Virus activation. Medical search

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.

This plant order includes 8 families, 66 genera, and about 1,800 species. These herbaceous perennials are mainly found in the wet tropics. Members include the banana family (MUSACEAE) and GINGER family (ZINGIBERACEAE).

An analog of DEOXYURIDINE that inhibits viral DNA synthesis. The drug is used as an antiviral agent.

The type species of LYMPHOCRYPTOVIRUS, subfamily GAMMAHERPESVIRINAE, infecting B-cells in humans. It is thought to be the causative agent of INFECTIOUS MONONUCLEOSIS and is strongly associated with oral hairy leukoplakia (LEUKOPLAKIA, HAIRY;), BURKITT LYMPHOMA; and other malignancies.

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.

Viruses whose genetic material is RNA.

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.

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.

Process of growing viruses in live animals, plants, or cultured cells.

The expelling of virus particles from the body. Important routes include the respiratory tract, genital tract, and intestinal tract. Virus shedding is an important means of vertical transmission (INFECTIOUS DISEASE TRANSMISSION, VERTICAL).

A general term for diseases produced by viruses.

A species of POLYOMAVIRUS originally isolated from Rhesus monkey kidney tissue. It produces malignancy in human and newborn hamster kidney cell cultures.

The assembly of VIRAL STRUCTURAL PROTEINS and nucleic acid (VIRAL DNA or VIRAL RNA) to form a VIRUS PARTICLE.

Viruses parasitic on plants higher than bacteria.

Viruses whose nucleic acid is DNA.

Viruses which lack a complete genome so that they cannot completely replicate or cannot form a protein coat. Some are host-dependent defectives, meaning they can replicate only in cell systems which provide the particular genetic function which they lack. Others, called SATELLITE VIRUSES, are able to replicate only when their genetic defect is complemented by a helper virus.

The type species of ALPHAVIRUS normally transmitted to birds by CULEX mosquitoes in Egypt, South Africa, India, Malaya, the Philippines, and Australia. It may be associated with fever in humans. Serotypes (differing by less than 17% in nucleotide sequence) include Babanki, Kyzylagach, and Ockelbo viruses.

The type species of MORBILLIVIRUS and the cause of the highly infectious human disease MEASLES, which affects mostly children.

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.

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.

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.

A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 3 and neuraminidase 2. The H3N2 subtype was responsible for the Hong Kong flu pandemic of 1968.

The type species of the genus ORTHOHEPADNAVIRUS which causes human HEPATITIS B and is also apparently a causal agent in human HEPATOCELLULAR CARCINOMA. The Dane particle is an intact hepatitis virion, named after its discoverer. Non-infectious spherical and tubular particles are also seen in the serum.

A species of FLAVIVIRUS, one of the Japanese encephalitis virus group (ENCEPHALITIS VIRUSES, JAPANESE). It can infect birds and mammals. In humans, it is seen most frequently in Africa, Asia, and Europe presenting as a silent infection or undifferentiated fever (WEST NILE FEVER). The virus appeared in North America for the first time in 1999. It is transmitted mainly by CULEX spp mosquitoes which feed primarily on birds, but it can also be carried by the Asian Tiger mosquito, AEDES albopictus, which feeds mainly on mammals.

A group of viruses in the PNEUMOVIRUS genus causing respiratory infections in various mammals. Humans and cattle are most affected but infections in goats and sheep have also been reported.

Ribonucleic acid that makes up the genetic material of viruses.

The functional hereditary units of VIRUSES.

Substances elaborated by viruses that have antigenic activity.

The type species of VESICULOVIRUS causing a disease symptomatically similar to FOOT-AND-MOUTH DISEASE in cattle, horses, and pigs. It may be transmitted to other species including humans, where it causes influenza-like symptoms.

The 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.

Proteins found in any species of virus.

Membrane glycoproteins from influenza viruses which are involved in hemagglutination, virus attachment, and envelope fusion. Fourteen distinct subtypes of HA glycoproteins and nine of NA glycoproteins have been identified from INFLUENZA A VIRUS; no subtypes have been identified for Influenza B or Influenza C viruses.

Viruses that produce tumors.

A CELL LINE derived from the kidney of the African green (vervet) monkey, (CERCOPITHECUS AETHIOPS) used primarily in virus replication studies and plaque assays.

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 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.

The type species of RUBULAVIRUS that causes an acute infectious disease in humans, affecting mainly children. Transmission occurs by droplet infection.

A species of RESPIROVIRUS also called hemadsorption virus 2 (HA2), which causes laryngotracheitis in humans, especially children.

Viruses which produce a mottled appearance of the leaves of plants.

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 in the genus HEPATOVIRUS containing one serotype and two strains: HUMAN HEPATITIS A VIRUS and Simian hepatitis A virus causing hepatitis in humans (HEPATITIS A) and primates, respectively.

A species of ALPHAVIRUS isolated in central, eastern, and southern Africa.

Group of alpharetroviruses (ALPHARETROVIRUS) producing sarcomata and other tumors in chickens and other fowl and also in pigeons, ducks, and RATS.

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 measurement of infection-blocking titer of ANTISERA by testing a series of dilutions for a given virus-antiserum interaction end-point, which is generally the dilution at which tissue cultures inoculated with the serum-virus mixtures demonstrate cytopathology (CPE) or the dilution at which 50% of test animals injected with serum-virus mixtures show infectivity (ID50) or die (LD50).

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.

The binding of virus particles to receptors on the host cell surface. For enveloped viruses, the virion ligand is usually a surface glycoprotein as is the cellular receptor. For non-enveloped viruses, the virus CAPSID serves as the ligand.

A species of POLYOMAVIRUS apparently infecting over 90% of children but not clearly associated with any clinical illness in childhood. The virus remains latent in the body throughout life and can be reactivated under certain circumstances.

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.

Viruses whose taxonomic relationships have not been established.

A species of POLYOMAVIRUS, originally isolated from the brain of a patient with progressive multifocal leukoencephalopathy. The patient's initials J.C. gave the virus its name. Infection is not accompanied by any apparent illness but serious demyelinating disease can appear later, probably following reactivation of latent virus.

The type species of ALPHARETROVIRUS producing latent or manifest lymphoid leukosis in fowl.

The relationships of groups of organisms as reflected by their genetic makeup.

Deoxyribonucleic acid that makes up the genetic material of viruses.

A family of RNA viruses causing INFLUENZA and other diseases. There are five recognized genera: INFLUENZAVIRUS A; INFLUENZAVIRUS B; INFLUENZAVIRUS C; ISAVIRUS; and THOGOTOVIRUS.

The type species of ORBIVIRUS causing a serious disease in sheep, especially lambs. It may also infect wild ruminants and other domestic animals.

Virus diseases caused by the ORTHOMYXOVIRIDAE.

Established cell cultures that have the potential to propagate indefinitely.

Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses.

The type species of RESPIROVIRUS in the subfamily PARAMYXOVIRINAE. It is the murine version of HUMAN PARAINFLUENZA VIRUS 1, distinguished by host range.

A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. It also infects rats and newborn hamsters. It is apparently transmitted to embryos in utero and to newborns through mother's milk.

Insertion of viral DNA into host-cell DNA. This includes integration of phage DNA into bacterial DNA; (LYSOGENY); to form a PROPHAGE or integration of retroviral DNA into cellular DNA to form a PROVIRUS.

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.

The outer protein protective shell of a virus, which protects the viral nucleic acid.

The type species of the FLAVIVIRUS genus. Principal vector transmission to humans is by AEDES spp. mosquitoes.

A genus of the family HERPESVIRIDAE, subfamily ALPHAHERPESVIRINAE, consisting of herpes simplex-like viruses. The type species is HERPESVIRUS 1, HUMAN.

The type species of TOBAMOVIRUS which causes mosaic disease of tobacco. Transmission occurs by mechanical inoculation.

Pneumovirus infections caused by the RESPIRATORY SYNCYTIAL VIRUSES. Humans and cattle are most affected but infections in goats and sheep have been reported.

The type species of LEPORIPOXVIRUS causing infectious myxomatosis, a severe generalized disease, in rabbits. Tumors are not always present.

Inactivation of viruses by non-immune related techniques. They include extremes of pH, HEAT treatment, ultraviolet radiation, IONIZING RADIATION; DESICCATION; ANTISEPTICS; DISINFECTANTS; organic solvents, and DETERGENTS.

A species of ORTHOPOXVIRUS that is the etiologic agent of COWPOX. It is closely related to but antigenically different from VACCINIA VIRUS.

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.

A species of ORTHOPOXVIRUS causing infections in humans. No infections have been reported since 1977 and the virus is now believed to be virtually extinct.

The type species of PNEUMOVIRUS and an important cause of lower respiratory disease in infants and young children. It frequently presents with bronchitis and bronchopneumonia and is further characterized by fever, cough, dyspnea, wheezing, and pallor.

A species of ARENAVIRUS, part of the Old World Arenaviruses (ARENAVIRUSES, OLD WORLD), and the etiologic agent of LASSA FEVER. LASSA VIRUS is a common infective agent in humans in West Africa. Its natural host is the multimammate mouse Mastomys natalensis.

A species of ALPHAVIRUS causing an acute dengue-like fever.

The type species in the genus NOROVIRUS, first isolated in 1968 from the stools of school children in Norwalk, Ohio, who were suffering from GASTROENTERITIS. The virions are non-enveloped spherical particles containing a single protein. Multiple strains are named after the places where outbreaks have occurred.

An acute viral infection in humans involving the respiratory tract. It is marked by inflammation of the NASAL MUCOSA; the PHARYNX; and conjunctiva, and by headache and severe, often generalized, myalgia.

A collection of single-stranded RNA viruses scattered across the Bunyaviridae, Flaviviridae, and Togaviridae families whose common property is the ability to induce encephalitic conditions in infected hosts.

Biological properties, processes, and activities of VIRUSES.

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.

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).

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 amino-terminal C/H1 domain of CREB binding protein mediates zta transcriptional activation of latent Epstein-Barr virus. (1/1814)

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

Bacteriophage inactivation at the air-water-solid interface in dynamic batch systems. (2/1814)

Bacteriophages have been widely used as surrogates for human enteric viruses in many studies on virus transport and fate. In this investigation, the fates of three bacteriophages, MS2, R17, and phiX174, were studied in a series of dynamic batch experiments. Both MS2 and R17 readily underwent inactivation in batch experiments where solutions of each phage were percolated through tubes packed with varying ratios of glass and Teflon beads. MS2 and R17 inactivation was the result of exposure to destructive forces at the dynamic air-water-solid interface. phiX174, however, did not undergo inactivation in similar studies, suggesting that this phage does not accumulate at air-water interfaces or is not affected by interfacial forces in the same manner. Other batch experiments showed that MS2 and R17 were increasingly inactivated during mixing in polypropylene tubes as the ionic strength of the solution was raised (phiX174 was not affected). By the addition of Tween 80 to suspensions of MS2 and R17, phage inactivation was prevented. Our data suggest that viral inactivation in simple dynamic batch experiments is dependent upon (i) the presence of a dynamic air-water-solid interface (where the solid is a hydrophobic surface), (ii) the ionic strength of the solution, (iii) the concentration of surface active compounds in the solution, and (iv) the type of virus used. (+info)

Activation in vivo of retroperitoneal fibromatosis-associated herpesvirus, a simian homologue of human herpesvirus-8. (3/1814)

Retroperitoneal fibromatosis-associated herpesvirus of rhesus macaques (RFHVMm) is a gammaherpesvirus closely related to human herpesvirus-8 (HHV-8), which is thought to be a necessary cofactor for the development of Kaposi's sarcoma (KS) in humans. Here, RFHVMm infection of rhesus macaques exposed to the D-type retrovirus simian retrovirus-2 (SRV-2) is described. Development of SRV-2 viraemia, infection with simian immunodeficiency virus or administration of cyclosporin A could result in persistent RFHVMm viraemia. From this, it is concluded that productive retrovirus infection or otherwise-induced immune suppression has the ability to activate this herpesvirus in vivo. Elevated levels of circulating interleukin-6, a cytokine that plays a central role in KS, were found in RFHVMm-viraemic animals. In viraemic animals, RFHVMm was found in tissues that are common sites for the development of AIDS-associated KS, especially the oral cavity. Together, these data suggest a common biology between RFHVMm infection of macaques and HHV-8 infection and pathogenesis in humans. (+info)

Requirements for measles virus induction of RANTES chemokine in human astrocytoma-derived U373 cells. (4/1814)

Interferons and chemokines play a critical role in regulating the host response to viral infection. Measles virus, a member of the Paramyxoviridae family, induces RANTES expression by astrocytes. We have examined the mechanism of this induction in U373 cells derived from a human astrocytoma. RANTES was induced in a dose- and time-dependent manner by measles virus infection. Inhibition of receptor binding by the anti-CD46 antibody TRA-2.10 and of virus-membrane fusion by the tripeptide X-Phe-Phe-Gly reduced RANTES expression. Formalin-inactivated virus, which can bind but not fuse, and extensively UV-irradiated virus, which can bind and fuse, were both ineffective. Therefore, virus binding to the cellular receptor CD46 and subsequent membrane fusion were necessary, but not sufficient, to induce RANTES. UV irradiation of virus for less than 10 min proportionally inhibited viral transcription and RANTES expression. RANTES induction was decreased in infected cells treated with ribavirin, which inhibits measles virus transcription. However, RANTES mRNA was superinduced by measles virus in the presence of cycloheximide. These data suggest that partial transcription of the viral genome is sufficient and necessary for RANTES induction, whereas viral protein synthesis and replication are not required. This hypothesis was supported by the fact that RANTES was induced through transient expression of the measles virus nucleocapsid gene but not by measles genes encoding P or L proteins or by leader RNA in A549 cells. Thus, transcription of specific portions of measles virus RNA, such as the nucleocapsid gene, appears able to generate the specific signaling required to induce RANTES gene expression. (+info)

Role for gamma interferon in control of herpes simplex virus type 1 reactivation. (5/1814)

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

Management of human cytomegalovirus infection and disease after allogeneic bone marrow transplantation. (6/1814)

BACKGROUND AND OBJECTIVE: Human cytomegalovirus (HCMV) infection and disease remain a major cause of morbidity and mortality after bone marrow transplantation. HCMV disease, especially pneumonitis, may be treated with ganciclovir and immunoglobulin but even so the outcome is poor with mortality rates of 30-70%. It is therefore imperative to treat HCMV infection before it develops into disease. The aim of this article is to describe the main strategies used to prevent HCMV infection and to improve the survival after CMV disease in bone marrow transplant recipients. INFORMATION SOURCES: In the present review, we examined personal papers in this field and articles published in journals covered by the Science Citation Index and Medline. STATE OF THE ART: Major advances have been made in preventing HCMV infection and disease through two different approaches, both of which reduce HCMV induced morbidity and mortality: In pre-emptive therapy, patients are given ganciclovir when HCMV infection is first identified and this is continued 3-4 months after transplantation; in prophylactic therapy ganciclovir is given to all patients at risk of HCMV disease from engraftment up to 3-4 months post transplantation. Each strategy has advantages and disadvantages and there is no evidence for the superiority of one over the other since the overall survival is the same and the incidence of death from HCMV disease is similar. PERSPECTIVES: The use of more sensitive tests such as HCMV PCR or antigenemia may improve the outcome but probably will not eradicate all HCMV disease. Future possible strategies could include adoptive transfer of CD8+ HCMV-specific cytotoxic T lymphocytes clones derived from the donor marrow or boosting donor or patient immunity using subunit anti-HCMV vaccines such as gB or pp65. (+info)

Induction of prophages of enterohemorrhagic Escherichia coli O157:H7 with norfloxacin. (7/1814)

Norfloxacin (NFLX) caused induction of prophages VT1 and VT2 of enterohemorrhagic Escherichia coli O157 at subinhibitory concentrations. In time course experiments, we observed the following sequential events: upon induction, the phage genomes underwent multiplication; the amount of stx genes increased; and subsequently, large quantities of toxins VT1 and VT2 were produced. Further studies showed that the molecular mechanism of prophage induction is closely related to the RecA system since the prophage VT2 was not induced with NFLX in a recA mutant strain. (+info)

Long-lasting protection by live attenuated simian immunodeficiency virus in cynomolgus monkeys: no detection of reactivation after stimulation with a recall antigen. (8/1814)

The infection of cynomolgus monkeys with an attenuated simian immunodeficiency virus (SIV) (C8) carrying a deletion in the nef gene results in a persistent infection associated with an extremely low viral burden in peripheral blood mononuclear cells. The aim of this study was to determine (1) the breadth of the protection after repeated challenges of monkeys with SIV homologous strains of different pathogenicity, (2) the genotypic stability of the live virus vaccine, (3) whether the protection might depend on cellular resistance to superinfection, and (4) whether immunogenic stimuli such as recall antigens could reactivate the replication of the C8 virus. To address these goals, the monkeys were challenged at 40 weeks after C8 infection with 50 MID50 of cloned SIVmac251, BK28 grown on macaque cells. They were protected as indicated by several criteria, including virus isolation, anamnestic serological responses, and viral diagnostic PCR. At 92 weeks after the first challenge, unfractionated peripheral blood mononuclear cells from protected monkeys were susceptible to the in vitro infection with SIVmac32H, spl. At 143 weeks after C8 infection, the four protected monkeys were rechallenged with 50 MID50 of the pathogenic SIVmac32H, spl grown on macaque cells. Once again, they were protected. The C8 virus remained genotypically stable, and depletion of CD4(+) cells was not observed during approximately 3 years of follow-up. In contrast, it was found that the infection with SIVmac32H, spl induced CD4(+) cell depletion in three of three control monkeys. Of importance, stimulation with tetanus toxoid, although capable of inducing specific humoral and T cell proliferative responses, failed to induce a detectable reactivation of C8 virus. (+info)

... these lead to enhanced replication and virus production. Often, lytic activation leads to cell death. Clinically, lytic ... Although the branching order of the herpes viruses has not yet been resolved, because herpes viruses and their hosts tend to ... "Virus Taxonomy: 2020 Release". International Committee on Taxonomy of Viruses (ICTV). March 2021. Retrieved 10 May 2021. John ... The avian infectious laryngotracheitis virus is phylogenetically distant from these two viruses and serves to underline ...

https://en.wikipedia.org/wiki/Herpesviridae

"Paramyxovirus Sendai virus V protein counteracts innate virus clearance through IRF-3 activation, but not via interferon, in ... Sendai virus was also used as a backbone for vaccine against respiratory syncytial virus (HRSV). This virus (HRSV), is a major ... The virus genome has high similarity with human parainfluenza virus 1 (HPIV-1) and the two viruses share common antigenic ... It was suggested that the mice used to passage the virus were infected with the mouse virus. Thus, mouse virus was later ...

https://en.wikipedia.org/wiki/Murine_respirovirus

"A Mechanism for the Activation of the Influenza Virus Transcriptase". Molecular Cell. 72 (2): 396. doi:10.1016/j.molcel.2018.10 ... Fodor's research focuses on the molecular biology of influenza viruses. An early highlight of his work was the development of a ... His more recent work focuses on the molecular mechanisms used by influenza viruses to copy their genetic information stored in ... Te Velthuis, Aartjan J. W.; Fodor, Ervin (August 2016). "Influenza virus RNA polymerase: insights into the mechanisms of viral ...

https://en.wikipedia.org/wiki/Ervin_Fodor

"Asparagine endopeptidase controls anti-influenza virus immune responses through TLR7 activation". PLOS Pathogens. 8 (8): ... Activation begins at pH 4.5. The chemical structure at this point shows that breaks which occurs at pH 4.5 can be healed under ... Antigen presenting is a key role in activation of immune system. It has been discovered that AEP plays role in this critical ... Enzyme is also important in processing of influenza virus and immune response using TLR7. AEP plays a critical role in TLR ...

https://en.wikipedia.org/wiki/Asparagine_endopeptidase

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Clausamines D-G inhibit early antigen activation of the Epstein-Barr virus. Leaf extracts have a mild effect on HIV-1 and HIV-2 ...

https://en.wikipedia.org/wiki/Clausena_anisata

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https://en.wikipedia.org/wiki/Ribonuclease_L

"Studying G protein-coupled receptor activation using split-tobacco etch virus assays". Analytical Biochemistry. 412 (2): 141-52 ... on the functional reconstitution of two previously inactive fragments derived from the NIa protease of the tobacco etch virus ( ...

https://en.wikipedia.org/wiki/Split_TEV

"Mutational definition of the human immunodeficiency virus type 1 Rev activation domain". Journal of Virology. 65 (8): 4248-54. ... Meyer BE, Meinkoth JL, Malim MH (April 1996). "Nuclear transport of human immunodeficiency virus type 1, visna virus, and ... Fischer U, Huber J, Boelens WC, Mattaj IW, Lührmann R (August 1995). "The HIV-1 Rev activation domain is a nuclear export ... Cochrane A, Kramer R, Ruben S, Levine J, Rosen CA (July 1989). "The human immunodeficiency virus rev protein is a nuclear ...

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October 2009). "Activation of MDA5 requires higher-order RNA structures generated during virus infection". Journal of Virology ... the genomic RNA of dsRNA viruses as well as replicative intermediates of both positive and negative sense RNA viruses. MDA5 has ... For many viruses, effective MDA5-mediated antiviral responses are dependent on functionally active LGP2. The signaling cascades ... November 2006). "Activation of Ras/Raf protects cells from melanoma differentiation-associated gene-5-induced apoptosis". Cell ...

https://en.wikipedia.org/wiki/MDA5

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"Transcriptional Activation of the Integrated Chromatin-Associated Human Immunodeficiency Virus Type 1 Promoter". Mol. Cell. ...

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"Transcriptional Activation of the Integrated Chromatin-Associated Human Immunodeficiency Virus Type 1 Promoter". Mol. Cell. ...

https://en.wikipedia.org/wiki/HIST1H2AD

"Transcriptional Activation of the Integrated Chromatin-Associated Human Immunodeficiency Virus Type 1 Promoter". Mol. Cell. ...

https://en.wikipedia.org/wiki/HIST1H2BA