Cowpox virus Ectromelia virus Monkeypox virus Raccoonpox virus Skunkpox virus Taterapox virus Vaccinia virus ... Canarypox virus Fowlpox virus Juncopox virus Mynahpox virus Pigeonpox virus Psittacinepox virus Quailpox virus Sparrowpox virus ...
... early genes are transcribed in the cytoplasm by viral RNA polymerase. Early expression begins at 30 minutes post-infection. ... Replication follows the DNA strand displacement model. DNA-templated transcription is the method of transcription. The virus ... Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment of the viral proteins to host ... papular stomatitis virus Camel contagious ecthyma virus Orf virus Parapoxvirus of red deer in New Zealand Pseudocowpox virus ...
"Trans-dominant inhibition of RNA viral replication can slow growth of drug-resistant viruses". Nature Genetics. 37 (7): 701-9. ... The consequences of a viral infection are always host-dependent. However, the virus itself poses a major challenge that a ... replication rate (the rate at which viral RNA or DNA is synthesized intracellularly for viral progeny production), viral load ( ... Attenuated RNA virus vaccines can revert to virulent forms. RNA viruses released in nature for pest control purposes can mutate ...
... early genes are transcribed by viral RNA polymerase. This occurs half an hour after the initial infection. Intermediate Phase: ... This triggers genomic DNA replication. Usually 100 minutes post-infection Late Phase: Between 140 minutes and 48 hours post- ... Virions are the complete form of a virus outside of the host cell that is capable of infection. Virions contain a core of RNA ... Viral proteins attach to the host glycosaminoglycans (GAGs). This brings about endocytosis which allows the virus penetration ...
Second, viral particles without genomic RNA could use other cellular RNAs as structural support during replication. As ... It is currently unknown how human infection of BLV occurs. Mason-Pfizer monkey virus packaging signal Mansky LM, Gajary LC ( ... Mutation or deletion of the RNA encapsidation (packaging) signal reduces RNA viral packaging, but still allows for the viral ... sequence of the bovine leukemia virus RNA packaging signal can influence efficient RNA packaging and virus replication". ...
Replication follows the positive stranded RNA virus replication model. Positive stranded RNA virus transcription, using the ... The replication process leaves a surplus of positive sense (+)RNA strands, and it is thought that not only does the viral RNA ... that infection of plants from tombusviruses contain defective interfering RNAs that are born directly from the viruses RNA ... Ahlum waterborne virus Bean mild mosaic virus Chenopodium necrosis virus Cucumber soil-borne virus Trailing lespedeza virus 1 ...
... and promotes viral RNA synthesis. Viruses in this family are often associated with respiratory infections, and are transmitted ... Plays a major role in forming a capsid around the viral genome. P - Phosphoprotein required for replication. Facilitates RNA- ... It is a negative-strand RNA virus that is the second most common cause of lower respiratory infection in young children. ... L - RNA dependent RNA polymerase. Required for replication. Adds a methylated guanosine cap and poly(A) tail to nascent mRNA. ...
A number of hosts of CaMV possess small RNA-based viral silencing mechanisms that serve to limit viral infection. The products ... "Alternative structures of the cauliflower mosaic virus 35 S RNA leader: implications for viral expression and replication". J ... Jul 2011). "Massive production of small RNAs from a non-coding region of Cauliflower mosaic virus in plant defense and viral ... but the viral particles contain DNA instead of RNA. Cauliflower mosaic virus (CaMV) is the type species of the family ...
In inactive viral infections the virus will not replicate itself but through replication of its host cell. This state can last ... In a productive infection, the provirus is transcribed into messenger RNA which directly produces new virus, which in turn will ... This state can be a stage of virus replication, or a state that persists over longer periods of time as either inactive viral ... This is known as lysogenic viral reproduction. Integration can result in a latent infection or a productive infection. ...
During viral replication, the integrated DNA provirus is transcribed into RNA, some of which then undergo RNA splicing to ... The integrated viral DNA may then lie dormant, in the latent stage of HIV infection.[67] To actively produce the virus, certain ... enveloped RNA viruses. Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double- ... Two RNA genomes are encapsidated in each HIV-1 particle (see Structure and genome of HIV). Upon infection and replication ...
Evidence suggests viral presence in mature erythrocytes is a result of replication of the virus in hematopoitic erythrocyte ... The double-stranded RNA viral genome is about 20,000 bp long and is divided into 12 segments, which are termed Seg-1 to Seg-12 ... is a viral infection (Coltivirus) transmitted from the bite of an infected Rocky Mountain wood tick (Dermacentor andersoni). It ... 1 April 1993). "Replication of Colorado tick fever virus within human hematopoietic progenitor cells". J. Virol. 67 (4): 2389- ...
Although in cultured cells ORF3 has not appeared essential for HEV RNA replication, viral assembly, or infection, it is ... DNA virus. HBV (B). RNA virus. CBV. HAV (A). HCV (C). HDV (D). HEV (E). HGV (G). ... positive HEV RNA then the person has HEV infection. *negative HEV RNA then there is no evidence of current or recent infection ... DNA virus. Human polyomavirus 2 Progressive multifocal leukoencephalopathy. RNA virus. MeV Subacute sclerosing panencephalitis ...
... inhibits the replication of number of enveloped RNA viruses including influenza A, HIV and the Ebola and Dengue viruses. ... Consequently pharmacological induction of IFITM3 potentially could be used to treat a number of viral infections. Protein ... occurring as an intermediate in RNA viruses replication) or by other proteins. It is able to phosphorylate the eukaryotic ... Antiviral proteins are proteins that are induced by human or animal cells to interfere with viral replication. These proteins ...
Twenty-six serotypes are now recognised for this virus. The virus particle consists of ten strands of double-stranded RNA ... "Functional mapping of bluetongue virus proteins and their interactions with host proteins during virus replication". Cell ... In cattle, goats and wild ruminants infection is usually asymptomatic despite high virus levels in blood. Red deer are an ... Viral survival and vector longevity is seen during milder winters. A significant contribution to the northward spread of ...
The virus attaches to the cell membrane of the host cell. It then injects its DNA or RNA into the host to initiate infection. ... Viral replication is the formation of biological viruses during the infection process in the target host cells. Viruses must ... Viruses with segmented genomes for which replication occurs in the cytoplasm and for which the viral RNA-dependent RNA ... Like most viruses with RNA genomes, double-stranded RNA viruses do not rely on host polymerases for replication to the extent ...
Blood samples are tested for viral RNA, viral antibodies or for the virus itself to confirm the diagnosis.[1][6] ... After infection, a secreted glycoprotein, small soluble glycoprotein (sGP or GP) is synthesised. EBOV replication overwhelms ... The four are Bundibugyo virus (BDBV), Sudan virus (SUDV), Taï Forest virus (TAFV) and one simply called Ebola virus (EBOV, ... or detecting antibodies against the virus in a person's blood.[98] Isolating the virus by cell culture, detecting the viral RNA ...
Ribavirin is a prodrug which appears to interfere with viral replication by inhibiting RNA-dependent nucleic acid synthesis, ... Lassa fever infections are difficult to distinguish from other viral hemorrhagic fevers such as Ebola and Marburg virus disease ... Lujo virus. References[edit]. *^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad "Lassa fever". WHO. March 2016 ... Confirmation is by laboratory testing to detect the virus's RNA, antibodies for the virus, or the virus itself in cell culture. ...
Other viral hemorrhagic fevers, such as Ebola virus, Lassa virus, Marburg virus, and Junin virus, must be excluded as the cause ... Yellow fever is caused by yellow fever virus, a 40- to 50-nm-wide enveloped RNA virus, the type species and namesake of the ... 2007). "Flaviviridae: The Viruses and Their Replication". In Knipe, D. M.; P. M. Howley (eds.). Fields Virology (5th ed.). ... The mechanism of action of ribavirin in reducing liver pathology in yellow fever virus infection may be similar to its activity ...
It has both icosahedral virus particles, viral RNA-dependent RNA polymerase and protease and viral replication proteins. But ... the discovery of viral replication in culture was also with poliovirus in 1949. This was the first time that infection virus ... strand RNA genome is replicated through a double-stranded RNA intermediate that is formed using viral RDRP (RNA-Dependent RNA ... Virus RNA polymerases use VPg as primer. VPg as primer uses both minus and plus strand RNA synthesis. Picornavirus replication ...
... the impact of viral infection is higher on archaea than on bacteria and virus-induced lysis of archaea accounts for up to one- ... the latter virus has the largest currently reported ssDNA genome. Defenses against these viruses may involve RNA interference ... Kelman LM; Kelman Z (2004). "Multiple origins of replication in archaea". Trends Microbiol. 12 (9): 399-401. doi:10.1016/j.tim. ... Archaea can be infected by double-stranded DNA viruses that are unrelated to any other form of virus and have a variety of ...
The TATA-binding protein (TBP) could also be targeted by viruses as a means of viral transcription.[6] ... and viral genes.[8][2] The TATA box was found in protein coding genes transcribed by RNA polymerase II.[2] ... "A novel HIV-1-encoded microRNA enhances its viral replication by targeting the TATA box region". Retrovirology. 11: 23. doi: ... "Expression and nuclear localization of the TATA-box-binding protein during baculovirus infection". The Journal of General ...
Replication follows the positive stranded RNA virus replication model. Positive stranded RNA virus transcription is the method ... Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment to host receptors, which mediates ... Most calicivirus infections do not call for medical attention, but those who are immunocompromised may need to be hospitalized ... Newbury-1 virus Genus Norovirus; type species: Norwalk virus Genus Sapovirus; type species: Sapporo virus Genus Vesivirus; type ...
This is mostly shown for plant RNA viruses. Viroplasm is the location within the infected cell where viral replication and ... may help to develop new therapeutic approaches against virus infections in animal and plant cells. Viral evolution Viral ... Presence of viroplasms is used to diagnose certain viral infections. Understanding the phenomena of virus aggregation and of ... A viroplasm is an inclusion body in a cell where viral replication and assembly occurs. They may be thought of as viral ...
... also plays a key role in viral proliferation,[11] directing the initiation of DNA replication for the virus as well as ... Adenovirus infection. RNA virus. Rotavirus. Norovirus. Astrovirus. Coronavirus. Hepatitis. DNA virus. HBV (B). RNA virus. CBV. ... DNA virus. JCV Progressive multifocal leukoencephalopathy. RNA virus. MeV Subacute sclerosing panencephalitis. LCV Lymphocytic ... RNA virus. HCV Hepatocellular carcinoma. Splenic marginal zone lymphoma. HTLV-I Adult T-cell leukemia/lymphoma. ...
The N protein contributes to viral replication, and coats the genomic RNA within the virion. Presently the soybean thrips ( ... The NSs protein is also a non-structural protein and contributes to suppression of RNA silencing during plant infection. ... Soybean vein necrosis virus (SVNV, previously: Soybean vein necrosis associated virus SVNaV) is a plant pathogenic virus of ... The genome of SVNV is a negative sense single stranded RNA virus (Group V) that has three segments (S, M, and L segments). The ...
At that point, the infection will persist indefinitely. In most viruses, DNA is transcribed into RNA, and then RNA is ... Viral life cycle. *Viral entry. *Viral replication. *Viral shedding. *Virus latency. *Viroplasm ... Such viruses are either single stranded RNA (e.g. HIV) or double stranded DNA (e.g. Hepatitis B virus) viruses. ... Feline leukemia virus and Feline immunodeficiency virus infections are treated with biologics, including the only ...
Some of the viruses evolved into DNA viruses to protect their genes from attack. Through the process of viral infection into ... Self-replication. The ability to self-replicate, or synthesize other RNA molecules; relatively short RNA molecules that can ... In segmented RNA viruses, "mating" can occur when a host cell is infected by at least two virus particles. If these viruses ... Atkins JF, Gesteland RF, Cech T (2006). The RNA world: the nature of modern RNA suggests a prebiotic RNA world. Plainview, N.Y ...
RNA silencing mechanisms are also important in the plant systemic response, as they can block virus replication.[40] The ... a situation that can arise in viral infections of host cells.[8] They were named "natural killer" because of the initial notion ... For example, the Influenza A virus produces NS1 protein, which can bind to host and viral RNA, interact with immune signaling ... which degrades viral RNA.[23] Some viruses evade this by producing molecules which interfere with IFN production. ...
Infection[edit]. Vesicular stomatitis virus is believed to be taken up by the autophagosome from the cytosol and translocated ... A subset of viruses and bacteria subvert the autophagic pathway to promote their own replication.[63] Galectin-8 has recently ... "Subversion of cellular autophagosomal machinery by RNA viruses". PLoS Biol. 3 (5): e156. doi:10.1371/journal.pbio.0030156. PMC ... autophagy can be distinguished by the type and degree of regulatory signaling during stress particularly after viral infection. ...
Despois de que o virus entra no corpo hai un período de rápida replicación viral, que fai que o virus sexa abondoso no sangue ... Martínez, edited by Miguel Angel (2010). RNA interference and viruses : current innovations and future trends. Norfolk: Caister ... Lawn SD (2004). "AIDS in Africa: the impact of co-infections on the pathogenesis of HIV-1 infection". J. Infect. Dis. 48 (1): 1 ... Blankson, JN (2010 Mar). "Control of HIV-1 replication in elite suppressors". Discovery medicine 9 (46): 261-6. PMID 20350494. ...
negative regulation of viral genome replication. • humoral immune response. • positive regulation of interleukin-8 production. ... response to virus. • positive regulation of osteoclast differentiation. • negative regulation of cytokine secretion involved in ... negative regulation of transcription from RNA polymerase II promoter. • positive regulation of NF-kappaB transcription factor ... "Programmed death-1-induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection". Nat. ...
Integration occurs following production of the double-stranded viral DNA by the viral RNA/DNA-dependent DNA polymerase reverse ... The main function of IN is to insert the viral DNA into the host chromosomal DNA, a step that is essential for HIV replication ... Early in 2010, scientists solved the crystal structure of IN from prototype foamy virus (PFV) assembled on viral DNA ends. In ... Integration is in part responsible for the persistence of retroviral infections. After integration, the viral gene expression ...
... the virus' genetic material (RNA or DNA) must be introduced to the cell. Replication between viruses is greatly varied and ... In these forms of viral infection, the illness is often treated by the body's own immune response, and therefore the virus is ... See also: Infection. Infections may be caused by bacteria, viruses, fungi, and parasites. The pathogen that causes the disease ... Most DNA viruses assemble in the nucleus while most RNA viruses develop solely in cytoplasm.[22][23] ...
Viruses can replicate only in living cells.[71] Influenza infection and replication is a multi-step process: First, the virus ... The central core contains the viral RNA genome and other viral proteins that package and protect this RNA. RNA tends to be ... In virus classification, influenza viruses are RNA viruses that make up four of the seven genera of the family Orthomyxoviridae ... Negative-sense vRNAs that form the genomes of future viruses, RNA-dependent RNA polymerase, and other viral proteins are ...
Several animal models have also suggested Chikungunya virus may establish persistent infections. In a mouse model, viral RNA ... Viral replication is highly cytopathic, but susceptible to type-I and -II interferon.[43] In vivo, in studies using living ... and false positives can occur with infection due to other related viruses, such as o'nyong'nyong virus and Semliki Forest virus ... Because high amounts of virus are present in the blood in the beginning of acute infection, the virus can be spread from a ...
3 substitutions per site per year during viral genome replication.[7] Mutations in the surface proteins allow the virus to ... As in all RNA viruses, mutations in influenza occur frequently because the virus' RNA polymerase has no proofreading mechanism ... After an infection, the body produces many more of these virus-specific immune receptors, which prevent re-infection by this ... a vaccine against a virus works by teaching the immune system to recognize the antigens exhibited by this virus. However, viral ...
As it is a group 7 virus, replication involves an RNA intermediate. Four main open reading frames are encoded (ORFs) and the ... cell to infect others or are immediately dismantled so the new viral genomes can enter the nucleus and magnify the infection. ... Viral Polymerase[edit]. Hepadnaviridae encode their own polymerase, rather than co-opting host machinery as some other viruses ... Replication[edit]. Hepadnaviruses replicate through an RNA intermediate (which they transcribe back into cDNA using reverse ...
HIV infected individuals who naturally suppress viral replication have elevated levels of p21 and its associated mRNA. p21 ... transcription initiation from RNA polymerase II promoter. • G1/S transition of mitotic cell cycle. • cytokine-mediated ... p21 mediates the resistance of hematopoietic cells to an infection with HIV[35] by complexing with the HIV integrase and ... significantly limiting production of new viruses.[36] ... regulation of transcription from RNA polymerase II promoter. • ...
... which allows pieces of RNA from different viruses to mix and form a novel type of virus as new virus particles are being ... This suggests that the virus is unlikely to cause severe infections similar to those caused by the 1918 pandemic flu virus or ... These genes were passed on to the new virus. Gene sequences for every viral gene were made available through the Global ... advantage over seasonal flu strains and that reassortment is unlikely at this time due to its currently at ease in replication ...
Variola virus Smallpox was caused by infection with Variola virus, which belongs to the genus Orthopoxvirus, the family ... and are the sites of viral replication. Guarnieri bodies are readily identified in skin biopsies stained with hematoxylin and ... the most important of which is a viral-associated DNA-dependent RNA polymerase. ... Four orthopoxviruses cause infection in humans: variola, vaccinia, cowpox, and monkeypox. Variola virus infects only humans in ...
By inhibiting the function of NCp7, the viral replication is affected and a non-functional virus that is unable to infect its ... helps integrate the viral RNA into budding virions, and is intimately involved in the replication of HIV-1 in both the early ... Studies suggest that NOBA and NOBP were able to inhibit HIV-1 infection by inhibiting reverse transcription without an apparent ... As zinc fingers are known to be involved in m-RNA regulation, reverse transcription, protection of synthesized viral DNA, ...
Template:Virus navs(edit talk links history). Usage in navbox code[ಬದಲಾಯಿಸಿ]. To be used in a parent navbox. All navs are set , ... Template:Protozoan infection navs(edit talk links history). *Template:Psych navs(edit talk links history) ({{Psychology navs ... replication. *cycle. *recombination. *repair. *binding proteins. *Transcription *factors. *regulators. *nucleic acids. *RNA ...
"Apoptosis induced by Oropouche virus infection in HeLa cells is dependent on virus protein expression". Virus Research. 149 (1 ... Viral multiplication in a stable strain of human malignant epithelial cells (strain HeLa) derived from an epidermoid carcinoma ... Since the cells' first mass replications, they have been used by scientists in various types of investigations including ... Further HeLa cells have also been used to define cancer markers in RNA, and have been used to establish an RNAi Based ...
"Sequence-specific cleavage of hepatitis C virus RNA by DNAzymes: inhibition of viral RNA translation and replication". The ... "Advancements in Nucleic Acid Based Therapeutics against Respiratory Viral Infections". Journal of Clinical Medicine. 8 (1): 6. ... influenza B virus by 10-23 catalytic motif containing DNA enzymes significantly inhibits viral RNA translation and replication ... "Potent Intracellular Knock-Down of Influenza A Virus M2 Gene Transcript by DNAzymes Considerably Reduces Viral Replication in ...
RNA viruses regulate autophagy and the role of autophagy in NS-RNA viral replication and in immune responses to virus infection ... RNA viruses regulate autophagy and the role of autophagy in NS-RNA viral replication and in immune responses to virus infection ... virus and immune response, then focus on the interplay between NS-RNA viruses and autophagy during virus infection. We have ... virus and immune response, then focus on the interplay between NS-RNA viruses and autophagy during virus infection. We have ...
... for the first time that both the cellular and virion-associated pools of many of these proteins actively contribute to viral ... To this end, we performed a small interfering RNA functional screen and found that 15 of these host proteins altered HSV-1 ... Recently, we performed the first comprehensive characterization of the mature herpes simplex virus type 1 (HSV-1) in which up ... Altogether, these findings underscore the power and biological relevance of combining proteomics and RNA interference to ...
Lentivirus Infections. Retroviridae Infections. RNA Virus Infections. Virus Diseases. Sexually Transmitted Diseases, Viral. ... Inflammation, Viral Replication, and Atherosclerosis in Treated HIV Infection. The safety and scientific validity of this study ... All plasma HIV RNA levels within the past year must be below conventional levels of detection (, 50 copies RNA/mL), although ... HIV-infected patients who are on a stable antiretroviral drug regimen for at least a year; all plasma HIV RNA levels within the ...
Hepatitis, Viral, Human. Virus Diseases. Enterovirus Infections. Picornaviridae Infections. RNA Virus Infections. ... Evaluation the Possible Influence of Transcatheter Arterial Chemoembolization on Hepatitis B Viral Replication. This study has ... Evaluation the Possible Influence of Transcatheter Arterial Chemoembolization on Hepatitis B Viral Replication. ... the first and the third month after TACE to investigate the influence of TACE on hepatitis B virus replication. This study will ...
The authors wish to add the following Acknowledgments and completed Table 1 to their paper published in Viruses [1], doi: ... Identification of Genes Critical for Resistance to Infection by West Nile Virus Using RNA-Seq Analysis ... Cyclophilins as Modulators of Viral Replication. Previous Article in Journal. ... Viruses 2013, 5, 1219-1230.. Viruses 2013, 5, 1682-1683. AMA Style. Bastos JCS, Kohn LK, Fantinatti-Garboggini F, Padilla MA, ...
In this review, we summarize the current knowledge about how RNA viruses, including influenza virus, poliovirus, coxsackievirus ... In this review, we summarize the current knowledge about how RNA viruses, including influenza virus, poliovirus, coxsackievirus ... enterovirus 71, Japanese encephalitis virus, hepatitis C virus, and dengue virus, regulate these processes. We also discuss ... enterovirus 71, Japanese encephalitis virus, hepatitis C virus, and dengue virus, regulate these processes. We also discuss ...
Diamond MS, Zachariah M, Harris E. Mycophenolic acid inhibits dengue virus infection by preventing replication of viral RNA. ... 在美國食品藥品監督管理局(FDA)已發出警告,指接受黴酚酸酯和黴酚酸的患者受機會性感染的風險有所增加,例如激活潛在的病毒感染,如帶狀皰疹、其他單純皰疹感染、鉅細胞
Host Gene Responses To Infections by From WHSmith today! FREE delivery to store or FREE UK delivery on all orders over £20 ... host innate and adapted immune responses to viral replication in target organs; (iii) virus-activated signal transduction ... Hantavirus Infection and Innate Immunity (N Sen et al.); Positive Single-Stranded RNA Virus: Impact of Filovirus Infection upon ... this volume explores state-of-the-art knowledge of the molecular mechanisms of RNA virus infection and host-virus interactions ...
"Mycophenolic acid inhibits dengue virus infection by preventing replication of viral RNA". Virology. 304 (2): 211-21. doi: ... such as activation of latent viral infections, including shingles, other herpes infections, cytomegalovirus, and BK virus ... A combination of mycophenolate and ribavirin has been found to stop infection by and replication of dengue virus in vitro. It ... This is a viral infection known as progressive multifocal leukoencephalopathy; it attacks the brain and is usually fatal. ...
Many of these RNA-binding proteins regulate viral replication and can be targeted to influence infection outcome. ... RBPs stimulated by the infection redistribute to viral replication factories and regulate the capacity of the virus to infect. ... to analyze the RNA-bound proteome during virus infection. More than 200 cellular RNA-binding proteins change their binding ... System-wide Profiling of RNA-Binding Proteins Uncovers Key Regulators of Virus Infection. ...
Friesland M et al. Sigma-1 receptor regulates early steps of viral RNA replication at the onset of hepatitis C virus infection. ... Adeyemi RO et al. Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication. PLoS Pathog ... Sola I et al. The polypyrimidine tract-binding protein affects coronavirus RNA accumulation levels and relocalizes viral RNAs ... Palma-Ocampo HK et al. Interferon lambda inhibits dengue virus replication in epithelial cells. Virol J 12:150 (2015). WB . ...
We exposed D. melanogaster to two challenges of a virus known to produce an antiviral RNAi response, to examine whether any ... Results In this experiment we found no evidence that prior exposure to Drosophila C Virus (DCV) protects flies from a ... in Drosophila melanogaster is an ideal candidate for providing a specific and acquired response to subsequent infection. ... Viral replication Is the Subject Area "Viral replication" applicable to this article? Yes. No. ...
Microbial infection) Plays an essential role in Aichi virus RNA replication by recruiting PI4KB at the viral replication sites ... Microbial infection) Plays an essential role in Aichi virus RNA replication by recruiting PI4KB at the viral replication sites ... this interaction allows the formation of a 3A/ACBD3/PI4KB complex in order to synthesize PI4P at the viral RNA replication ... ACBD3 CRISPR as ready-to-use vector or virus: Non-viral , Lenti- , Adeno- , AAV- , siRNA - Browse All ...
... particularly during viral RNA replication and virion assembly. We also develop systems to study clinical HCV infection as part ... Our group study molecular aspects of hepatitis C virus infection and replication, specifically mechanisms of virus entry; ... My laboratory is focussed on the study of emerging viral infections with 2 main themes - acute hepatitis C infection and new ... Viral hepatitis. The focus of the hepatitis programme is hepatitis C virus (HCV), which afflicts approximately 3% of the global ...
The HCV exhibits substantial heterogeneity as a result of mutations occurring during viral replication.5This rapid mutation ... Acquisition of HCV infection from human milk has not been documented,30 31 although HCV RNA has been detected in human milk. ... 1992) Prevalence of hepatitis B and C viruses and human immunodeficiency virus infections in women of reproductive age. Br J ... Because antibodies elicited by one virus type do not recognize other virus types, previous infection does not protect against ...
Over the last century, the elucidation of viral oncogenic roles in many cancer types has provided fundamental knowledge on... ... Viral infections cause at least 10%-15% of all human carcinomas. ... by RNA interference allows for inhibition of HIV-1 replication ... In hepatocytes infected with duck hepatitis B virus, the template for viral RNA synthesis is amplified by an intracellular ... Viral infections cause at least 10%-15% of all human carcinomas. Over the last century, the elucidation of viral oncogenic ...
... and druggable target for antiviral intervention of a wide range of RNA virus infections. Inhibition of Membrane-Bound Viral RNA ... Gosert R, Kanjanahaluethai A, Egger D, Bienz K, Baker SC (2002) RNA replication of mouse hepatitis virus takes place at double- ... Ahlquist P (2006) Parallels among positive-strand RNA viruses, reverse- transcribing viruses and double-stranded RNA viruses. ... Thus, although RNA synthesis appears to be unaffected and viral RNA detected in preparations of extracellular virus was ribonu ...
Describes new CDC guidance for testing and follow-up of healthcare personnel potentially exposed to hepatitis C virus through ... Human serum facilitates hepatitis C virus infection, and neutralizing responses inversely correlate with viral replication ... Dynamics of HCV RNA levels during acute hepatitis C virus infection. J Med Virol 2014; 86: 1722-9. ... Acute infection with a single hepatitis C virus strain in dialysis patients: Analysis of adaptive immune response and viral ...
... leading to disruption of the viral RNA replication complex, blockage of HCV RNA production, and inhibition of viral replication ... HCV is a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family; HCV infection is associated with the ... viral RNA-dependent HBV DNA polymerase and, so, the replication of viral DNA and transcription. Check for active clinical ... The E1B protein causes p53 inactivation in host cells, which promotes viral replication. Deletion of E1B prevents replication ...
HIV Infections. Hepatitis C, Chronic. Hepatitis, Viral, Human. Virus Diseases. Flaviviridae Infections. RNA Virus Infections. ... Lentivirus Infections. Retroviridae Infections. Sexually Transmitted Diseases, Viral. Sexually Transmitted Diseases. Slow Virus ... Detectable HIV RNA and HCV RNA HIV and HCV co-infected with detectable HIV RNA and HCV RNA ... and Hepatitis C virus (HCV) co-infection (HIV/HCV) have a more rapid and progressive course of HCV infection, leading to fatty ...
Pur-α also serves as cellular host factor for the infection of RNA viruses like JC virus and HIV (7-10), most likely by ... Its best-studied family member, Pur-α, acts as a transcriptional regulator, as host factor for viral replication, and as ... 2001) Coordinate effects of human immunodeficiency virus type 1 protein Tat and cellular protein Puralpha on DNA replication ... The observed selective reduction of RNA binding by Pur-α (I-II/R65A, R142A) (see Fig. 4D) indicates that the tested RNA and DNA ...
... viral replication protein stability that may underlie chronic viral infections for some small genome DNA and RNA viruses. ... replication proteins is a unique form of latency that may promote chronic viral persistence for some small DNA and RNA viruses. ... is required for long-term virus persistence. There is no known latency mechanism for chronic small DNA virus infections. Merkel ... Viral latency is required for long-term persistence and allows viruses to evade host immune surveillance. We find that Merkel ...
We report the fatal case of a patient in China who was infected with an A(H7N9) virus having a polybasic amino acid sequence at ... Enhanced surveillance is needed to determine whether this highly pathogenic avian influenza A(H7N9) virus will continue to ... Most of the A(H7N9) viruses previously reported have been of low pathogenicity. ... virus RNA. Viral RNA was detectable in the patients endotracheal aspirate at high levels (,4 log RNA copies/mL) until day 17 ( ...
Binding to different sites within the viral RNA suggests that AUF1 may negatively regulate infection by these viruses using ... 4). Viral RNA synthesis was inhibited at a time during infection when there is a detectable increase in viral RNA (Fig. 2) and ... Inhibition of viral RNA synthesis during infection leads to reduced accumulation of viral proteins in cells. Viral proteinase ... Since AUF1 may regulate viral RNA stability by binding to regions of RNA outside the 3′ NCR, a direct measurement of viral RNA ...
These modifications -- chemical tags known as methyl groups -- influence viral replication and the human immune response. ... Researchers at University of California San Diego School of Medicine have discovered that Zika virus infection leads to ... modifications of both viral and human genetic material. ... Zika virus infection alters human and viral RNA. University of ... Zika virus infection alters human and viral RNA Findings may influence vaccine and therapy development ...
RNA2 (2.9 kb) encodes the 2a protein (94 kDa), the RNA-dependent RNA polymerase, responsible for replication of the viral ... 3a and coat protein are essential for systemic infection in plants but not RNA replication. Lucas, R. W.; Larson, S. B.; ... Brome mosaic virus (BMV) is a small (28 nm, 86S), positive-stranded, icosahedral RNA plant virus belonging to the genus ... "Effects of deletions in the N-terminal basic arm of brome mosaic virus coat protein on RNA packaging and systemic infection". ...
CKS1B and MAP2K5 significantly inhibited hepatitis C viral RNA replication. PACSIN1, by contrast, inhibited hepatitis C virus ... Title: Identification of novel human kinases that suppress hepatitis C virus infection. ... Project title: HPA RNA-seq normal tissues. *Description: RNA-seq was performed of tissue samples from 95 human individuals ... Model RNAs and proteins are also reported here.. Reference GRCh38.p13 Primary Assembly. Genomic * NC_000015.10 Reference GRCh38 ...
Lentivirus Infections. Retroviridae Infections. RNA Virus Infections. Virus Diseases. Sexually Transmitted Diseases, Viral. ... Dehydroepiandrosterone Effects on HIV-1 Replication. The safety and scientific validity of this study is the responsibility of ... Active opportunistic infections or malignancy other than localized cutaneous KS lesions. *Concurrent or prior use within the ... This studys purpose is to learn how dehydroepiandrosterone (DHEA) affects the HIV virus, the immune system, hormone levels, ...
HCV, like many other viruses, exploit host cellular machinery for productive infection. However, unlike other RNA viruses, HCV ... great strides have been made in characterizing the virus and functions of viral genes as well as in unraveling the replication ... Hepatitis C virus infection activates an innate pathway involving IKK-α in lipogenesis and viral assembly.. Li Q, Pène V, ... and viral hepatitis-associated hepatocellular carcinoma (HCC).. Current Research. Infection with hepatitis B and C viruses ...
  • We also review recent advances in understanding how NS-RNA viral proteins perturb autophagy and how autophagy-related proteins contribute to NS-RNA virus replication, pathogenesis and antiviral immunity. (
  • The compendium of RNA-binding proteins (RBPs) has been greatly expanded by the development of RNA-interactome capture (RIC). (
  • More than 200 cellular RNA-binding proteins change their binding activity in response to this challenge, mainly driven by transcript availability. (
  • Many of these RNA-binding proteins regulate viral replication and can be targeted to influence infection outcome. (
  • Zinc finger proteins designed to specifically target duck hepatitis B virus covalently closed circular DNA inhibit viral transcription in tissue culture. (
  • 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. (
  • Other than proteins involved in the innate immune response, few host factors have been identified that restrict picornavirus replication. (
  • As part of the alteration of the host cell landscape to promote virus replication, picornaviruses modify lipid metabolism and reorganize membrane architecture to form replication complexes, downregulate host cell transcription and translation to redirect cellular resources to favor viral replication, and disrupt nucleocytoplasmic trafficking to relocate nuclear proteins required for replication into the cytoplasm ( 1 - 4 ). (
  • However, the dependence on cellular proteins to promote each step of the virus replication cycle provides opportunities for viral interactions with cellular restriction factors. (
  • Among the viral gene products, the accessory proteins HBeAg and HBX are not essential for replication in vitro but appear to be important for viral infection in vivo. (
  • In human cells, RNA is the genetic material that carries instructions from the DNA in a cell's nucleus out to the cytoplasm, where molecular machinery uses those instructions to build proteins. (
  • These viruses hijack the host's cellular machinery to translate its RNA to proteins. (
  • Many of the positive-strand RNA viruses that belong to the alphavirus family share a high degree of similarity in proteins involved in genomic replication and synthesis. (
  • The methyltransferase domain shows sequence similarity to other alphavirus m7G methyltransferases and guanyltransferases, called nsP1 proteins, involved in RNA capping. (
  • The dicistronic RNA3 (2.1 kb) encodes for two proteins, the 3a protein (involved in cell-to-cell migration during infection) and the coat protein (for RNA encapsidation and vascular spread), which is expressed from a subgenomic replication intermediate mRNA, called RNA4 (0.9 kb). (
  • The structural proteins comprise the building blocks for the virion and the nonstructural proteins replicate the viral RNA [ 7 ]. (
  • While it is known that the membrane-associated viral protein 6K2 plays a role in the process, the contribution of host proteins has been poorly defined. (
  • Nonstructural (NS) proteins are not part of the virus coat and are thought to participate in the formation of these viral replication compartments (RCs). (
  • Here, we used tick-borne encephalitis virus (TBEV) as a model for the flaviviruses and developed a stable human cell line in which the expression of NS proteins can be induced without viral RNA replication. (
  • We show that the expression of six NS proteins is sufficient to induce infection-like dilation of the endoplasmic reticulum (ER) and the formation of RC-like membrane invaginations. (
  • We propose that the NS proteins drive the remodeling of ER membranes and that viral RNA, RNA replication, viral polymerase, and TBEV structural proteins are not required. (
  • Expression of the individual viral components of the replication machinery in cells demonstrates that the 3 viral proteins required for replication are sufficient to drive cytoplasmic phase separation. (
  • By 4 h postinfection (hpi), however, electron-dense structures appear in the cytoplasm, which are enriched in proteins required for RNA synthesis, namely, the nucleocapsid protein (N), the phosphoprotein (P), and the multifunctional large protein (L). Once formed, these compartments become the major sites of RNA synthesis ( 3 - 5 ). (
  • A number of DNA and RNA viruses encode proteins that target critical cell cycle regulators to achieve cellular conditions that are beneficial for viral replication. (
  • However, viruses encode a limited number of proteins able to interact with RNA and thus hijack cellular RNA-binding proteins to replicate and spread. (
  • In addition, the antiviral 'arsenal' of the host cells includes specialised RNA-binding proteins that recognise viral RNA and intermediaries of replication. (
  • Therefore, cellular RNA-binding proteins are critical players in the virus-host cell battlefield. (
  • Unfortunately, the complement of cellular RNA-binding proteins that engage with viral RNA remains largely unknown. (
  • In this webcast, the speakers will describe a recently developed approach, called viral RNA interactome capture (vRIC), to comprehensively discover the proteins that interact with viral RNA in infected cells with high specificity and depth. (
  • To test if these cellular proteins are important for virus infection, the researchers then developed a high-throughput viral fitness assay to follow viral gene expression kinetics in near real time. (
  • Rather the amino acid is necessary for the expression of the late viral functions such as synthesis of viral coat proteins and production of complete infectious virions. (
  • Arginine is involved in the synthesis of viral proteins and it has been hypothesised that arginine is necessary for the formation of a functional protein that is essential for virion maturation. (
  • Sequence-specific degradation of mRNA by short interfering RNA (siRNA) allows the selective inhibition of viral proteins that are critical for human immunodeficiency virus type 1 (HIV-1) replication. (
  • The genome RNA serves as both mRNA for translation of viral proteins and the template for RNA replication. (
  • Although structural proteins are clearly dispensable for RNA replication, recent evidence points to an important role of several non-structural proteins in particle assembly and release, turning their designation on its head. (
  • In the present review, the molecular and cellular aspects of the HCV life cycle and the role of viral proteins in pathological liver conditions caused by HCV infection are described. (
  • The outer proteins of the virus both protect the viral genome (which may be deoxyribonucleic acid or, unlike cellular genomes, ribonucleic acid) and enable it to identify and infect suitable target cells. (
  • The initial interaction between a virus and its host cell is mediated by proteins (often with attached sugars) on the surface of the virus and by proteins and other structures on the host cell. (
  • Genes expressed later are generally for the proteins that make up the virus particle (structural proteins) or those involved in viral assembly. (
  • Coat proteins (CPs) are the most abundant protein produced during a viral infection. (
  • The cells that exhibited cytoplasmic capsid proteins also contained virus nucleic acids, indicating that these proteins were synthesized by the infected cells and not through uptake from the culture medium. (
  • DENV contains a relatively short positive-stranded RNA genome, which encodes ten viral proteins. (
  • The viral genome codes four nonstructural proteins that are associated with viral RNA replication. (
  • The subgenomic RNA, which codes the structural proteins, is transcribed from the negative template strand. (
  • The replication of genomic and subgenomic RNA strands is associated with replication complexes composed of the nonstructural proteins. (
  • Transfection of plasmids expressing viral replicase proteins and template RNA can also induce formation of replication complexes in addition to live virus infection. (
  • demonstrated that the signaling proteins Fas-associated via death domain (FADD) and receptor-interacting protein 1 (RIP1) were essential for the production of type I IFNs in response to infection with vesicular stomatitis virus (VSV) and transfection with poly I:C ( 6 ). (
  • Novel data analysis tools will be developed to identify signatures of mutation and variant post-translational modification in viral proteins, using mass spectra collected from purified viruses by the Hutchinson group. (
  • Maps of protein-level diversity will be compared to next-generation sequencing of the viral genome and transcriptome, in order to map of sites in viral proteins which can tolerate variation and sites which select against it. (
  • Viral RNA molecules are copied by one of the virus's own proteins and so before the viral RNA can be replicated, it must first be translated to form viral proteins. (
  • When and where replication begins depends on the concentration of translated proteins around the RNA and so replication tends to begin in particular areas of the cell at different times. (
  • We have analyzed the levels of viral proteins and transcripts, as well as the viral replicative forms, in the presence of the constructed pSUPER vectors. (
  • We show that RNAi is an efficient approach in reducing the level of HBV transcripts and proteins and in suppression of HBV replication. (
  • In this study, we present a series of experiments showing a significant reduction in hepatitis B virus (HBV) transcripts and proteins in cell culture, as well as in the viral replicative forms, induced by siRNA-producing vectors. (
  • Therefore, using RNAi as an anti-HBV tool seems to have some important advantages: First, specifically targeting the viral transcripts and proteins severely impairs its replication and promotes its eradication, without activating nonspecific cellular responses, hence minimizing undesirable side effects. (
  • The potato mop-top virus (PMTV) triple gene block 2 (TGB2) movement proteins fused to monomeric red fluorescent protein (mRFP-TGB2) was expressed under the control of the PMTV subgenomic promoter from a PMTV vector. (
  • This comprehensive compilation of the altered gene expression profiles and signal transduction pathways in host cells in response to the majority of human/animal RNA viruses opens new directions for basic and clinical research on viral pathogenesis, and also provides valuable biomarkers for researchers to select gene targets in the development of diagnostic tests and antiviral therapeutics for a number of infectious diseases. (
  • Sera will be used in an in-vitro hepatocyte model of hepatitis C infection to better understand the pathogenesis of HIV/HCV co-infection, and to gain insight into intracellular mechanisms. (
  • HCV gene products have been shown to interact with many host factors and to induce cellular alterations vital for viral replication, persistence and pathogenesis. (
  • We have taken three approaches to study HCV infection and pathogenesis. (
  • Further investigations on this overwhelming generation of DI-RNA may provide important insights into the understanding of H7N9 viral replication and pathogenesis. (
  • Gaining insight into the pathogenesis of these viruses is thus relevant to thoroughly understand them and identify new treatment and prevention options. (
  • The general objectives would be to characterize the susceptibility, pathogenesis, and virus-vector-host interactions of BTV, RVFV, and VSV in mammalian and invertebrate cell cultures and hosts. (
  • The characterization of viral populations that successfully initiate infection, and also those that drive progression to chronicity is instrumental for understanding pathogenesis and vaccine design. (
  • Studies of ISAV-induced apoptosis may provide a clearer picture of the cellular mechanisms of viral persistence and pathogenesis in ISAV infection. (
  • However, the interplay between MSCs and virus is like a double-edge sword, and it also provides beneficial effects such as allowing the proliferation and function of antiviral specific effector cells instead of suppressing them, serving as an ideal tool for study of viral pathogenesis, and protecting hosts against viral challenge by using the antimicrobial activity. (
  • Investigating in details the relationship between autophagy and viral replication will greatly improve our knowledge of the pathogenesis of ChikV and provide insight for the design of candidate antiviral therapeutics. (
  • A new study published on the online preprint server bioRxiv * in June 2020 reports the successful use of three primate species to model the infection, pathogenesis, and clinical features associated with COVID-19. (
  • In conclusion, sensitive molecular assays are important tools for reviewing pathogenesis of FeLV infection. (
  • To apply molecular, biochemical and functional genomic tools to identify and characterize structural and functional interactions among the virus, viral gene products, cellular pathways and the host. (
  • The nonsegmented negative-strand (NNS) RNA virus vesicular stomatitis virus (VSV) is capable of transcribing its genomic RNA initially in the absence of any apparent specialized replication compartment ( 3 ). (
  • The 11,161-nucleotide genomic RNA of VSV is found completely encased within a sheath of 1,240 N protein molecules ( 9 ). (
  • Lavia P, Mileo AM, Giordano A, Paggi MG (2003) Emerging roles of DNA tumor viruses in cell proliferation: new insights into genomic instability. (
  • Their observations reveal that influenza polymerase dimerization as a feature that can restrict the reassortment of genomic viral RNA segments, a major evolutionary mechanism of influenza viruses, and could become an attractive target for antiviral drug development. (
  • Curing patients with viral infections is a public health problem due to antigen alterations and drug resistance caused by the high genomic mutation rate. (
  • New antiviral drug design leading to transcriptional reduction of Influenza viral genomic RNA segments. (
  • This is a critical requirement, as many inactivated viruses that carry the required antigens or genomic sequence could persist over a relatively long period in the environment ( 13 ). (
  • As a unique genomic entity, the influenza A virus RNP has been extensively studied since the 1960s. (
  • Viral coat protein (CP), genomic RNA and fluorescently-labeled TGB2 were detected in plastid preparations isolated from the infected leaves, and viral RNA was localized to chloroplasts in infected tissues. (
  • K22 exerts most potent antiviral activity after virus entry during an early step of the viral life cycle. (
  • Collectively, this study proposes an evolutionary conserved step in the life cycle of positive-stranded RNA viruses, the recruitment of cellular membranes for viral replication, as vulnerable and, most importantly, druggable target for antiviral intervention. (
  • We expect this mode of action to serve as a paradigm for the development of potent antiviral drugs to combat many animal and human virus infections. (
  • Our results identify a cooperative function for retrotransposons and antiviral RNAi in the control of lethal acute infection for the establishment of viral persistence. (
  • Outside of the antiviral activity of the innate immune system, few host factors have been identified that restrict picornavirus replication. (
  • Understanding how these viruses replicate and targeting key points in their life cycle can help advance antiviral treatments worldwide. (
  • His main research interests are influenza viruses, HIV, and antiviral immunology. (
  • It confers antiviral properties by blocking viral entry, [140] Moscona A. Medical management of influenza infection. (
  • IFN-induced antiviral protein which performs as an inhibitor of cellular and viral processes, cell migration, proliferation, signaling, as well as viral replication. (
  • While some treatment strategies may focus on letting down the blood-brain barrier that blocks the entry of many molecules to the brain to allow the antiviral drug to have access to infected brain tissue, this could be counterproductive by allowing the virus to enter as well, fear the researchers. (
  • When introduced into mice, a family of short, triphosphorylated stem-loop RNAs (SLRs) induces a potent interferon response and the activation of specific genes essential for antiviral defense. (
  • RIG-I activation by RNA leads to the induction of type I interferon (IFN) genes through the activation of its adaptor molecule, mitochondrial antiviral signaling protein (MAVS) ( 5 ). (
  • Effective recognition of viral infection and subsequent triggering of antiviral innate immune responses are essential for the host antiviral defense, which is tightly regulated by multiple regulators, including microRNAs. (
  • Upon viral infection, host innate immunity is the first line of antiviral defense, designed to recognize viral components and produce proinflammatory cytokines and type I IFN ( 1 - 3 ). (
  • Type I IFN plays critical roles in antiviral immune response mainly through induction of cellular resistance to viral infection and apoptosis of virus-infected cells. (
  • There are no currently available specific antiviral therapies for non-polio Enterovirus infections. (
  • Wageningen University is seeking commercial partners interested in developing a new class of antiviral drugs based on RNA compounds able to reduce viral replication levels and potentially applicable to all Influenza viruses, including new pandemic strains. (
  • Current options to reduce the impact of Influenza virus infections include vaccination and the use of antiviral drugs. (
  • Antiviral drugs have the advantage to be immediately applicable and thereby may help to contain an emerging pandemic virus at its emergence. (
  • The antiviral RNA compounds proposed in this invention act on a very conserved mechanism within Influenza viruses that is different from the currently available classes of emerging drugs, thus offering possibilities for new antiviral drug design and for solutions to the above described limitations. (
  • Since the RNA compounds rely on a sequence which is conserved among all Influenza (A, B and C) viruses, the RNA compounds can be functional as antiviral drug against all Influenza viruses, including new, emerging pandemic strains. (
  • We found that the antiviral activity of tat shRNA was abolished due to the emergence of viral quasispecies harboring a point mutation in the shRNA target region. (
  • Alternatively, similar to present antiviral drug therapy paradigms, DNA constructs expressing multiple siRNAs need to be developed that target different regions of the viral genome, thereby reducing the probability of generating escape mutants. (
  • A new direct-acting antiviral (DAA) for chronic hepatitis C virus (HCV) infection is available in Australia. (
  • Retinoic acid-inducible gene I (RIG-I), a pivotal cytosolic sensor, recognizes viral RNAs to initiate antiviral innate immunity. (
  • Among these PRRs, retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) serve as cytoplasmic RNA sensors that recognize viral RNA and trigger signaling cascades that induce antiviral mediators, such as type I interferons (IFNs) and proinflammatory cytokines ( 2 ). (
  • Analogous to other RNA virus infections, development of effective vaccines and antiviral treatments has been constrained by the ability of these viruses to swiftly overcome evolutionary pressures such as host immunity and antiviral drugs [5] - [7] . (
  • We also showed that viral mRNA increased steadily throughout the infection, in spite of the increased levels of IFN-α and Mx, indicating that these genes have little or no antiviral effect on ISAV in Atlantic salmon cells. (
  • Despite the nearly 400 million new infections estimated annually, no vaccines or specific antiviral therapeutics are currently available. (
  • Our findings suggest that inhibition of translation elongation, an obligate step in the viral replication cycle, may provide a general antiviral strategy against fast-replicating RNA viruses. (
  • Despite these staggering numbers, there is currently no vaccine, nor antiviral drugs available to prevent or to treat infection. (
  • Due to the intrinsically high mutation rate of RNA viruses, resistance to antiviral drugs that act against viral targets ( e.g. , inhibitors of viral proteases and polymerases) can occur rapidly. (
  • Since the immune system clears DENV and other acute viral pathogens if given sufficient time, the goal of antiviral therapy against these pathogens may be to shorten the duration of the infection and decrease viral burden by inhibiting replication, thereby reducing transmission and the incidence of severe disease. (
  • Heralded by this work, additional strategies for inhibiting DENV and other RNA viruses via host targets through repurposing of known drugs or validation of new targets and antiviral entities are of considerable interest. (
  • Mice lacking the adaptor protein that initiates an antiviral response downstream of the RNA helicases retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) have recently been described. (
  • These studies highlight the essential and nonredundant role of nucleic acid recognition in the induction of type I interferon production and raise important questions regarding the nature of cell-autonomous virus detection in coordinating the antiviral response. (
  • These cytokines, originally identified as a soluble activity that blocked virus spread among cultured cells ( 1 , 2 ), have several essential functions in the antiviral response. (
  • Type I IFNs act in both an autocrine and paracrine fashion by inducing the expression of hundreds of genes that together establish an "antiviral state," which restricts the spread of virus among neighboring cells. (
  • These lines of investigations will lead to new insights how these small noncoding RNAs regulate expression of cellular and viral mRNAs and may point to new venues for antiviral therapeutics against HCV. (
  • The antiviral effect is sequence-specific and does not depend on active viral replication. (
  • 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. (
  • Michael holds a PhD in virology and has studied RNA virus replication and the innate immune response to viral infections at the Universities of Freiburg and Heidelberg (Germany), the Pasteur Institute in Paris (France) and the Scripps Research Institute in La Jolla (U.S.A). He currently conducts research at the University of Canberra and the CSIRO Black Mountain Laboratories where he works with rabbit caliciviruses. (
  • This is the first comprehensive book on human/animal gene responses to RNA viral infections, including prevalent, emerging and re-emerging RNA viruses such as HIV, SARS-CoV, West Nile virus, influenza virus and many others. (
  • Enhanced surveillance is needed to determine whether this highly pathogenic avian influenza A(H7N9) virus will continue to spread. (
  • Avian influenza A(H7N9) viruses with zoonotic potential emerged in East China in early 2013. (
  • The A(H7N9) virus is a low pathogenicity avian influenza (LPAI) virus that typically causes no signs of disease in birds and has become enzootic in poultry. (
  • Prevention and therapy, evolution and emerging viruses receive particular attention and specific chapters address the major infectious challenges posed by HIV, pandemic influenza and BSE. (
  • The indication is for patients in whom other treatments for influenza, including the inhaled formulation of zanamivir, are unsuitable, and/or the patient's influenza virus is known or suspected to be resistant to other treatments. (
  • [140] Moscona A. Medical management of influenza infection. (
  • Amantadine-oseltamivir combination therapy for H5N1 influenza virus infection in mice. (
  • Effects of the combination of favipiravir (T-705) and oseltamivir on influenza A virus infections in mice. (
  • An in vitro study suggests that amantadine and oseltamivir combination therapy may reduce the emergence of drug-resistant influenza A virus. (
  • Currently under development, this agent targets host respiratory cells rather than the influenza virus itself, specifically the sialic acid receptor used by the influenza virus to attach to the airway epithelium. (
  • Studies have shown in vitro effectiveness against both influenza A and B, and in vitro and in vivo effectiveness against human parainfluenza viruses. (
  • DAS181, a novel sialidase fusion protein, protects mice from lethal avian influenza H5N1 virus infection. (
  • Cyanovirin-N is a protein that interacts with the haemagglutinin cell surface protein of both influenza A and influenza B viruses in vitro. (
  • Influenza defective interfering (DI) particles are replication-incompetent viruses carrying large internal deletion in the genome. (
  • Despite reports of DI particles present in seasonal influenza A H1N1 infections, their existence in human infections by the avian influenza A viruses, such as H7N9, has not been studied. (
  • Influenza DI-RNA is known as a defective viral RNA with single large internal deletion. (
  • Pandemic influenza A virus (IAV) outbreaks occur when strains from animal reservoirs acquire the ability to infect and spread among humans. (
  • Influenza A viruses (IAVs) are negative-sense, single-stranded RNA viruses with a segmented genome. (
  • One well-established factor is the influenza RNA-dependent RNA polymerase (RdRP): this enzyme catalyzes replication of the viral genome and transcription of viral messenger RNAs (mRNAs) 3 . (
  • New insights on how subunits of the influenza virus polymerase co-evolve to ensure efficient viral RNA replication are provided by a study published October 3 in the PLOS Pathogens journal, by researchers from the Institut Pasteur and the CNRS (French National Center for Scientific Research). (
  • Because of their yearly recurrence and the potential emergence of pandemic viruses, influenza viruses represent a worldwide major public health threat. (
  • Enhancing fundamental knowledge about the RNA-polymerase of influenza viruses, which is an enzyme that consists of three subunits (i.e., a heterotrimer) and ensures transcription and replication of the viral genome, is essential to reach the goal of better prevention and treatment of disease. (
  • Wageningen University's scientists have identified RNA compounds that are preferentially being used during the initiation of the Influenza virus genome transcription. (
  • In vivo inhibition of influenza A virus replication by RNA interference targeting the PB2 subunit via intratracheal delivery. (
  • Influenza virus infection is a major threat to human health. (
  • In this study, we constructed a series of DNA vector-based short hairpin RNAs (shRNAs) that target various genes of the influenza A virus using the polymerase III U6-RNA promoter to prevent influenza virus infection in vitro and in a mouse model. (
  • Three sets of DNA vector-based shRNA, two targeting genes encoding the polymerase acidic protein (PA) and one targeting polymerase basic protein 2 (PB2), efficiently inhibited the replication of influenza virus A/WSN/33(H1N1) in vitro. (
  • We also successfully prevented influenza virus A/WSN/33(H1N1) infection in a C57BL/6 mouse model by intratracheal delivery of anti-PB2 shRNA. (
  • Our findings suggest that the PB2-targeting shRNA plasmid showed potential for use as an RNAi-based therapeutic for influenza virus infection. (
  • RIG-I, the most important RLR, recognizes a wide variety of RNA viruses, including influenza A virus (IAV), Sendai virus (SeV), respiratory syncytial virus (RSV), and vesicular stomatitis virus (VSV) ( 2 ). (
  • The genome of influenza A viruses consists of eight segments of single-stranded, negative-sense RNA that are encapsidated as individual rod-shaped ribonucleoprotein complexes (RNPs). (
  • Influenza A virus RNPs play important roles during virus infection by directing viral RNA replication and transcription, intracellular transport of the viral RNA, gene reassortment as well as viral genome packaging into progeny particles. (
  • Lower Respiratory Tract Infections (LRTI) induced by Corona (SARS-CoV-2, SARS-CoV, MERS-CoV) or Para-influenza (RSV) viruses, pandemic strains of Influenza virus, and others often result in severe and life threatening conditions. (
  • This project will consider influenza viruses, a genus which includes both endemic and emerging threats to human health. (
  • In contrast to humans, the entire genomes of some viruses, including Zika and HIV, are made up of RNA instead of DNA. (
  • 5. The Process of Infection: I. Attachment of Viruses and the Entry of Their Genomes into the Target Cell. (
  • These molecules can include viral genomes, replication intermediates, and any other species containing a stable RNA duplex that is terminated with a 5′-triphosphate or diphosphate group ( 3 , 4 ). (
  • For viruses with RNA genomes, those that carry out RNA synthesis in the cytoplasm outnumber those that do so in the nucleus by about 10:1. (
  • To replicate their genomes in cells and generate new progeny, viruses typically require factors provided by the cells that they have infected. (
  • Seven basic replication strategies exist based on genome type (including DNA or RNA and single‐ or double‐stranded genomes) but these may vary widely within a specific type. (
  • Some viruses have genomes in multiple parts (segments) and must have ways to make sure that all of the necessary segments are packaged. (
  • This review focuses on the regulatory roles that phosphorylation of CPs has in the life cycle of viruses with RNA genomes. (
  • Recent studies have revealed that DNA forms of arboviral RNA genomes play a significant role in viral persistence in mosquitoes. (
  • This is in large part due to the highly error-prone replication of RNA virus genomes, which results in rapid evolution. (
  • The replication complex repeatedly copies this archival viral RNA chromosome to produce new progeny genomes that are released through a membranous neck on the vesicle into the cytoplasm, where they are incorporated as the payload of new infectious virions. (
  • The development of in vitro systems including infectious cell cultures affords the opportunity to fully characterize viral replication and virus-cell interactions. (
  • Nevertheless, significant efforts have been directed at developing cell culture models to elucidate the viral lifecycle in vitro. (
  • A recombinant sialidase fusion protein effectively inhibits human parainfluenza viral infection in vitro and in vivo. (
  • Influence of L-lysine amino acid on the HIV-1 RNA replication in vitro. (
  • CD8 + lymphocytes from infected individuals have been shown to inhibit HIV-1 replication in vitro ( 1 ). (
  • Positive in vitro and ex vivo results to date suggest that this new RNA molecules will show greater efficacy against pandemic virus strains. (
  • Staff will maintain collections, generate virus preparations by in vitro growth in cell culture, and purify RNA from the virus preparations. (
  • By using a quantitative real-time PCR approach we analyzed the regulation of key apoptosis related genes during early stages of ISAV infection in vitro. (
  • Moreover, high susceptibilities of MSCs to viral infections in vitro could reflect the destructive outcomes that might impair the clinical efficacy of MSCs infusion. (
  • Since monocytes in peripheral blood are precursors of macrophages, we investigated the effect of cell maturation on virus replication under limited control conditions in vitro by inoculating blood leukocytes with virus and retarding the maturation of monocytes to macrophages during cultivation in serum-free medium. (
  • The catalytic DNA molecule inhibits JEV replication in vitro in cultured cells and in vivo in the mouse brain. (
  • The researchers also demonstrated efficient inhibition of virus in cells that line the human airways and are the natural port of entry for respiratory viruses. (
  • 1. Targeting Membrane-Bound Viral RNA Synthesis Reveals Potent Inhibition of Diverse Coronaviruses Including the Middle East Respiratory Syndrome Virus Anna Lundin1. (
  • Specifically, the formation of double membrane vesicles (DMVs), a hallmark of coronavirus replication, was greatly impaired upon K22 treatment accompanied by near-complete inhibition of viral RNA synthesis. (
  • Importantly, K22 inhibitsa broad range of coronaviruses, including Middle East respiratory syndrome coronavirus(MERS CoV), and efficient inhibition wasachieved in primary human epithelia cultures representing the entry port of human coronavirus infection. (
  • Mechanistic target of rapamycin inhibition by either nutrient starvation or use of an active site inhibitor reduces Skp2 levels and stabilizes LT, leading to enhanced MCV replication and transmission. (
  • The work presented here addresses the mechanism of AUF1 inhibition of the replication of poliovirus and CVB3. (
  • Furthermore, siRNA must be capable of sustained inhibition of the rapid replication kinetics of HIV-1 infection ( 9 ). (
  • Inhibition of protein kinase C promotes dengue virus replication. (
  • Results of the inhibition and activation on viral entry/replication and host cell survival were examined. (
  • Proteasome Inhibition Suppresses Dengue Virus Egress in Antibody Dependent Infection. (
  • We show here that proteasome inhibition decouples infectious virus production from viral RNA replication in antibody-dependent infection of THP-1 cells. (
  • Proteasome inhibition decouples infectious DENV2 production from viral RNA replication in THP-1 cells. (
  • To demonstrate that proteasome inhibition with clasto lactacystin β-lactone (β-lactone), a widely used proteasome inhibitor, indeed did not alter virus entry at non-toxic levels (Fig 1A), we measured DiD (1,1'-dioctadecyl-3,3,3',3'-tetramethylindodicarbocyanine, 4-chlorobenzenesulfonate salt)-labeled DENV in β-lactone treated cells. (
  • To test the effect of ChikV-induced-autophagy on viral replication, we blocked the autophagic process, either by pharmacological (3-MA) or genetic inhibition (siRNA against the transcript of Beclin 1, an autophagic protein), and analyzed the percentage of infected cells and the viral RNA load released in the supernatant. (
  • Moreover, we found that inhibition of autophagy, either by biochemical reagent and RNA interference, dramatically decreases ChikV replication. (
  • Recently, nucleoside analogs, which directly affect viral replication by inhibition of its reverse transcriptase activity, were shown to be highly effective in the clearance of HBV-DNA from serum. (
  • MCV can sense stresses in its intracellular environment, such as nutrient loss, through SCF E3 ligase activities, and responds by initiating active viral transmission. (
  • To establish a successful infection, many plant RNA viruses remodel host cellular membranes to create a viral replication organelle that facilitates replication and intracellular movement of the viral RNAs ( Laliberté and Zheng, 2014 ). (
  • Flaviviruses are known to cause remodeling of intracellular membranes into small cavities, where replication of the viral RNA takes place. (
  • Similar to other flaviviruses, TBEV exploits intracellular membranes to build RCs for viral replication. (
  • RNA replication takes place at specialized intracellular membrane structures called 'membranous webs' or 'membrane-associated foci', whereas viral assembly probably occurs on lipid droplets and endoplasmic reticulum. (
  • Viruses are obligate intracellular parasites, relying on their host cells to provide the basic machinery to allow them to replicate. (
  • In contrary, activation of PKC effectively suppressed intracellular viral number. (
  • Interestingly, infection with positive-strand RNA viruses may result in the rearrangement of intracellular membranes, constituting scaffolds for viral genome replication [ 2 ]. (
  • These cells sample endocytosed material but do not detect the presence of intracellular infection. (
  • Multiple generations within a single cell infection provide opportunities for significant accumulation of mutations per viral genome and for intracellular selection. (
  • The life history strategies of viruses are largely reflected by their mode of intracellular replication. (
  • With EF-Tu may provide a stabilizing scaffold for the beta (catalytic) subunit, implicated in the elongation step of viral RNA synthesis where it fixes EF-Tu in an open conformation. (
  • Here we screened a collection of 16671 diverse compounds for anti-human coronavirus 229E activity and identified an inhibitor, designated K22, that specifically targets membrane-bound coronaviral RNA synthesis. (
  • K22-resistant viruses contained substitutions in non-structural protein 6 (nsp6), a membrane-spanning integral component of the viral replication complex implicated in DMV formation, corroborating that K22 targets membrane bound viral RNA synthesis. (
  • We demonstrate that AUF1 knockdown in human cells results in increased viral translation, RNA synthesis, and virus production. (
  • Triggered by double-stranded RNAs that form during viral RNA synthesis, the innate immune system is the best-described process that restricts virus replication, and as a result, picornaviruses have evolved numerous strategies to counteract this response ( 5 , 6 ). (
  • Nonsegmented negative-strand (NNS) RNA viruses, which include some of the most significant human, animal, and plant pathogens extant, form inclusions that are sites of RNA synthesis and are not circumscribed by a membrane. (
  • IMPORTANCE RNA viruses compartmentalize their replication machinery to evade detection by host pattern recognition receptors and concentrate the machinery of RNA synthesis. (
  • RNA viruses typically establish specialized organelles in the cytoplasm in which RNA synthesis occurs ( 1 , 2 ). (
  • This raises the question of how the machinery necessary for RNA synthesis is contained within this viroplasm. (
  • Here we combine metabolic pulse labeling and quantitative proteomics to monitor protein synthesis upon infection of human cells with a human- and a bird-adapted IAV strain and observe striking differences in viral protein synthesis. (
  • RNA is a central molecule in RNA virus biology, acting not only as a messenger of protein synthesis, but also as a genome. (
  • Amino acids play an important role in virus-related infections as they are needed for protein synthesis and they also regulate many metabolic pathways, including gene expression. (
  • Arginine is not involved in the early steps of virus replication at the level of viral DNA synthesis. (
  • It is necessary before the synthesis of virus DNA and the second requirement is associated with the formation of mature virions. (
  • In the absence of arginine, viral DNA synthesis continues undisturbed, whereas the formation of virions is inhibited. (
  • This review describes how RNA viruses achieve this balance by regulating the synthesis of Type I and Type III interferons. (
  • The impacts of altered host miRNAs on cellular processes, including immune escape, apoptosis, signal transduction, shutdown of host protein synthesis and viral replication, are discussed. (
  • In a productive infection, recognition of external structures on the cell is followed by entry, alteration of cellular function to support a time‐dependent cycle of virus‐specific macromolecular synthesis, assembly of the next generation of virus particles, and release from the cell. (
  • Accumulating evidence suggests that phosphorylation of viral CPs is involved in the regulation of the viral infection process from enabling virion disassembly to regulation of viral protein synthesis and replication. (
  • All viruses lack their own translational apparatus and rely entirely upon the host cell's protein synthesis machinery. (
  • The synthesis of viral RNA/mRNA is a key step in viral replication and could be used as a positive indication of infection ( 1 ). (
  • An Intrinsically Disordered Peptide from Ebola Virus VP35 Controls Viral RNA Synthesis by Modulating Nucleoprotein-RNA Interactions. (
  • article{Leung2015AnID, title={An Intrinsically Disordered Peptide from Ebola Virus VP35 Controls Viral RNA Synthesis by Modulating Nucleoprotein-RNA Interactions. (
  • During viral RNA synthesis, Ebola virus (EBOV) nucleoprotein (NP) alternates between an RNA-template-bound form and a template-free form to provide the viral polymerase access to the RNA template. (
  • Recently, a new vector system called pSUPER (suppression of endogenous RNA), which directs the synthesis of siRNAs and persistently suppresses gene expression in mammalian cells, has been developed. (
  • Is the Subject Area "RNA interference" applicable to this article? (
  • We found here that the persistence of RNA viruses in Drosophila melanogaster was achieved through the combined action of cellular reverse-transcriptase activity and the RNA-mediated interference (RNAi) pathway. (
  • The aim of this study was to characterize the potency and durability of virus-specific RNA interference (RNAi) in cell lines that stably express short hairpin RNA (shRNA) targeting the HIV-1 transactivator protein gene tat . (
  • Silencing of gene expression by RNA interference (RNAi) offers a new tool with potential therapeutic applications for the treatment of chronic viral infections such as those with human immunodeficiency virus type 1 (HIV-1) ( 3 , 4 , 6 - 8 , 10 , 11 ). (
  • vDNA formation is more extensive in RNA interference (RNAi)-deficient Aedes albopictus -derived C6/36 cells compared to RNAi-proficient mosquito cells. (
  • A cell can initiate RNA interference when it detects viral infection, which works by decreasing the influence of the virus's genetic material in relation to the cell's usual material. (
  • RNA interference (RNAi) is the process whereby double-stranded RNA (dsRNA) induces the sequence-specific degradation of homologous messenger RNA (mRNA).4 This process is mediated by 21 to 23 nucleotides, called small interfering RNAs (siRNA), cleaved from dsRNA. (
  • RNA interference (RNAi) is the process of sequence-specific gene silencing, initiated by double-stranded RNA (dsRNA) that is homologous in sequence to the target gene. (
  • 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. (
  • Merkel cell polyomavirus (MCV) causes an aggressive skin cancer after prolonged infection and requires an active large T (LT) phosphoprotein helicase to replicate. (
  • Unlike A(H5N1) viruses, A(H7N9) viruses efficiently infect and replicate in ex vivo cultures of the human bronchus ( 9 ) and are transmitted between ferrets, albeit inefficiently, by the airborne route ( 10 ), indicating the substantial potential for efficient human-to-human transmission. (
  • RNA viruses that replicate in the cell cytoplasm typically concentrate their replication machinery within specialized compartments. (
  • A single virus particle (virion) cannot replicate or express genetic material (DNA, RNA) without a host cell. (
  • Once within the cell, viruses move to specific sites where they can replicate. (
  • Viruses replicate at various locations within the cell. (
  • Most DNA viruses infecting eukaryotic cells replicate in the nucleus (with the exception of the nucleocytoplasmic large DNA viruses) while most RNA viruses replicate in the cytoplasm (since the DNA replication machinery within the nucleus it usually of little use to them). (
  • Hepatitis C virus (HCV) has been reported to replicate in peripheral blood mononuclear cells (PBMCs), particularly in patients coinfected with HCV and human immunodeficiency virus (HIV). (
  • They lack the ability to replicate on their own, so viruses are merely tiny packets of DNA or RNA genes enfolded in a protein coating, on the hunt for a cell they can dominate. (
  • The immune system also kicks into gear when it identifies a virus by producing antibodies that bind to the virus and render it unable to replicate. (
  • Knockdown of each of these E3 ligases enhances LT stability and promotes MCV genome replication. (
  • 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. (
  • Given this massive investment of resources, viral RNA genome replication is arguably one of the most important processes in infection, and It is already a major target for virus control," Ahlquist says. (
  • Ahlquist and his team previously showed that in each such genome replication complex, a copy of the viral RNA genome or chromosome is protected inside the spherule vesicle to function as a replication template. (
  • By contrast, polyinosinic:polycytidylic acid [poly(I:C)], which binds and activates multiple RNA sensors, induces type III interferons and several unique ISGs. (
  • In this paper, we show that RNA virus infection induces miR-155 expression in macrophages via TLR/MyD88-independent but retinoic acid-inducible gene I/JNK/NF-κB-dependent pathway. (
  • To study how TBEV induces membrane remodeling, we developed an inducible stable cell system expressing the TBEV NS polyprotein in the absence of viral RNA replication. (
  • The group screened for cDNAs that could enhance the activation of an IFN regulatory factor 3 (IRF3) reporter after transfection with polyinosinic-polycytidylic acid (poly I:C)-a synthetic double-stranded (ds)RNA polymer that potently induces the production of type I IFNs. (
  • This prior work further showed that the key viral protein that induces the replication vesicles and copies the viral RNA resides in a striking ring or crown structure that sits atop the cytoplasmic side of the spherule neck that connects with the cytoplasm. (
  • The cellular mRNA decay protein AUF1 acts as a restriction factor during infection by picornaviruses, including poliovirus, coxsackievirus, and human rhinovirus. (
  • Our findings suggest that AUF1 restriction of poliovirus and CVB3 replication uses a common mechanism through the viral IRES, which is distinct from the canonical role that AUF1 plays in regulated mRNA decay in uninfected host cells. (
  • Some RNA viruses do this by using their viral genome as an mRNA when they enter their host cell, whereas those that require transcription to produce mRNAs have to carry a suitable (and often rather large) polymerase within the virus particle. (
  • Although integrated cell culture-reverse transcription-PCR (RT-PCR) assay has been used to provide rapid detection of infectious viruses ( 6 ) by probing the presence of viral mRNA, this method requires additional mRNA extraction, RT-PCRs, and gel analysis, leading to the potential for contamination. (
  • Since a large portion of viral mRNA is synthesized early in the infectious cycle ( 1 ), in situ detection of viral mRNA directly from cell cultures may be used as a very sensitive and specific indicator for infectious viruses without amplification. (
  • HCV, picornavirsues and some insect viruses) and cellular mRNA molecules. (
  • Phylogenetic analyses of the A(H7N9) hemagglutinin (HA) genes showed that the viruses that emerged in the Yangtze River Delta region in 2013 rapidly spread to other parts of South and South East China and that distinct virus clades became established in these different geographic regions ( 7 ). (
  • While many gaps in our knowledge of HCV exist, great strides have been made in characterizing the virus and functions of viral genes as well as in unraveling the replication pathway and immunologic mechanisms of liver injury. (
  • The sequence similarities of RNA replication genes and strategies for BMV have been shown to extend to a wide range of plant and animal viruses beyond the alphaviruses, including many other positive-strand RNA viruses from other families. (
  • Hopefully, by increasing the level of ZBP1 protein production in the brain, by enhancing the expression of the ZBP1 genes, the virus will be eliminated from the brain and encephalitis will not occur following infection. (
  • Different viral genes are expressed at different stages of replication. (
  • Simple DNA viruses can use (or induce the production of) the cellular DNA synthetic machinery, whereas more complex viruses carry genes for the enzymes they need, making the process of replication more efficient. (
  • Effect of infectious salmon anemia virus (ISAV) infection on expression of apoptosis related genes in Atlantic salmon (Salmo salar L.) cells. (
  • In the present study we wanted to investigate the effect of ISAV infection on the expression of apoptosis related genes in Atlantic Salmon (Salmo salar L.) cells. (
  • In each positive-strand RNA virus, most of the viral genes are devoted to a single process: replicating the viral RNA genome. (
  • However, certain viral and cellular mRNAs, notably encoding proto-oncogenes and regulatory genes, contain long 5' noncoding regions with multiple AUG codons. (
  • and (iv) the small interfering RNA/microRNA-mediated gene silencing pathway, a recently characterized new host defense mechanism against viral infection.Organized into 27 highly accessible and well-illustrated chapters, this volume explores state-of-the-art knowledge of the molecular mechanisms of RNA virus infection and host-virus interactions. (
  • Over the last century, the elucidation of viral oncogenic roles in many cancer types has provided fundamental knowledge on carcinogenetic mechanisms and established a basis for the early intervention of virus-related cancers. (
  • Binding to different sites within the viral RNA suggests that AUF1 may negatively regulate infection by these viruses using different mechanisms. (
  • Given the worldwide distribution and prevalence of picornaviruses, it is important to gain insight into the host mechanisms used to restrict infection. (
  • The purpose of our research is to understand the mechanisms of disease and to improve treatment and prevention of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, and viral hepatitis-associated hepatocellular carcinoma (HCC). (
  • To achieve this goal, we must understand at the molecular, cellular and genetic levels the viral life cycle, viral mechanisms for productive and persistent infection, virus-host interactions, and host immune responses. (
  • 15. Mechanisms in Virus Latency. (
  • Vrati's early researches at THSTI focused on JEV life-cycle like receptor binding and entry mechanisms, molecular mechanisms of virus replication, assembly, egress as well as the clinical development of an oral rotavirus vaccine. (
  • Although beneficial for the viral life cycle, virus-mediated alterations in normal cell cycle control mechanisms could have detrimental effects on cellular physiology and may ultimately contribute to pathologies associated with the viral infection, including cell transformation and cancer progression and maintenance. (
  • Dayaram T, Marriott SJ (2008) Effect of transforming viruses on molecular mechanisms associated with cancer. (
  • Defining the immune mechanisms responsible for controlling HIV-1 replication during primary and chronic infection will be important for understanding the immunopathogenesis of AIDS. (
  • The mechanisms of T-cell priming and expansion following infections of the central nervous system (CNS) are poorly understood due to several unique characteristics of the CNS. (
  • Virus replication peaks at day 5 p.i. and is largely controlled by CD8 + cytotoxic T lymphocytes (CTL) via both perforin- and gamma interferon (IFN-γ)-mediated mechanisms ( 18 , 20 , 24 , 30 ). (
  • Once bound to the host cell, viruses enter by a range of mechanisms, often involving uptake into vacuoles, although other routes such as fusion with the cell membrane may be used. (
  • Already many molecular mechanisms of innate immune evasion by +ssRNA viruses have been identified. (
  • It has developed multiple mechanisms to sense invading viruses, and subsequent signal transduction pathways are targeted at the initial containment of infection in the body. (
  • The overall goals of this research project will be two-fold: 1) completion of animal studies (RVFV infection of deer and vector transmission mechanisms for arboviruses), and 2) complete the necessary analytical laboratory work in support of these studies. (
  • molecular mechanisms of plant resistance and evolution of viral pathogenicity. (
  • Areas of interests include gene expression and replication and RNA and DNA viruses, mechanisms of plant resistance to viral infections and resistance-breaking by RNA viruses, recombination, and evolution of RNA viruses. (
  • Background: Ribavirin (RBV) is a potential partner of interferon-based therapy and recently approved therapy using direct acting antivirals for patients with chronic hepatitis C. However, the precise mechanisms underlying RBV action against hepatitis C virus (HCV) replication are not yet. (
  • Continuous genetic variation and selection of virus subpopulations in the course of RNA virus replications are intimately related to viral disease mechanisms. (
  • Flavivirus is a positive-sense, single-stranded RNA viral genus, with members causing severe diseases in humans such as tick-borne encephalitis, yellow fever, and dengue fever. (
  • In this study, we show that primary human placental trophoblasts from non-exposed donors (n = 20) can be infected by primary passage ZIKV-FLR isolate, and uniquely allowed for ZIKV viral RNA replication when compared to dengue virus (DENV). (
  • Samples from 252 patients with dengue virus (n = 93), West Nile virus (n = 34), Japanese encephalitis virus (n = 25), chikungunya virus (n = 19) or Plasmodium spp. (
  • Cross-reactivity with high-level dengue virus antibodies was not detected. (
  • Human +ssRNA viruses that currently have a large impact on public health include dengue virus (DENV) and the more recent (re-)emerging viruses such as chikungunya virus (CHIKV) and Zika virus (ZIKV) [ 1 ]. (
  • Dengue virus (DENV) is a member of the Flaviviridae family, transmitted to human via mosquito. (
  • Dengue virus, a member of the Flaviviridae family, is a mosquito-borne pathogen and the causative agent of dengue fever. (
  • We identified lactimidomycin (LTM), a recently established inhibitor of translation elongation, as a potent inhibitor of dengue virus 2 infection in cell culture. (
  • Dengue virus 2 (DENV2), a member of the Flaviviridae family, is an enveloped, positive-strand RNA virus and the causative agent of dengue fever. (
  • Dengue infection can be serious, potentially leading to hemorrhagic fever, shock syndrome, and death. (
  • The complete 3'UTR of DENV-1 was sequenced from 13 patients suffering from the severe form of dengue virus infection (dengue hemorrhagic fever). (
  • The mosquito-borne dengue virus (DENV) is a cause of significant global health burden, with an estimated 390 million infections occurring annually. (
  • The positive-strand RNA viruses addressed in this work are the largest of six genetic classes of viruses and include many important pathogens such as the Zika, dengue and chikungunya viruses, as well as coronaviruses like SARS-CoV-2, cause of the current COVID-19 pandemic. (
  • In addition, the viral and host functions for productive and persistent infection in vivo are poorly understood. (
  • Using RNA sequencing, we provide the first in vivo genome-wide view of the expression networks that are initiated upon RIG-I activation. (
  • Cells isolated directly from the brain exhibit virus-specific ex vivo cytolysis between days 7 and 9 p.i. ( 1 , 2 , 19 ), a function not observed in cells derived from either spleen or CLN ( 4 , 29 ). (
  • Inhibitions of PKC by a PKC-specific chemical inhibitor or siRNA suppressed NS5 phosphorylation in vivo, increased viral replication and reduced viability of the DENV-infected cells. (
  • When combined with nuclease-resistant MBs, this method could be useful not only for the real-time detection of infectious viruses but is also useful to study the life cycle of viral processing in vivo. (
  • Visna lentiviruses have a natural tropism for cells of the macrophage lineage of sheep and goats, but virus replication in these cells in vivo is restricted so that only small quantities of virus are produced. (
  • In 'Type-I and III Interferon Production in Response to RNA Viruses,' Elizabeth Reid and Bryan Charleston, the Pirbright Institute (Surrey, UK), review the most recent studies looking at how RNA virus infections are able to induce multiple signaling pathways in host cells. (
  • Previous studies have shown that several RNA viruses induce apoptosis in host-cells. (
  • Here we show that replication compartments of vesicular stomatitis virus (VSV) have the properties of liquid-like compartments that form by phase separation. (
  • Specifically, the objectives include maintaining and further developing the USDA-Agricultural Research Service (ARS), Arthropod-Borne Animal Disease Research Unit (ABADRU) exotic bluetongue virus (BTV), Rift Valley fever virus (RVFV), and vesicular stomatitis virus (VSV) research through animal studies. (
  • We show that Kunjin virus and Modoc virus, two other members of the Flaviviridae family, as well as vesicular stomatitis virus and poliovirus 1, are also sensitive to LTM. (
  • Ensemble Structure of the Highly Flexible Complex Formed between Vesicular Stomatitis Virus Unassembled Nucleoprotein and its Phosphoprotein Chaperone. (
  • This protein-RNA complex (N-RNA) is used as the template by L for transcription of the viral mRNAs and for RNA replication. (
  • Assay sensitivity was examined using sera from 27 patients with reverse transcription (RT)-PCR-confirmed and 85 with suspected ZIKV infection. (
  • Once made dysfunctional, these RNA compounds can reduce viral genome transcription and replication levels and therefore the level of virus titers and the development of infection. (
  • Only a few monocytes were susceptible to infection, and virus replication did not extend beyond a low level of transcription of viral RNA. (
  • Filovirus replication and transcription. (
  • Homo-oligomerization of Marburgvirus VP35 is essential for its function in replication and transcription. (
  • These high mutation rates should also affect viral gene transcription. (
  • My laboratory is focussed on the study of emerging viral infections with 2 main themes - acute hepatitis C infection and new and emerging infections in sub-Saharan Africa. (
  • 3) Guidance for laboratory testing of the patient who is the source of the blood or body fluid is also updated in consideration of the increasing incidence of acute HCV infection among growing numbers of persons who inject drugs. (
  • CDC now recommends the 4-6 month post-exposure anti-HCV test out of an abundance of caution because of the potential for periods of intermittent aviremia during acute infection described in several earlier publications, primarily when older HCV RNA testing methodologies were used. (
  • Most patients with A(H7N9) disease primarily had viral pneumonia, with some progressing to acute respiratory distress syndrome (ARDS). (
  • ) and reflects updated guidance from professional organizations that recommend treatment for acute HCV infection. (
  • CD8 + T cells control acute infection of the central nervous system (CNS) by neurotropic mouse hepatitis virus but do not suffice to achieve sterile immunity. (
  • To trace T-cell expansion and infiltration into the CNS during the course of acute viral infection, BALB/c mice were infected intracerebrally with 1,000 PFU of the JHMV 2.2-V-1 variant ( 11 ). (
  • HCV (hepatitis C virus) infects nearly 3% of the population worldwide and has emerged as a major causative agent of liver disease, resulting in acute and chronic infections that can lead to fibrosis, cirrhosis and hepatocellular carcinoma. (
  • A comprehensive and longitudinal analysis of the viral population was conducted in four subjects followed from very early acute infection to resolution of disease outcome. (
  • Phylogenetic analysis of reassembled viral variants revealed acute infection was dominated by two sequential bottleneck events, irrespective of subsequent chronicity or clearance. (
  • These results provide the first detailed analysis of early within-host evolution of HCV, indicating strong selective forces limit viral evolution in the acute phase of infection. (
  • Infection persists in approximately 70% of acute cases, leading to chronic hepatitis, and ultimately cirrhosis and the associated complications of liver failure and hepatocellular carcinoma [2] . (
  • Intensive studies of the immune modulation and tissue regeneration over the past few years have demonstrated the great potential of MSCs for the prevention and treatment of steroid-resistant acute graft-versus-host disease (GvHD), immune-related disorders, and viral diseases. (
  • The presence of true antibody shows that the patient has been infected with the virus but does not indicate whether the infection is acute, resolved or chronic. (
  • While ZIKV causes acute human diseases, infections of vector mosquitoes are basically non-pathogenic, allowing persistent infections and conferring lifelong ability to transmit the virus. (
  • Infectious bursal disease (IBD) is an acute, highly contagious, and immunosuppressive avian disease caused by IBD virus (IBDV). (
  • The first step involved a 3-day study of acute infection in four macaques who were exposed via ocular, intratracheal, and intranasal routes, developing signs of infection such as a doubling of the C reactive protein (CRP), reduced serum protein and hemoglobin, and increasing serum CO2 levels. (
  • Macaques, therefore, developed clinical disease with acute infection but no significant weight loss or fever. (
  • Hepatitis B virus (HBV) is a 3.2-kb DNA virus, replicating almost exclusively in the liver.1 Although effective recombinant vaccines are available, HBV infection is still a major global health problem: Each year, acute and chronic HBV infection causes about 1 million deaths. (
  • We have selected some exemplary NS-RNA viruses and will describe how these NS-RNA viruses regulate autophagy and the role of autophagy in NS-RNA viral replication and in immune responses to virus infection. (
  • RBPs stimulated by the infection redistribute to viral replication factories and regulate the capacity of the virus to infect. (
  • AUF1 is shown to negatively regulate translation of a poliovirus and CVB3 IRES reporter RNA during infection but not in uninfected cells. (
  • Cis -acting RNA elements within the genome regulate RNA replication by forming secondary structures that interact with each other and trans -acting factors. (
  • CPs have been shown to regulate the infection processes of RNA viruses, including RNA replication and gene expression. (
  • Gene Expression in DNA Viruses and Reverse-Transcribing Viruses. (
  • Gene Expression and its Regulation in RNA Viruses. (
  • 3. The Structure of Virus Particles. (
  • Cellular attachment of HCV particles and their interaction with apolipoprotein E, which is essential for HCV infectivity, were significantly reduced by CA. These results indicate that CA inhibits HCV entry via its direct effect on viral particles and TA inhibits HCV RNA replication and particle egression as well as entry into host cells. (
  • The absence of essential amino acids may result in empty virus particles that are free of viral nucleic acids (DNA or RNA). (
  • however, simple intra-nasal application of our "Semi-live" RNA Vaccines (middle panel) ensures a full mucosal protection by the provision of secreted anti-viral IgA antibodies (right panel: Y-shaped antibodies intercepting all red punctured virus particles). (
  • We measure production of RNA and poliovirus particles through the infection cycle, and use these data to infer the parameters of our model. (
  • Using an approach that combined a genetically engineered, site-specific tag with labeling by nanoscale gold particles visible in cryo-EM, the researchers found that the C-terminal polymerase end of the viral RNA replication protein is positioned at the apex of the crown, leaving the N-terminal capping domain at the bottom of the structure to interact with the membrane. (
  • Novel Coronavirus SARS-CoV-2 Transmission electron micrograph of SARS-CoV-2 virus particles, isolated from a patient. (
  • Like other positive-strand RNA viruses, the Turnip mosaic virus (TuMV) infection leads to the formation of viral vesicles at the endoplasmic reticulum (ER). (
  • For positive-strand RNA viruses, RNA replication occurs in a virus-induced membrane-associated replication organelle. (
  • A positive-strand RNA virus of the Flaviviridae family, HCV contains a single-stranded RNA genome of approx. (
  • This 12 Kb positive-strand RNA virus contains two open reading frames (ORFs). (
  • Newswise - For the first time, scientists at the Morgridge Institute for Research have generated near atomic resolution images of a major viral protein complex responsible for replicating the RNA genome of a member of the positive-strand RNA viruses, the large class of viruses that includes coronaviruses and many other pathogens. (
  • This protein contains RNA polymerase and RNA capping domains- two enzymatic domains that are conserved across numerous positive-strand RNA viruses for synthesizing new viral genome copies-plus other domains for multimerizing, binding membranes and other functions. (
  • Thus far, virus-specific RNAi has been achieved through transient transfection of either synthetic siRNA molecules or vectors containing siRNA expression cassettes. (
  • Small interfering RNA (siRNA) is a promising approach for the prevention and treatment of viral infections. (
  • To answer these questions, we developed "comparative RIC" and applied it to cells challenged with an RNA virus called sindbis (SINV). (
  • In summary, RNA availability controls RBP localization and function in SINV-infected cells. (
  • 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. (
  • By applying the technology of induced pluripotent stem cells and hepatocyte differentiation, we have established useful cell model systems to study viral replication and virus-cell interaction. (
  • Human cells modify viral RNA with m6A as a means to get rid of the infection. (
  • Cells can chemically modify RNA to influence protein production. (
  • To unravel the role of m6A in Zika virus infection of human cells growing in the laboratory, the researchers removed the human enzymes responsible for adding methyl groups to viral RNA. (
  • Without m6A, the viral RNA was more stable and viral replication increased, as compared to human cells with normal methylation enzymes. (
  • 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. (
  • Soon after infection, activated HIV-specific cytotoxic T lymphocytes, mediated primarily by CD8+ cells, were detected in 17 of 23 patients (74 percent). (
  • Patients with low frequencies of Env-specific memory cytotoxic T lymphocytes (or none) in early infection had a more rapid decline to less than 300 CD4+ cells per cubic millimeter (P = 0.05). (
  • A research team has discovered a protein without which cells infected by viruses cannot trigger an immune response, leading to 100% mortality with even non-disease-producing strains. (
  • By killing off the infected host cell, this short-circuits the normal viral program of hijacking the host cell's machinery to create numerous viral copies, assemble them and release them to infect new host cells. (
  • Prior research by the same scientists has shown the steep rise in ZBP1 expression in mouse brains and mouse cells following viral infection. (
  • Viral replication was much higher in brain cells and embryonic fibroblasts from mice without ZBP1 expression after infecting with either pathogenic or nonpathogenic strains of West Nile virus, as well as of Zika virus . (
  • Single Molecule Real Time (SMRT) sequencing was first applied and long-read sequencing analysis showed that a variety of H7N9 DI-RNA species were present in the patient samples and human bronchial epithelial cells. (
  • Taken together, we reveal the diversity and characteristics of DI-RNAs found in H7N9-infected patients, cells and animals. (
  • Cells derived from the glassy-winged sharpshooter, Homalodisca vitripennis, support infection and replication of viral RNA from a clone of Homalodisca coagulata virus 1 (HoCV-1). (
  • Similar structures have been observed in cells infected with related viruses, including rabies virus (RABV [ 4 , 5 ]), Ebola virus ( 6 ), and measles virus ( 7 ). (
  • Despite these differences in receptor binding, many avian viruses are internalized by human cells and initiate expression of the viral genome. (
  • In contrast, some viruses can arrest cells in a particular phase of the cell cycle that is favorable for replication of the specific virus. (
  • Cell cycle arrest may inhibit early cell death of infected cells, allow the cells to evade immune defenses, or help promote virus assembly. (
  • When arginine is not available, herpes viruses in cells are unable to complete a single replication cycle and cell damage is evident in infected cells. (
  • Respiratory and intestinal infections caused by RNA viruses stimulate infected cells to produce interferons, which can act alone or in combination to block virus replication. (
  • Important differences between the presence of IFN receptors on cells and new evidence that specific types of IFNs can control RNA virus infection are explored in a review article in Journal of Interferon & Cytokine Research (JICR), a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. (
  • Eliminating CD8 + lymphocytes from monkeys during chronic SIV infection resulted in a rapid and marked increase in viremia that was again suppressed coincident with the reappearance of SIV-specific CD8 + T cells. (
  • As in HIV-1 infection of humans, primary infection of rhesus monkeys with SIVmac is characterized by an intense burst of virus replication followed by an abrupt decline in viremia presumably due to the emergence of immune responses that suppress virus replication ( 7 ) or, potentially, to exhaustion of target cells ( 8 ). (
  • To determine the lag between T-cell priming and optimal activity within the CNS, the accumulation of virus-specific CD8 + T cells in the CNS relative to that in peripheral lymphoid organs was assessed by using gamma interferon-specific ELISPOT assays and class I tetramer staining. (
  • Virus-specific CD8 + T cells were first detected in the cervical lymph nodes. (
  • Cytolytic activity correlates with a high frequency of virus-specific CD8 + T cells in the CNS compared with barely detectable levels in the periphery ( 1 , 2 , 19 ). (
  • It is further unclear to what extent virus-specific T cells expand within the CNS or prior to CNS entry. (
  • RNA viruses need to carry or produce their own polymerase to make RNA from an RNA template, since such enzymes are not present at useful levels in cells. (
  • Bolin, S. R. 2002-01-01 00:00:00 The kinetics of porcine circovirus type 2 (PCV2) replication in PK15 cells was examined. (
  • Viral antigens were observed in a few cells at 18 hour postinfection (h p.i.) and cell-free progeny viruses began to appear at about 30 h p.i. (
  • These results indicated that PKC may act as a restricting mechanism that modulates the DENV replication and represses the viral outburst in the host cells. (
  • Biopsied lymph nodes from the 7 symptomatic patients contained substantially higher copy numbers of HIV-1 RNA and DNA than did peripheral blood mononuclear cells (PBMC). (
  • In the first method, mammalian cells were infected with viruses and replication complexes were blocked on the plasma membrane by drug treatment to prevent transport to endolysosomal vesicles. (
  • Oyster Mushroom Laccase Inhibits Hepatitis C Virus Entry into Peripheral Blood Cells and Hepatoma Cells. (
  • The number of fluorescent cells also increased in a dose-responsive manner, enabling the direct quantification of infectious viral dosages by direct counting of fluorescent foci. (
  • Molecular and imaging analyses in β-lactone treated THP-1 cells suggest that proteasome function does not prevent virus assembly but rather DENV egress. (
  • C) Alexa Fluor 647 labeled DENV2 opsonized with h3H5 were internalized in cells pre-treated with DMSO or β-lactone, while genistein prevented the uptake of virus at 2 hpi. (
  • Here we provide the first evidence that hallmarks of autophagy are specifically found in HEK.293 infected cells and are involved in ChikV replication. (
  • To test the capacity of ChikV to mobilize the autophagic machinery, we performed fluorescence microscopy experiments on HEK.GFP.LC3 stable cells, and followed the LC3 distribution during the time course of ChikV infection. (
  • These respiratory viruses attach, enter and destroy lung cells thereby causing airway destruction and high-grade bronchial inflammation. (
  • For this reason, " vir 4 vac " has set out a novel concept ensuring full mucosal protection by fully abrogating already all initial contacts of respiratory viruses to respiratory tract and lung cells (see Figure below). (
  • Davey MW , Dalgarno L . Semliki Forest virus replication in cultured Aedes albopictus cells: studies on the establishment of persistence. (
  • Role of extracellular virus on the maintenance of the persistent infection induced in Aedes albopictus (mosquito) cells by Sindbis virus. (
  • One restricting factor suggested in previous studies is that virus replication is dependent on the maturity of the cells: the more mature the cell, the less restrictive the replication of the virus. (
  • Using enzyme markers that identified the cells in their resting monocytic stage (peroxidase) and mature macrophage stage (acid phosphatase) along with quantitative in situ hybridization and immunocytochemistry with viral reagents to trace the efficiency of virus replication, we correlated virus replication with cell maturation. (
  • In the acid phosphatase-positive, maturing macrophage, susceptibility of the cells to infection was increased and virus replication was greatly amplified to the level of translation of viral polypeptides. (
  • In addition, type I IFNs enhance the function of natural killer (NK) cells and the differentiation of virus-specific cytotoxic T lymphocytes (CTLs), both of which recognize and eliminate virus-infected cells. (
  • First, TLRs specific for viral nucleic acids are expressed by only a small fraction of specialized cells, whereas almost all cells produce type I IFNs when infected with virus or transfected with nucleic acids. (
  • Second, the TLRs that sense nucleic acids are localized in the endosomes of sentinel cells that are generally not infected with virus. (
  • Thus, although TLRs can detect viral infection, a second, more widely expressed receptor system must signal the presence of virus from within all cells. (
  • The current study aimed to develop a non-human model to recapture the diversity of human responses to the viral infection and to understand the early events that take place in infected cells in the lungs. (
  • Alongside this, there was a fall in the number and relative proportion of neutrophils, probably because these immune cells were recruited to the lung tissue by the infection-associated cellular signals. (
  • The present invention also relates to the method of treatment of Japanese encephalitis comprising the steps of introducing the catalytic DNA molecule or DNAzyme into the infected cells under conditions suitable for cleavage and reduction of viral titres. (
  • 32. A method of treatment of Japanese Encephalitis and related infectious diseases in animals comprising the steps of introducing said catalytic DNA molecule of claim 25 into infected cells under conditions suitable for cleavage and reduction of infectious Japanese Encephalitis virus or other infectious micro-organisms. (
  • Our laboratory has been been studying the mechanism by which a liver-specific microRNA, miR-122, regulates the amplification of the hepatitis C virus (HCV) genome in cultured cells. (
  • Viruses will also spread to nearby cells and begin the process again. (
  • The immune system also releases T-cells, which work to kill the virus. (
  • Because it has been shown that RNAi can be accomplished in cultured mammalian cells by introducing small interfering RNAs (siRNAs), much effort has been invested in exploiting this phenomenon for experimental and therapeutic means. (
  • There are no specific treatments for infection, and vaccines exist for only two picornaviruses: poliovirus and hepatitis A virus. (
  • Given the magnitude and severity of both viral infections as a global public health problem, it is imperative to develop and implement effective prophylactic vaccines and better therapeutic regimens. (
  • But these findings are also something researchers should keep in mind as they are designing new Zika virus vaccines and treatments that target the viral genome -- some approaches won't work unless they take methylation into account. (
  • 21. Vaccines and Antivirals: The Prevention and Treatment of Virus Diseases. (
  • Vaccines cannot provide immunity against new strains of viruses and manufacturing capacity may be insufficient when coping with sudden high demands. (
  • Novel first-in-class intra-nasally applicable safe recombinant " vir 4 vac " RNA vaccines constitute a very safe and efficacious way of preventing serious infections of respiratory corona and paramyxoviruses as well as other respiratory viruses. (
  • Scientists from the MPI of Biochemistry in Martinsried have generated Sendai virus "Semi-live" RNA Vaccines (the " vir 4 vac " platform) which are characterized by highest safety features ensured by a full replication deficiency of our vaccine vectors, which guarantees prevention of any uncontrolled spread, amplification, persistence and potential mutations of our recombinant vaccines within vaccinated people. (
  • Our RNA-Vectored "Semi-live" Vaccines mimic the natural viral infection process of all respiratory viruses (see Figure above) and there-by achieve protection directly in the airways (via simple intranasal application of our safe RNA-Vectored Vaccines). (
  • By mapping sites of protein conservation and plasticity it will expand our understanding of targets for the immune response, including by 'universal' vaccines, and provide a rational basis for viral protein engineering. (
  • To prevent such infections, scientists have extensively studied the poliovirus and have developed effective vaccines against it that have eliminated the virus from all but a few countries. (
  • By applying sensitive molecular assays, efficacious commonly used FeLV vaccines that protect cats from antigenaemia were found not to prevent proviral integration and minimal viral replication after challenge. (
  • These antibodies target the glycoprotein (GP) on the Ebola virus surface, thereby blocking attachment and entry of the virus on host cell membranes. (
  • Viruses that require a lipid envelope (enveloped viruses) can acquire this from a range of cellular sources, including the plasma membrane or internal membranes. (
  • Within an infected cell, viral RNA replication occurs at modified cellular membranes, often in association with spherules, virus-induced vesicles approximately 50-100 nanometers in size. (
  • The results reveal a novel association of TGB2 and vRNA with chloroplasts, and suggest viral replication is associated with chloroplast membranes, and that TGB2 plays a novel role in targeting the virus to chloroplasts. (
  • Next, Rana and team will investigate the role of RNA modifications in the viral life cycle, and how the human immune response is altered by various Zika virus strains. (
  • Astrocytes are infected predominantly by lymphotropic strains, but infections with monocytotropic strains have also been described. (
  • We show that impaired production of M1 from bird-adapted strains is caused by increased splicing of the M segment RNA to alternative isoforms. (
  • ARS-ABADRU and Kansas State University scientists will collaboratively investigate development of diagnostic tests of exotic and endemic strains of both viruses in high containment facilities. (
  • Given their genetic flexibility, these viruses have therefore developed multiple strategies to evade the innate immune response in order to optimize their replication capacity. (
  • Apoptosis is a genetically controlled process of cell suicide in response to a variety of stimuli and is considered a part of the innate immune response to virus infection, limiting the time and cellular machinery available for viral replication. (
  • These alterations are mainly driven by the loss of cellular mRNAs and the emergence of viral RNA. (
  • Specifically, we are addressing the following questions: Which cellular and viral mRNAs can be translated by internal ribosome binding? (
  • Once released from the ER, the viral vesicles mature intracellularly and then move intercellularly. (
  • We found that the replication of TuMV and the cell-to-cell movement of its replication vesicles are impaired in rhd3 . (
  • This defect can be tracked to a delayed maturation of the viral vesicles from the replication incompetent to the competent state. (
  • Furthermore, 6K2 can relocate RHD3 from the ER to viral vesicles. (
  • However, a Golgi-localized mutated 6K2 GV is unable to interact and relocate RHD3 to viral vesicles. (
  • We conclude that the maturation of TuMV replication vesicles requires RHD3 for efficient viral replication and movement. (
  • remodels the ER to generate viral vesicles. (
  • The replication complexes are housed in membrane invaginations called spherules on the plasma membrane and endolysosomal vesicles. (
  • Hantavirus Infection and Innate Immunity (N Sen et al. (
  • Early in human immunodeficiency virus type 1 (HIV-1) infection there is a decline in viral replication that has been attributed to host immunity, but the components of this response, particularly the ability of cytotoxic T lymphocytes to control viral burden and influence the outcome of disease, are poorly understood. (
  • Clinical evidence suggests that cellular immunity is involved in controlling human immunodeficiency virus-1 (HIV-1) replication. (
  • These results confirm the importance of cell-mediated immunity in controlling HIV-1 infection and support the exploration of vaccination approaches for preventing infection that will elicit these immune responses. (
  • We directly assessed the role of cellular immunity in controlling HIV-1 infection by means of the SIV of macaques (SIVmac)/rhesus monkey model of AIDS ( 4 ). (
  • However, the diversity of protein products that result, and how these could affect infection and immunity, is unclear. (
  • Antibiotics have no effect on viruses, though vaccinations will provide immunity. (
  • Investigators in the Division of Infectious Diseases and the Departments of Biochemistry and Molecular Biology of The George Washington University Medical Center are carrying out a research study to determine why patients with Human Immunodeficiency Virus (HIV) and Hepatitis C virus (HCV) co-infection (HIV/HCV) have a more rapid and progressive course of HCV infection, leading to fatty infiltration of the liver and cirrhosis. (
  • Both the RNA duplex and 5′-triphosphate moieties are important for specific, high-affinity binding and signaling by RIG-I ( 9 - 11 ), and through a series of recent crystal structures and functional studies of RNA recognition by the RIG-I receptor, the molecular basis for these effects has been elucidated ( 3 , 12 ). (
  • Umeå University, Faculty of Medicine, Molecular Infection Medicine Sweden (MIMS). (
  • Systems-level approaches have provided important insights into the molecular details of host-virus interaction 15 . (
  • The interferon system plays a critical role in maintaining an optimum equilibrium between virus replication and host survival,' says co-editor-in-chief Ganes C. Sen, PhD, chairman of the Department of Molecular Genetics at Cleveland Clinic Foundation in Ohio. (
  • My research focuses on molecular plant-virus interactions. (
  • By directly visualizing newly synthesized viral RNA with molecular beacons (MBs), we have developed a generalized method for the rapid and sensitive detection of infectious viruses from cell culture. (
  • They found a cytoplasmic sensor protein, ZBP1, which is essential in recognizing the presence of a virus by the accumulation of RNA in response to the infection. (
  • For NNS RNA viruses, the replication compartment is a cytoplasmic inclusion that is not circumscribed by a cellular membrane. (
  • To further investigate the association of PMTV infection with chloroplasts, ultrastructural studies of thin sections of PMTV-infected potato and Nicotiana benthamiana leaves by electron microscopy revealed abnormal chloroplasts with cytoplasmic inclusions and terminal projections. (
  • Our in silico analyses indicated that the non-structural protein 5 (NS5), especially the RNA-dependent RNA polymerase (RdRp) domain, contains conserved phosphorylation sites for protein kinase C (PKC). (
  • The rapid rate of evolution in RNA viruses is driven by a highly error-prone RNA-dependent RNA polymerase (RdRp). (
  • Because antibodies elicited by one virus type do not recognize other virus types, previous infection does not protect against reinfection with the same or different genotypes of the virus. (
  • This new guidance includes three important updates: 1) This report updates the post-exposure laboratory testing algorithm for the exposed HCP with testing for antibodies to HCV four to six months after exposure which was not included in the 2016 algorithm, based on current understanding of early HCV infection viral dynamics. (
  • By inhibiting viral replication, ZBP1 signaling provides precious time to the body to create antibodies and clear the virus from the host. (
  • The second option is to test the source patient for antibodies to hepatitis C virus (anti-HCV), then if positive, test for HCV RNA. (
  • They are also developing small molecules to target specific RNA structures as a means to treat Zika virus infections. (
  • Consequently, host cell receptor molecules that potentiate HCV infection were identified over a decade after the virus was discovered. (
  • Viruses with genetic information made up of molecules of RNA can multiply quickly, but not very accurately. (
  • The present invention relates to synthetic catalytic DNA molecules or DNAzymes which specifically cleave the RNA sequences of the Japanese Encephalitis Viral genome and is useful in treating Japanese Encephalitis infection. (
  • Previously, we reported that coffee extract and its constituents, caffeic acid (CA) and p-coumaric acid, inhibit infection by the hepatitis C virus (HCV). (
  • These compounds appear to selectively inhibit Caspase 8 as a method of preventing infective viral particle release. (
  • Our group study the functions of virus and host components during hepatitis C infection, particularly during viral RNA replication and virion assembly. (
  • Mutations at two of these phosphoreceptor sites [serine (S)220 and S239] in the full viral genome increase LT levels and promote MCV virion production and transmission, which can be neutralized with anti-capsid antibody. (
  • CP phosphorylation also affects viral trafficking and virion assembly. (
  • Chronic hepatitis B infection is the common etiology for the development of HCC. (
  • Hepatitis C virus (HCV) has become the most significant cause of chronic liver disease of infectious etiology in the United States. (
  • Most cases of blood-borne non-A, non-B hepatitis have been proven to be caused by hepatitis C virus (HCV) infection, one of the most common causes of chronic hepatitis in developed societies. (
  • 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. (
  • There is no known latency mechanism for chronic small DNA virus infections. (
  • Infection with hepatitis B and C viruses affects more than 10 percent of the world population and is the most common etiology of chronic liver disease and hepatocellular carcinoma, which is the fourth leading cause of death from cancer in the world. (
  • The draft genome sequence of an S. chromogenes isolate (MU 970) recovered from the milk of a cow with a chronic intramammary infection is reported here. (
  • However, the possibility of chronic infection also exists. (
  • The listing is Authority Required , General Schedule and Section 100, for the treatment of chronic HCV infection in patients with HCV genotypes 1-6. (
  • Hepatitis C is a pandemic human RNA virus, which commonly causes chronic infection and liver disease. (
  • In the two subjects who developed chronic infection, this second bottleneck was followed by the emergence of a new viral population, which evolved from the founder variants via a selective sweep with fixation in a small number of mutated sites. (
  • Hepatitis C virus (HCV) infection is a major cause of chronic liver disease, resulting in substantial morbidity and mortality worldwide, with between 123 and 170 million persons infected [1] . (
  • Among the 350 million people with chronic infection, the risk of dying from HBV-related diseases, such as end-stage cirrhosis and hepatocellular carcinoma (HCC) is between 15% to 25%.2 Since the early 1990s, chronically infected patients have been treated with recombinant interferons that are effective only in limited cases. (
  • DENV infection is common in tropical areas and occasionally causes life-threatening symptoms. (
  • The characteristics of DENV-1 viruses, isolated during the 2001-2002 outbreak in Indonesia were studied. (
  • DENV interacts with host cell factors to complete its life cycle although this virus-host interplay remains to be fully elucidated. (
  • Genetic analysis of A(H7N9) viruses has revealed some adaptations in the virus HA that allow binding to the sialic acid receptors on the epithelium of the mammalian upper respiratory tract. (
  • Researchers at University of California San Diego School of Medicine have discovered that Zika virus infection leads to modifications of both viral and human genetic material. (
  • The loss of essential genetic information causes abortive viral replication, which can be rescued by co-infection with a helper virus that possesses an intact genome. (
  • Although Middle East respiratory syndrome-coronavirus (MERS-CoV) does not infect large numbers of people like the afore-mentioned viruses, 35% of diagnosed patients die of MERS [ 2 ], and considering the virus' genetic possibilities, any change that increases transmissibility between humans would mean a serious public health threat that is considered worth preparing for. (
  • With so many different generations of virus coexisting in a cell, there are a lot of opportunities for new genetic combinations to occur and for viruses to evolve new abilities. (
  • with each new replication, the host cell produces more viral material than it does normal genetic material. (
  • The HCV exhibits substantial heterogeneity as a result of mutations occurring during viral replication. (
  • Upon infection in humans, these viruses rapidly acquire mutations in the viral polymerase basic 2 (PB2) gene ( 8 ). (
  • This means that many errors, or mutations, occur when the RNA is copied to create new viruses. (
  • The advantage of this rapid, but mistake-filled, RNA replication process is that some of the mutations will be beneficial to the virus. (
  • Or do the new copies of the RNA also get copied themselves in a 'geometric replication mode' that increases the likelihood of mutations and enables the virus to evolve more rapidly? (
  • This means that in a single infected cell there are multiple generations of RNA, and each generation may undergo distinct mutations that are passed on to the next set of RNA copies. (
  • Those virus-retrotransposon DNA chimeras produced transcripts processed by the RNAi machinery, which in turn inhibited viral replication. (
  • Our results suggest that, in order for RNAi to durably suppress HIV-1 replication, it may be necessary to target highly conserved regions of the viral genome. (
  • In conclusion, our data suggest that RNAi may provide a powerful therapeutic tool, acting both on replication-competent and on replication-incompetent HBV. (
  • In addition, the numerous potential targets for RNAi along the viral genome make it possible to target conserved regions, limiting the viral ability to create escape mutants. (
  • Such structures were first observed in the cell bodies of neurons from humans infected with rabies virus and were termed Negri bodies. (
  • The species barriers that hinder most avian IAVs from successfully infecting humans are effective at several steps in the viral life cycle. (
  • Chikungunya Virus (ChikV) is an Alphavirus of the Togaviridae family transmitted to humans through arthropods bites (mosquitoes of the Aedes genus). (
  • The poliovirus is an RNA virus that can cause paralysis and death in humans. (
  • Unfortunately for humans, some viral infections outpace the immune system. (
  • In panels B and C, primary human trophoblasts infected with ZIKV-FLR strain were analyzed at 5 days post-infection for the presence of viral replicative complexes ( B ) and envelope glycoprotein expression ( C ) by immunofluorescence, in three different unrelated placental donors. (
  • Bronchoalveolar lavage (BAL), nasal swabs, and nasopharyngeal swabs, as well as oropharyngeal swabs, taken at 1-3 days from infection, showed the presence of viral RNA, whereas it was not detected in similar pre-infection samples. (
  • Quantitative analysis of viral burden in tissues from adults and children with symptomatic human immunodeficiency virus type 1 infection assessed by polymerase chain reaction. (
  • The amount of human immunodeficiency virus type 1 (HIV-1) in various tissues was investigated by polymerase chain reaction (PCR) in 16 patients with end-stage HIV-1 infection and 7 patients with symptomatic but less advanced disease. (
  • SCID/uPA mice transplanted with human hepatocytes susceptible to HCV infection and transgenic mouse models have been useful as small animal models. (
  • When ZBP1 signaling is turned off, or absent, on the other hand, as in knockout mice, the study found even when they were infected by a strain of West Nile virus that was engineered to not produce disease (a non-pathogenic strain), every single mouse died. (
  • On the other hand, an active ZBP1 pathway led to limited replication, and prevented the development of brain inflammation in mice infected with the West Nile virus. (
  • The study thus shows that ZBP1 is required to limit the replication of West Nile and Zika viruses, and that this pathway is essential in activating effective immune responses to West Nile virus infection in mice. (
  • The short length (10 to 14 base pairs) and robust function of SLRs in mice demonstrate that RIG-I forms active signaling complexes without oligomerizing on RNA. (
  • In addition, we examined the expression of DI-RNAs in mice infected with sublethal dose of H7N9 virus at different time points. (
  • Mice infected with the reduced-virulence 2.2-V-1 JHMV variant clear infectious virus from the CNS by day 12 postinfection (p.i.) ( 2 , 18 , 24 ) but still develop immune-mediated demyelination ( 11 , 20 , 25 ). (
  • Wiegand MA, Gori-Savellini G, Gandolfo C, Papa G, Kaufmann C, Felder E, Ginori A, Disanto MG, Spina D, Cusi MG. Repiratory syncytial virus (RSV) vaccine vectored by a stable chimeric and replication-deficient Sendai virus protects mice without inducing enhanced disease. (
  • Third, mice lacking the adaptor protein MyD88, which are unable to activate most TLR signaling pathways, are remarkably resistant to infection with several viruses ( 4 ). (
  • However, most published descriptions of HCV-exposed HCP focus on source anti-HCV test results rather than tests for HCV RNA (nucleic acid tests, or NAT) [ 8 ] and limited published data are available to confirm the lack of risk to HCP[ 9-12 ]. (
  • DNA- and RNA-binding studies confirmed that PUR domains are indeed functional nucleic-acid binding domains. (
  • The first option is to test the source patient with a nucleic acid test (NAT) for HCV RNA. (
  • Detection of nucleic acids is a fundamental means of viral recognition in both prokaryotes and eukaryotes, although the types of receptors that recognize nucleic acids and the responses induced by these receptors vary greatly across phyla. (
  • Meanwhile, rapidly evolving genomeediting techniques targeting viral DNA/RNA have emerged as novel therapeutic strategies for treating virusrelated carcinogenesis and have begun showing promising results. (
  • The availability of culture systems and small animal models has greatly facilitated the elucidation of fundamental knowledge of the virus and the evaluation of vaccine and therapeutic candidates. (
  • This work suggests novel therapeutic approaches to the problem of combating NNS RNA viral infections. (
  • Saha A, Kaul R, Murakami M, Robertson ES (2010) Tumor viruses and cancer biology: modulating signaling pathways for therapeutic intervention. (
  • Patients with hepatocellular carcinoma caused by hepatitis B virus who will be treated by transcatheter arterial chemoembolization were included. (
  • Shlomai A, de Jong YP, Rice CM. Virus associated malignancies: the role of viral hepatitis in hepatocellular carcinoma. (
  • Hepatitis D virus (HDV) is responsible for fulminant hepatitis and liver failure and accelerates evolution toward cirrhosis and hepatocellular carcinoma in hepatitis B virus (HBV)-infected patients. (
  • After that, we decided to investigate m6A RNA in Zika virus as well, since we didn't want to miss out on this important information the way we missed it for 30 years of HIV research," Rana said. (
  • When Zika virus infects a human cell, Rana's team found, the cell modifies viral RNA with m6A as a means to get rid of the infection. (
  • In addition, they found that this host response to Zika viral infection also induced specific m6A modifications on human RNA. (
  • These human RNA changes were not present in the absence of Zika virus. (
  • In contrast, silencing the human enzymes that remove methyl groups -- increasing m6A methylation, in other words -- decreased Zika virus production. (
  • It could help develop new treatment methods for viruses that target the nervous system such as the Zika or West Nile Encephalitis virus . (
  • The study focused on how to control the replication of 2 modern-day killer viruses, the West Nile and Zika viruses. (
  • The Zika virus is spread by the Aedes mosquito which can breed in the south of the US, up to Florida and Texas. (
  • In the majority of cases of Zika or West Nile virus attack, the person doesn't even know because of a healthy immune response, and this limits our knowledge of actual infection statistics and of the natural course of infection. (
  • Primary Human Placental Trophoblasts are Permissive for Zika Virus (ZIKV) Replication. (
  • Zika virus (ZIKV) is an emerging mosquito-borne (Aedes genus) arbovirus of the Flaviviridae family. (
  • Serological diagnosis of Zika virus (ZIKV) infections is challenging due to high cross-reactivity between flaviviruses. (
  • Rapid risk assessment: Zika virus epidemic in the Americas: potential association with microcephaly and Guillain-Barré syndrome. (
  • Zika Virus in the Americas--Yet Another Arbovirus Threat. (
  • Zika virus (ZIKV) is a mosquito-borne flavivirus and has historically been reported to cause mild symptomatic diseases during human infections. (
  • Higgs S . Zika virus: emergence and emergency. (
  • Probable non-vector-borne transmission of Zika virus, Colorado, USA. (
  • Potential sexual transmission of Zika virus. (
  • Rapid spread of Zika virus in the Americas-implications for public health preparedness for mass gatherings at the 2016 Brazil Olympic games. (
  • Guillain-barré syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study. (
  • Zika virus associated with microcephaly. (
  • This guidance provides CDC recommendations for laboratory testing and follow-up of health care personnel (HCP) who have been potentially exposed to hepatitis C virus (HCV) through an exposure to blood or other infectious body fluid. (
  • Follow-up testing for HCP exposed to blood or body fluids from a source who tests anti-HCV positive but HCV RNA negative is not currently recommended, as source persons with that laboratory result profile are not considered infectious. (
  • Chimpanzee challenge studies have suggested that there is an infectious titer (chimpanzee infective dose) required to transmit infection, and that this level of inoculum is different in other animal models (humanized liver-mouse models). (
  • Dove B, Brooks G, Bicknell K, Wurm T, Hiscox JA (2006) Cell cycle perturbations induced by infection with the coronavirus infectious bronchitis virus and their effect on virus replication. (
  • Arginine is required for the replication of human adenovirus type 2 (common cold) and is essential for the production of complete infectious virions. (
  • The dormant nature of these viruses may be explained by the availability of arginine during various stages of the infectious process. (
  • Infectious salmon anemia virus (ISAV) is the causative agent of an important viral disease threatening the Atlantic salmon aquaculture in Norway and many other countries. (
  • Rapid detection of infectious viruses is of central importance for public health risk assessment. (
  • The ability to detect infectious viruses is of critical importance in medical diagnostic and environmental/agricultural protection ( 18 ). (
  • Current methods to assess the presence of infectious viruses are based on mammalian cell culture and rely on the production of visible cytopathic effects (CPE) ( 15 ). (
  • RNA viruses are major threats to human and animal health and account for the majority of emerging infectious diseases. (
  • Rna Viruses: Host Gene Responses To Inf. (
  • Host Signaling Responses to Coxsackievirus Infection (G Gao et al. (
  • Double-Stranded RNA Virus: Host Signaling Responses to Reovirus Infection (D Pan et al. (
  • virus-host interactions and identifying factors contributing to virus-associated progression of liver disease. (
  • 5 This rapid mutation appears to be a mechanism that allows the virus to escape immune surveillance by the host and to maintain persistent infection. (
  • Its best-studied family member, Pur-α, acts as a transcriptional regulator, as host factor for viral replication, and as cofactor for mRNP localization in dendrites. (
  • Pur-α also serves as cellular host factor for the infection of RNA viruses like JC virus and HIV ( 7 - 10 ), most likely by augmenting viral replication ( 11 , 12 ). (
  • Viral latency is required for long-term persistence and allows viruses to evade host immune surveillance. (
  • The work presented here seeks to define the mechanism of action for the host restriction factor AUF1 during infection by poliovirus and CVB3. (
  • HCV, like many other viruses, exploit host cellular machinery for productive infection. (
  • However, unlike other RNA viruses, HCV has a high propensity to cause persistent infection despite an active host immune response. (
  • For HBV, the replication and virus-host interactions have been studied in great detail and many of the pathways have been elucidated. (
  • Portion of thesis entitled Characterization of Brome Mosaic Virus RNA3 interaction with GCD10, a tRNA binding host factor from yeast. (
  • 14. Animal Virus-Host Interactions. (
  • Thus, we identify M segment RNA splicing as a viral host range determinant. (
  • Subversion of the cellular machinery that controls replication of the infected host cell is a common activity of many viruses. (
  • Movement between hosts is entirely passive, but once they encounter a suitable host cell viruses can begin a cycle that can produce hundreds of new viruses within a very short time. (
  • However, while laboratory experiments focus on productive infections where the host cell is rapidly turned into a virus factory, many other types of infection exist, some of them allowing the virus to exist alongside its host for long periods of time. (
  • However, research addressing the effect of host innate immune evasion on the pathology caused by viral infections is less prevalent in the literature, though very relevant and interesting. (
  • Thus, the viral life cycle is necessarily rely on or regulated by host factors. (
  • According to Researchers Catherine Jopling and colleagues, HCV could ease viral replication by binding its RNA genome to host-cell microRNA (miRNA). (
  • The outcome of primary HCV infection is driven by the interplay between rapid viral evolution and host adaptive immune responses [3] , [4] . (
  • The spectrum of host response categories was refined by investigating plasma viral RNA loads. (
  • Once a virus infects a cell, it tries to take over its host completely, much as Napoleon spread the French influence with every country he fought. (
  • Left unchecked, the virus will cause the death of the host cell. (
  • In this review, we briefly introduce autophagy, viral xenophagy and the interaction among autophagy, virus and immune response, then focus on the interplay between NS-RNA viruses and autophagy during virus infection. (
  • These modifications -- chemical tags known as methyl groups -- influence viral replication and the human immune response. (
  • Since interferons have been implicated in inflammatory diseases and immunopathology in addition to their protective role in infection, antagonizing the immune response may have an ambiguous effect on the clinical outcome of the viral disease. (
  • Sofosbuvir is an inhibitor of HCV NS5B nucleotide polymerase, essential for viral replication. (
  • Specifically, we have found that miR-122 interacts with the 5' end of the viral RNA and is essential for viral replication. (
  • Besides K22 resistance, the nsp6 mutants induced a reduced number of DMVs, displayed decreased specific infectivity, while RNA synthesiswasnot affected. (
  • however, there are reports of virus resistance to both inhibitors [ 4 ]. (
  • A neomycin resistance cassette including the simian virus 40 (SV40) early promoter and the SV40 early polyadenylation signal was cloned into Bgl II and Cla I sites of pCMV-H1-MCS. (
  • This allows viruses to rapidly evolve, for example, to develop resistance against drugs. (
  • The envelope surrounds a capsid that contains a positive sense single-stranded RNA genome approximately 9,600 nucleotides long encoding a 3000-amino-acid polyprotein. (
  • Although much progress has been achieved in dissecting the interplay between viruses and cellular autophagic machinery, it is not well understood how the cellular autophagic pathway is utilized by viruses and manipulated to their own advantage. (
  • How the replication machinery that forms this inclusion remains associated in the absence of a membrane has been an enduring mystery. (
  • Viruses alter the cellular machinery to facilitate the production of the next generation of viruses, and repress cellular and immunological controls that attempt to prevent this. (
  • Indeed, André Lwoff noted the absence of ribosomes and the cellular translation machinery as a defining feature of viruses ( Lwoff, 1957 ). (
  • In stably transgenic potato, we obtained very poor expression of Narita 104 virus capsid protein (NaVCP) despite the use of a strong constitutive promoter (dual enhancer 35S) driving the native coding sequence. (
  • Comparative studies using real time PCR analysis from cDNA samples revealed lower accumulation of full length transcripts of NaVCP as compared to those from a gene encoding Norwalk Virus capsid protein (a related Genogroup I Norovirus) in transiently transfected plants. (
  • Viral transcripts were detected by 18 h p.i. and the capsid protein RNA of 950 nucleotides (nt) was the most abundant RNA species. (