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)

TY - JOUR. T1 - Chronic herpesvirus reactivation occurs in aging. AU - Stowe, Raymond P.. AU - Kozlova, Elena V.. AU - Yetman, Deborah L.. AU - Walling, Dennis M.. AU - Goodwin, James. AU - Glaser, Ronald. PY - 2007/6. Y1 - 2007/6. N2 - The aged immune system is characterized by clonal expansions of CD8+ T cells of which a substantial portion are directed against Epstein-Barr virus (EBV) and cytomegalovirus (CMV). It is unknown if these expansions represent increased viral reactivation or simply reflect an accumulation over time. We investigated herpesvirus reactivation in young and old subjects co-infected with CMV and EBV. Using molecular and serological techniques, we found significant increases in both the frequency and magnitude of EBV and CMV reactivation in elderly subjects. CMV DNA was frequently detected in the urine of elderly subjects; EBV load in peripheral blood was also significantly increased. Notably, EBV DNA in plasma was detected in a majority of the elderly subjects which was ...
TY - JOUR. T1 - Monitoring and Preemptive Rituximab Therapy for Epstein-Barr Virus Reactivation after Antithymocyte Globulin Containing Nonmyeloablative Conditioning for Umbilical Cord Blood Transplantation. AU - Blaes, Anne H.. AU - Cao, Qing. AU - Wagner, John E.. AU - Young, Jo Anne H. AU - Weisdorf, Daniel J.. AU - Brunstein, Claudio G.. N1 - Funding Information: Financial disclosure: This work was supported in part by grants from the National Cancer Institute PO1-CA65493 (J.E.W., C.G.B) and the Childrens Cancer Research Fund (J.E.W.). PY - 2010/2. Y1 - 2010/2. N2 - Epstein Barr viremia (EBV) and posttransplantation lymphoproliferative disorder (PTLD) are complications of hematopoietic stem cell transplantation (HSCT). The use of antithymocyte globulin (ATG) in recipients of umbilical cord HSCT is a known risk factor for the development of PTLD. In this high-risk population, we implemented an EBV monitoring program with preemptive therapy with rituximab (375 mg/m2 intravenously [i.v.]) for ...
Currently available medicines in the BCR-ABL TKIs class of drugs include Gleevec and Iclusig, as well as Tasigna, Bosulif, and Sprycel.. These BCR-ABL tyrosine kinase inhibitors (TKIs) are used for the treatment of specific types of blood cancers, including Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) and Ph+ acute lymphoblastic leukemia (ALL), and less commonly, other types of cancers.. In May 2016 Health Canada issued a safety warning, BCR-ABL Tyrosine Kinase Inhibitors [GLEEVEC (imatinib mesylate), TASIGNA (nilotinib), BOSULIF (bosutinib), SPRYCEL (dasatinib), ICLUSIG (ponatinib hydrochloride)] - Risk of Hepatitis B Reactivation, which did not receive much public attention in the US.. From that May 2016 Health Canada document, we get the following detailed safety information about these drugs:. ...
HBV is endemic in Taiwan. Mass vaccination started in 1984 [13, 14]. However, the prevalence of HBV is still high in the general population. This is the first large cohort study to compare the incidence of HBV reactivation in different subtypes of hematological malignancy. In this retrospective cohort, 286 (14.6%) of 1962 patients were HBV carriers. HBV reactivation is critical for the clinical care of patients with hematological malignancy receiving chemotherapy. The incidence of HBV reactivation was 10.4 per 100 person-years in this study. This epidemiological result is similar to those of previous studies of lymphoma (10.4 per 100 person-years) [5] and AML (9.5 per 100 person-years) [23].. HBV reactivation in cancer patients receiving cytotoxic chemotherapy has been noted for 3 decades [3, 24, 25], especially in patients with lymphoma [4, 5], patients treated with corticosteroids [6, 7] and rituximab [8, 9], as well as in patients undergoing stem cell and bone marrow transplantation [10, 11]. ...
This paper describes the clinical case of an anti-HBc-positive and anti-HBs-positive patient undergoing prolonged immunosuppression who developed HBV reactivation 3 months after the suspension of prolonged (4 years) LMV prophylaxis. At HBV reactivation, the patient showed an atypical serological profile characterized by HBsAg negativity and anti-HBs positivity (with a high antibody titer of 505 mIU/ml). These results corroborate recently published studies showing that a substantial proportion (10% to 80%) of patients who tested positive for anti-HBc and anti-HBs remained HBsAg-negative despite the reuptake of viral replication [12-14]. Overall, our results suggest that this immunological profile is critical in the management of patients who are at risk of HBV reactivation and strongly support the use of serum HBV-DNA (rather than HBsAg) for the diagnosis of HBV reactivation.. HBsAg negativity may be related to the high degree of genetic variability in HBsAg observed in patients who develop ...
Harrison C, Kiladjian JJ, Al-Ali HK et al (2012) JAK inhibition with ruxolitinib versus best available therapy for myelofibrosis. N Engl J Med 366:787-798PubMedCrossRefGoogle Scholar ...
Atıf İçin Kopyala Beysel S., YEGİN Z. A. , Yagci M. TURKISH JOURNAL OF GASTROENTEROLOGY, cilt.21, sa.2, ss.197-198, 2010 (SCI İndekslerine Giren Dergi) ...
Throughout the process of virus-host coevolution, herpesviruses have developed an array of immunomodulatory mechanisms to avoid detection and destruction by the hosts immune system. Although loss of immune control can lead to herpesvirus reactivation from latency and result in serious disease (2, 3, 4), delayed primary infection with herpesviruses in affluent societies (1, 2) coincides with higher incidence of allergic disorders (32), which in contrast indicates a beneficial role for these viruses.. In connection with this, our group has previously reported an inverse association between EBV seropositivity and IgE sensitization in 2-year-old children (25). Recent observations from our laboratory did not provide support for a Th1-biased cytokine profile in EBV SP children (26), which could have explained the protection against the allergic phenotype (32, 33). However, latent herpesvirus infections in mice result in potentiated innate activity and increased systemic IFN-γ levels (29). To ...
Ok I guess the first thoughts are that people are trying to get something for nothing. I would like to suggest a feature: Move. All I would like to do is maintain the functionality of the VM. Just one licensed copy. I re-image my Host hard drive every couple months, install updates, and create an image of that. This way if something goes horribly wrong Malware or other, I can have a working system in a few minutes. Each time I did this with VirtualBox, the Guest activation is lost. If I could Move the Licensed and activated VM back to the newly re-imaged Host, Id stand on my head and eat bug. The move feature would prevent the VM Guest from being used anywhere else. I used RouterSim software to study for my CCNA. I could move the simulator around with me. It was a great time saver ...
Prodromal symptoms include wue paresthesiaitching, and pain where lumbosacral nerves innervate herpes skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome herrpes experienced can reduce the appearance simplex duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop and are less painful and heal faster within 5-10 days without antiviral treatment than those occurring during the primary infection.. The causes of reactivation are uncertain, but several potential triggers have been documented. A study showed the protein VP16 plays a key role in qque of the dormant virus.. Reactivation due to other infections que the likely source of qur historic terms cold sore and fever hedpes. Other identified triggers include local injury to the face, lips, eyes, or mouth; trauma; surgery; radiotherapy ; and exposure to wind, ultraviolet lightor sunlight.. The frequency and severity ...
A drug originally meant to treating cancer seems to have another unexpected but equally amazing potential, that of treating HIV. JQ1, named after chemist and research scientist Jun Qi, is already in early stages of human trials as a cancer drug. The anti-cancer medicine can also treat heart failure and…
I have written about antivirals in the past, and thought that it was time to do an update. EBV, HHV5 and other virus in CFSValganciclovir, HHV-6, EBV and CFSValganciclovir antiviral and CFSValacyclovir, EBV and CFS Valacyclovir which reported some patients with complete resolution of symptoms). Myths of Chronic EBV and Lyme Viral re-activation is common with ME/CFS…
Rapid Reactivation of Extralymphoid CD4 T Cells during Secondary Infection. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Latency-associated transcript (LAT) significantly enhances the spontaneous reactivation phenotype of herpes simplex virus type 1 (HSV-1). The mechanism by which LAT accomplishes this has been elusive. To determine if LATs antiapoptosis activity is involved, the authors used a rabbit eye model to analyze the spontaneous reactivation phenotype of an HSV-1 mutant in which LAT was replaced by an unrelated antiapoptosis gene. This virus, dLAT-cpIAP, contains the open reading frame of the baculovirus inhibitor of apoptosis protein gene (cpIAP) in place of LAT, under control of the LAT promoter. The authors report here that in a rabbit ocular model of infection, dLAT-cpIAP had a spontaneous reactivation phenotype similar to wild-type virus and significantly higher than LAT(-) viruses. This was consistent with their previous findings using the mouse trigeminal ganglia explant-induced reactivation model. Whether LAT (and in the case of dLAT-cpIAP, cpIAP) enhances the spontaneous reactivation phenotype ...
Clinical trial for Chronic | Lymphocytic Leukemia | Chronic Lymphocytic Leukemia , The Incidence of Hepatitis B Reactivations in Patients Affected by Chronic Lymphocytic Leukemia With Ibrutinib
Chronic viral infections are difficult to treat, and new approaches are needed, particularly those aimed at reducing reactivation by enhancing immune responses. Herpes simplex virus (HSV) establishes latency and reactivates frequently, and breakthrough reactivation can occur despite suppressive antiviral therapy. Virus-specific T cells are important to control HSV, and proliferation of activated T cells requires increased metabolism of glutamine. Here, we found that supplementation with oral glutamine reduced virus reactivation in latently HSV-1-infected mice and HSV-2-infected guinea pigs. Transcriptome analysis of trigeminal ganglia from latently HSV-1-infected, glutamine-treated WT mice showed upregulation of several IFN-γ-inducible genes. In contrast to WT mice, supplemental glutamine was ineffective in reducing the rate of HSV-1 reactivation in latently HSV-1-infected IFN-γ-KO mice. Mice treated with glutamine also had higher numbers of HSV-specific IFN-γ-producing CD8 T cells in ...
Murine gammaherpesvirus 68 (γHV68) infection of mice results in the establishment of a chronic infection, which is largely maintained through latent infection of B lymphocytes. Acute virus replication is almost entirely cleared by 2 weeks postinfection. Spontaneous reactivation of γHV68 from latently infected splenocytes upon ex vivo culture can readily be detected at the early stages of infection (e.g., day 16). However, by 6 weeks postinfection, very little spontaneous reactivation is detected upon explant into tissue culture. Here we report that stimulation of latently infected splenic B cells harvested at late times postinfection with cross-linking surface immunoglobulin (Ig), in conjunction with anti-CD40 antibody treatment, triggers virus reactivation. As expected, this treatment resulted in B-cell activation, as assessed by upregulation of CD69 on B cells, and ultimately B-cell proliferation. Since anti-Ig/anti-CD40 stimulation resulted in splenic B-cell proliferation, we assessed ...
Morbidity and mortality of ICU patients is increased by the development of a immunosuppression systemic (IS). This IS develops in the early hours of hospitalization and is responsible for severe infections, including viral reactivations (Cytomegalovirus or Herpes Simplex Virus). Viral reactivation was associated with increased morbidity and mortality in intensive care units. In clinical practice, they are searched at the onset of organ failure or unexplained fever. The investigators wish to conduct this research in the stroke patients to assess the predictive power of these viral reactivations on the duration of mechanical ventilation ...
Herpes simplex viruses cause considerable morbidity and mortality. They undergo a lytic, productive infection at the mucosal sites and spread into sensory gangl...
Discussion. HBV reactivation is a potentially fatal condition with mortality rates reported as high as 25%.4 In our study the rate of HBV reactivation in patients with previously resolved infection was approximately 2%, resulting in death in one patient. This highlights the importance of assessing potential risk factors for reactivation since prophylaxis can prevent its occurrence.. Only 4 retrospective studies addressed the risk of reactivation in HBsAg-negative and anti-HBc-positive KTR.7-9,13 The number of patients was small and reactivation rates varied from 0 to 6.5%. Risk factors for reactivation included older age, presence of rejection, use of rituximab and loss/absence of anti-HBs, but findings were not consistent among the 4 studies possibly due to the small number of cases in each study. We found that 13.9% of the patients with resolved HBV infection and positive anti-HBs titers lost immunity. In our series, older age and presence of BPAR were independent risk factors for loss of ...
Kidney transplant programs now have the ability to perform reactivation of multiple candidates simultaneously whose current candidate status is
J Infect Dis. 2014 Mar 5. [Epub ahead of print] Focal encephalitis following varicella-zoster virus reactivation without rash in a healthy immunized...
The FDAs approval of rituximab-abbs is based on a review of evidence that included extensive structural and functional characterization, animal data, human pharmacokinetic data, clinical immunogenicity data, and other clinical data that demonstrate rituximab-abbs is biosimilar to rituximab. Rituximab-abbs has been approved as a biosimilar, not as an interchangeable product.. The most common side effects of rituximab-abbs are infusion reactions, fever, lymphopenia, chills, infection, and asthenia. Health-care providers are advised to monitor patients for tumor-lysis syndrome, adverse cardiac reactions, renal toxicity, and bowel obstruction and perforation. Patients should not receive vaccinations while in treatment.. Like rituximab, the labeling for rituximab-abbs contains a boxed warning to alert health-care professionals and patients about increased risks of the following: fatal infusion reactions; severe skin and mouth reactions, some with fatal outcomes; hepatitis B virus reactivation, which ...
Human cytomegalovirus (HCMV) latency is typically harmless but reactivation can be largely detrimental to immune compromised hosts. We modeled latency and reactivation using a traceable HCMV laboratory strain expressing the Gaussia luciferase reporter gene (HCMV/GLuc) in order to interrogate the viral modulatory effects on the human adaptive immunity. Humanized mice with long-term (more than 17 weeks) steady human T and B cell immune reconstitutions were infected with HCMV/GLuc and 7 weeks later were further treated with granulocyte-colony stimulating factor (G-CSF) to induce viral reactivations. Whole body bio-luminescence imaging analyses clearly differentiated mice with latent viral infections vs. reactivations. Foci of vigorous viral reactivations were detectable in liver, lymph nodes and salivary glands. The number of viral genome copies in various tissues increased upon reactivations and were detectable in sorted human CD14+, CD169+, and CD34+ cells. Compared with non-infected controls, ...
Human cytomegalovirus (CMV) is a viral pathogen that infects both genders, who remain asymptomatic unless they receive immunosuppressive medications or acquire infections that trigger reactivation of latent pathogen. to six months. Neutralization titers created in immunized mice are equal to titers discovered clinically after organic infections. This viral vaccine, expressing gB produced from CMV stress […]. ...
A team of researchers from the University of California, Davis (UC Davis), recently tested if idiopathic headshaking in horses could be similar to a condition in humans--trigeminal nerve pain caused by the reactivation of a latent virus.
The Therapeutic Goods Administration (TGA) has issued a safety update regarding the potential for hepatitis B virus (HBV) reactivation in patients taking BCR-ABL tyrosine kinase inhibitors (TKI). This safety update follows a review of clinical trial and post-marketing data from the European Medicines Agency (EMA). Reports of HBV reactivation have included cases of acute hepatic failure and fulminant hepatitis leading to liver transplantation or death.. Affected TKIs available in Australia include imatinib, nilotinib, dasatinib, and ponatinib. These agents are indicated for specific blood cancers including chronic myeloid leukaemia (CML) and acute lymphoblastic leukaemia (ALL).. Reactivation of HBV is a well-known complication of immunosuppressive therapy in patients with chronic hepatitis B. While this is now considered a class effect of BCR-ABL TKIs, the mechanism of virus reactivation and frequency of occurrence is not known. Patients who are chronically infected are at a higher risk of ...
Epstein-Barr virus (EBV) associated lymphoproliferative disorder (LPD) after immunosuppressive therapy for aplastic anemia (AA) is extremely rare in a nontransplant setting and has not been well described. This report describes a severe AA patient in whom fatal EBV-LPD developed after being treated with rabbit antithymocyte globulins (ATG) and cyclosporine A (CsA). An 81-year-old man was diagnosed as having severe AA. He was started on CsA followed by administration of ATG for five consecutive days. One month after the start of ATG, persistent fever which was not responsive to antibiotics or antifungal agents developed and atypical lymphocytes emerged in peripheral blood. Repeated blood cultures were negative. An extremely high level of EBV virus in his peripheral blood plasma was detected by means of a quantitative real-time PCR assay. Even after the cessation of CsA, the fever persisted and the peripheral atypical lymphocytes proliferated rapidly. The patient suffered from respiratory failure, liver
Reactivation of hepatitis B in patients who were previously infected with the hepatitis B virus (HBV) and had received concomitant TNF-blocking agents, including very rare cases (, 0.01%) with Etanercept , has been reported. In some instances, hepatitis B reactivation occurring in conjunction with TNF-blocker therapy has been fatal. The majority of these reports have occurred in patients concomitantly receiving other medications that suppress the immune system, which may also contribute to hepatitis B reactivation. Patients at risk for HBV infection should be evaluated for prior evidence of HBV infection before initiating TNF-blocker therapy. Prescribers should exercise caution in prescribing TNF blockers in patients previously infected with HBV. Adequate data are not available on the safety or efficacy of treating patients who are carriers of HBV with anti-viral therapy in conjunction with TNF-blocker therapy to prevent HBV reactivation. Patients previously infected with HBV and require ...
Immunosuppressive chemotherapy can lead to Hepatitis B virus reactivation resulting in Hepatitis. Previous history of HBV infection is a major risk factor. Here we report a 66 yr old male, with Follicular lymphoma stage 4. He was planned for B-R (Bendamustine-Rituximab) regimen. As the creatinine clearance was 31 ml/min, it was decided to initiate chemo with R-CVP(Rituximab-Cyclophosphomide, Vincristine, Prednisolone) regimen and then switch to B-R regimen, once the creatinine clearance improves. Hepatitis B surface antigen was tested and found to be negative. Post cycle 1 his creatinine clearance improved to 42 ml/min and then he was started with B-R regimen. After 16 days of post cycle 3, he developed cough, wheeze, high eosinophils and fever. It was found to be due to rituximab induced interstitial lung disease, hence the drug was stopped and he was started on steroids, levofloxacin, montelukast. He was continued with CVP regimen. After 5 cycles, his transaminases started going up and a repeat test
The European Medicines Agency is to review the safety of direct-acting antivirals used to treat patients with chronic hepatitis C infection.
Chronic hepatitis B (CHB) caused by hepatitis B virus (HBV) infection remains a major global health problem affecting an estimated 350 million people worldwide with more than 786000 individuals dying annually due to complications of CHB, including cirrhosis and liver cancer. CHB is the leading cause of hepatocellular carcinoma (HCC) accounting for at least 50% of newly diagnosed cases. Furthermore, HCC is the third leading cause of cancer-related mortality in the world with a dismal 5 year survival and the fastest growing rate of cancer death in North America.. Liver transplantation (LT) is the most effective treatment in patients with CHB-related liver failure, cirrhosis and HCC. However, HBV reactivation following LT emerges as a major clinical challenge. Prophylaxis with high-dose hepatitis B immunoglobulin (HBIG) and anti-viral drugs have achieved remarkable progress in LT by suppressing viral replication and improving long-term survival.. Before its introduction, reinfection with HBV after ...
BACKGROUND: The diagnosis and management of BK virus (BKV) reactivation following renal transplantation continues to be a significant clinical problem. Following reactivation of latent virus, impaired cellular immunity enables sustained viral replication to occur in urothelial cells, which potentially leads to the development of BKV-associated nephropathy (BKVAN). Current guidelines recommend regular surveillance for BKV reactivation through the detection of infected urothelial cells in urine (decoy cells) or viral nucleic acid in urine or blood. However, these methods have variable sensitivity and cannot routinely distinguish between different viral subtypes. We therefore asked whether mass spectrometry might be able to overcome these limitations and provide an additional non-invasive technique for the surveillance of BKV and identification of recipients at increased risk of BKVAN. RESULTS: Here we describe a mass spectrometry (MS)-based method for the detection of BKV derived proteins directly
Herpes simplex virus type 1 (HSV‐1) is a common human pathogen which attains a life‐long latent state in sensory neurones after initial infection at the periphery. The establishment of latency and the subsequent episodes of reactivation are fundamental to the clinical importance of herpes simplex viruses and undoubtedly contribute substantially to their evolutionary success, as latency allows the virus to evade the immune system. The pattern of viral gene expression during lytic infection, when at least 76 genes are expressed from the 152 kb genome (McGeoch et al., 1993 and references therein), contrasts with that of latency when only one active viral transcription unit of unknown function has been detected (for a review see Fraser et al., 1992). HSV‐1 genes can be divided into Immediate‐Early (IE), Early and Late temporal classes depending on their time‐course of synthesis and requirements for prior viral gene expression and DNA replication (reviewed by Roizman and Sears, 1990). ...
BACKGROUND:. Despite progress in understanding the pathophysiology of human cytomegalovirus (HCMV) infections, its manifestations in the immune compromised host are frequently associated with high morbidity and mortality. In this setting, HCMV disease can develop e.g. following immune suppression as a result of reactivation of latent HCMV acquired earlier in life. The mechanisms leading to establishment of latent infections and their subsequent reactivation are not clear. It is also unknown whether HCMV exists in a latent form with limited viral gene expression or as a persistent infection with normal virus transcription.. DESIGN NARRATIVE:. The specific aims of the study were to: 1) examine the percentage of HCMV positive donors whose bone marrow progenitors contained HCMV DNA using nested PCR and determine if virus could be rescued from those cells. 2) Analyze the HCMV life cycle in hematopoietic progenitor and stem cells. 3) identify and analyze HCMV gene expression in in vivo infected ...
Free resource for searching and exporting immune epitopes. Includes more than 95% of all published infectious disease, allergy, autoimmune, and transplant epitope data.
Some mammalian carcinogens and their metabolites affect the viability of Salmonella typhimurium strains, as indicated by a decrease in colony formation, and also induce prophage. We determined the minimum concentration required for prophage induction and the maximum prophage induction frequency for each carcinogen. The latter value was determined by the ratio of the number of induced phage particles relative to that of spontaneously induced phage particles in the controls. This value is constant for each carcinogen, regardless of its concentration. Since damage of the bacterial genome results in prophage induction, the reactivity of each compound with the genome may be indicated by the minimum concentration required for prophage induction and the maximum frequency of prophage induction. Carcinogens unable to affect bacterial viability are also unable to induce prophage. Failure to induce prophage indicates a requirement for metabolic activation by mammalian enzymes. Interaction of these ...
TY - JOUR. T1 - Prevention of activation of HIV-1 by antiviral agents in OM-10.1 cells. AU - Feorino, P. M.. AU - Butera, S. T.. AU - Folks, T. M.. AU - Schinazi, R. F.. PY - 1993. Y1 - 1993. N2 - The development of a reliable and simple system for evaluating compounds that could prevent activation of latent HIV would allow us to devise new therapeutic approaches. These compounds could eventually be used in combination with drugs that are effective against acute and chronic infections. The OM-10.1 cell line is a chronically infected clone which remains CD4+ until HIV-1 activation with tumour necrosis factor-α. A variety of compounds are known to have antiviral properties against either acutely or chronically infected cells were evaluated for their ability to inhibit HIV induced expression in these cells. We also examined the effect of several compounds that interact with biochemical pathways that may interfere with or enhance the reactivation process. These included nucleoside analogues, ...
Use of TNF blockers, which includes HUMIRA, may well enhance the threat of reactivation of hepatitis B virus (HBV) in individuals who are Serious carriers of the virus. In some circumstances, HBV reactivation developing in conjunction with TNF blocker therapy is lethal. Many these reviews have occurred in clients concomitantly getting other remedies that suppress the immune technique, which can also lead to HBV reactivation. Examine clients at risk for HBV infection for prior evidence of HBV infection right before initiating TNF blocker therapy. Training warning in prescribing TNF blockers for clients determined as carriers of HBV. Satisfactory facts are not readily available on the safety or efficacy of treating sufferers who will be carriers of HBV with anti-viral therapy along with TNF blocker therapy to prevent HBV reactivation ...
Utilization of TNF blockers, such as HUMIRA, might enhance the threat of reactivation of hepatitis B virus (HBV) in patients who will be chronic carriers of this virus. In some instances, HBV reactivation occurring together with TNF blocker therapy is deadly. Many these experiences have transpired in clients concomitantly getting other medicines that suppress the immune system, which can also lead to HBV reactivation. Assess patients in danger for HBV an infection for prior evidence of HBV infection before initiating TNF blocker therapy. Exercise warning in prescribing TNF blockers for people discovered as carriers of HBV. Enough information are usually not obtainable on the safety or efficacy of treating people that are carriers of HBV with anti-viral therapy along with TNF blocker therapy to stop HBV reactivation ...
Use of TNF blockers, which includes HUMIRA, might enhance the danger of reactivation of hepatitis B virus (HBV) in sufferers that are Continual carriers of this virus. In some situations, HBV reactivation transpiring at the side of TNF blocker therapy has long been fatal. The majority of these stories have transpired in sufferers concomitantly getting other remedies that suppress the immune process, which can also add to HBV reactivation. Consider people at risk for HBV infection for prior proof of HBV an infection in advance of initiating TNF blocker therapy. Training caution in prescribing TNF blockers for patients discovered as carriers of HBV. Adequate details will not be accessible on the protection or visit this website efficacy of dealing with patients who will be carriers of HBV with anti-viral therapy together with TNF blocker therapy to avoid HBV reactivation ...
Utilization of TNF blockers, together with HUMIRA, may possibly increase the danger of reactivation of hepatitis B virus (HBV) in people who will be Serious carriers of the virus. In a few cases, HBV reactivation occurring along side TNF blocker therapy has been lethal. The vast majority of these stories have transpired in patients concomitantly acquiring other drugs that suppress the immune technique, which may also lead to HBV reactivation. Evaluate individuals at risk for HBV an infection for prior evidence of HBV infection prior to initiating TNF blocker therapy. Exercising warning in prescribing TNF blockers for sufferers recognized as carriers of HBV. Ample info will not be obtainable on the security or efficacy of treating patients whore carriers of HBV with anti-viral therapy along with TNF blocker therapy to stop HBV reactivation ...
Utilization of TNF blockers, such as HUMIRA, may perhaps boost the risk of reactivation of hepatitis B virus (HBV) in people who are Continual carriers of the virus. In a few scenarios, HBV reactivation happening at the side of TNF blocker therapy continues to be lethal. Nearly all of these experiences have transpired in people concomitantly getting other prescription drugs that suppress the immune method, which may also lead to HBV reactivation. Examine clients in danger for HBV infection for prior evidence of HBV an infection before initiating TNF blocker therapy. Training warning in prescribing TNF blockers for individuals identified as carriers of HBV. Suitable information usually are not obtainable on the security or efficacy of treating sufferers that are carriers of HBV with anti-viral therapy along side TNF blocker therapy to stop HBV reactivation ...
We are aware that relapses in MS are frequently triggered by infections; about a third of relapses are known to be preceded by infections. These are typically viral infections.We have no idea how many relapses are triggered by reactivation of dormant viral infections, such as VZV, CMV and EBV. The latter is one of the hypotheses underpinning the viral hypothesis of autoimmunity, i.e. that viral infections drive autoimmunity by stimulating or boosting the immune system that allows the autoimmune cells to be easily triggered to damage self. How do we test this hypothesis? It may have been tested already, but we dont know it. Does interferon beta and interferon alpha, which are antiviral agents work in MS by suppressing viral infections? Some of the original data on exogenous viral infections (colds, flu, etc.) suggests that interferon-beta does not reduce these types of infections, but we dont have data on the impact of these agents on reactivation of persistent viral infections, in particular ...
Fig. 4. EBV lytic cycle genes activated by Rta alone or together with Z(S186A). Cells were either untreated (lane 1), chemically induced with TPA and sodium butyrate (lane 2), or transfected with 10 μg of plasmid DNA (lanes 3 to 10). In lanes 4, 6, and 8, cells received 5 μg of activator and 5 μg of empty vector. In lanes 3, 5, and 7, cells received only vector pRTS (lane 3), pBXG1 (lane 5), or pCMV (lane 7). In lanes 9 and 10, Rta was transfected with ZEBRA and the mutant Z(S186A), respectively. Total RNA prepared 30 h following transfection was analyzed by Northern blotting using probes for the indicated genes (see Materials and Methods). The blot was stripped between probes. Classification of the genes according to primary activator(s) is indicated to the right (see Discussion). The extra band above the expected size of the BRLF1 mRNA in lane 10 is most likely the result of an Rta-activated transcript from the Z(S186A) expression vector. ...
Cancer-associated fibroblasts (CAF) comprise the majority of stromal cells in breast cancers, yet their precise origins and relative functional contributions to malignant progression remain uncertain. Local invasion leads to the proximity of cancer cells and adipocytes, which respond by phenotypical changes to generate fibroblast-like cells termed as adipocyte-derived fibroblasts (ADF) here. These cells exhibit enhanced secretion of fibronectin and collagen I, increased migratory/invasive abilities, and increased expression of the CAF marker FSP-1 but not α-SMA. Generation of the ADF phenotype depends on reactivation of the Wnt/β-catenin pathway in response to Wnt3a secreted by tumor cells. Tumor cells cocultivated with ADFs in two-dimensional or spheroid culture display increased invasive capabilities. In clinical specimens of breast cancer, we confirmed the presence of this new stromal subpopulation. By defining a new stromal cell population, our results offer new opportunities for ...
Background: Efforts to disrupt the establishment and maintenance of the latent reservoir have focused on the shock-and-kill therapeutic approach to reverse HIV latency from CD4+ T cells with subsequent killing of the infected cells. The X-linked inhibitor of apoptosis protein (XIAP) is up regulated in latently infected cell lines. In this study, we investigated whether this molecular signature existed in primary latently-infected resting central memory CD4+ T cells and whether this could be used to selectively target and kill latent HIV harboring cells.. Methods: CCL19-treated naïve CD4+ T cells isolated from HIV-uninfected donors were infected with HIV then expanded in the presence of IL2 for 12 d. Memory CD4+ T cells were then isolated and cultured in the presence of IL7 for a further 20 d then analyzed by flow cytometry. HIV integration was analyzed by Alu-LTR qPCR. Expression of XIAP was assessed using Western blotting. HIV p24 antigen was quantified by ELISA. Long-lived, resting memory ...
Looking for online definition of cross reactivation in the Medical Dictionary? cross reactivation explanation free. What is cross reactivation? Meaning of cross reactivation medical term. What does cross reactivation mean?
For rheumatoid arthritis (RA) patients, one to three doses of tocilizumab may increase the risk of hepatitis B virus (HBV) reactivation
Tuberculosis (Tb) still is the most prevalent bacterial infectious disease in humans and continues to be a major cause of morbidity and mortality in impoverished regions in the tropics. The causative agent, Mycobacterium tuberculosis is carried by an estimated 2-3 billion people globally, but in most cases it lies dormant and the immune system is able to prevent it from spreading in the body. A relatively small proportion (5-10%) of infected people will develop active disease during their lifetime. However the immune system fails to achieve sterile eradication of the tubercle bacillus. The enormous reservoir of latent Tb patients constantly leads to new active Tb cases and transmission of the disease, thus perpetuating the epidemic. Reactivation can occur after years or decades of clinical latency, and the risk of reactivation increases with conditions that modulate the immune status of the host such as immunosuppressive therapy, malnutrition or comorbidities. The Research group Coinfection is ...
In article ,30DE9342E2D at, DANDERSON at PRL.PULMONARY.UBC.CA writes: , ,An immunization attempt would be interesting but I have ,a mechanistic question. Do these patients with zoster have a ,depressed cellular response in the face of a sufficient humoral ,response. Is the mechanism of this selective immunosuppression ,known?? As far as I know, the situation in zoster is not well understood (as is the case with most viral pathogenesis questions, of course). The related virus, herpes simplex virus, has been studied in more detail (and I know more about it, note the cunning switch of fields). With HSV reactivation, the virus seems to reactivate in spite of a perfectly competent humoral immune response. There is often a *moderate* suppression of the cellular immune response, concurrent with the reactivation. The most probable explanation is that HSV takes advantage of this suppression to show overt symptoms, but it is almost equally possible that some of this immune suppression ...
In an active area of research known as HIV-1 cure research, the purposeful reactivation of latent/dormant HIV-1 in memory T cells, which induces death of the infected cell or alerts the immune system to the presence of the virus, is known as the
I write about whats new in virology from the molecular biology point of view, covering topics such as human papiloma virus, hepatitis C, herpes simplex, and other viruses, especially those occurring in the body in a latent state. Read more ...
This MATLAB function returns filtered state probabilities FS from conducting optimal conditional inference of the probabilities of the operative latent states in the regime-switching data Y.
"Human Immunodeficiency Virus Type 1 Vpr Induces Apoptosis through Caspase Activation." Journal of Virology, April 2000, pp. ... These include enveloped viruses such as HIV, HSV, SARS or smallpox. Prior to budding, the virus may put its own receptor onto ... Although this process is primarily used by non-enveloped viruses, enveloped viruses may also use this. HIV is an example of an ... This is used primarily by non-enveloped viruses, although enveloped viruses display this too. An example is the use of ...
Le Page C, Génin P, Baines MG, Hiscott J (2000). "Interferon activation and innate immunity". Rev Immunogenet. 2 (3): 374-86. ... I: dsDNA viruses. II: ssDNA viruses. III: dsRNA viruses. IV: (+)ssRNA viruses. V: (−)ssRNA viruses. VI: ssRNA-RT viruses. VII: ... A virus has either RNA or DNA genes and is called an RNA virus or a DNA virus respectively. The vast majority of viruses have ... All viruses reproduce this way, and there are no free-living viruses.[1][2] Viruses are everywhere in the environment, and all ...
... these lead to enhanced replication and virus production. Often, lytic activation leads to cell death. Clinically, lytic ... "Virus Taxonomy: 2019 Release". International Committee on Taxonomy of Viruses. Retrieved 9 May 2020. John ... Although the branching order of the herpes viruses has not yet been resolved, because herpes viruses and their hosts tend to ... Chromatin dynamics regulate the transcription competency of entire herpes virus genomes. When the virus enters a cell, the ...
"Transcriptional Activation of the Integrated Chromatin-Associated Human Immunodeficiency Virus Type 1 Promoter". Mol. Cell. ...
... has been shown to inhibit hepatitis C virus (HCV) infection in vitro.[25] It has weak in vitro activity against human ... Additionally, honokiol regulates the nuclear factor kappa B (NF-κB) activation pathway, an upstream effector of vascular ... Calcium overloading can also cause damage by over-activation of calcium-stimulated enzymes. Honokiol can reduce calcium influx ... Honokiol also blocks inflammatory factor production in glial cells through the inhibition on NF-κB activation.[21][22] This ...
Lin WJ, Li J, Lee YF, Yeh SD, Altuwaijri S, Ou JH, Chang C (Mar 2003). "Suppression of hepatitis B virus core promoter by the ... "TAK1 is critical for IkappaB kinase-mediated activation of the NF-kappaB pathway". Journal of Molecular Biology. 326 (1): 105- ... Lin WJ, Li J, Lee YF, Yeh SD, Altuwaijri S, Ou JH, Chang C (Mar 2003). "Suppression of hepatitis B virus core promoter by the ... "Raf kinase inhibitor protein interacts with NF-kappaB-inducing kinase and TAK1 and inhibits NF-kappaB activation". Molecular ...
"Genome activation by raspberry bushy dwarf virus coat protein". Journal of General Virology. 90 (Pt 3): 747-53. doi:10.1099/vir ... Positive stranded RNA virus transcription is the method of transcription. The virus exits the host cell by tubule-guided viral ... Viruses are enriched by antibodies in the PCR microwells, followed by lysis of the virus particles, then reverse transcription ... Idaeovirus is a genus of positive-sense ssRNA viruses that contains one species: Raspberry bushy dwarf virus (RBDV). Although ...
"Env length and N-linked glycosylation following transmission of human immunodeficiency virus Type 1 subtype B viruses". ... "Tubular cell HIV-1 gp120 expression induces caspase 8 activation and apoptosis". Ren Fail. 31 (4): 303-12. doi:10.1080/ ... gp120 can also easily be shed from the surface of the virus and captured by T cells due to its loose binding with gp41. A ... Gp120 is essential for virus entry into cells as it plays a vital role in attachment to specific cell surface receptors. These ...
This kinase is important for T-cell activation. It is required for the activation of the transcription factors NF-kappaB and AP ... Gupta S, Aggarwal S, Kim C, Gollapudi S (1994). "Human immunodeficiency virus-1 recombinant gp120 induces changes in protein ... platelet activation. • Fc-epsilon receptor signaling pathway. • protein phosphorylation. • negative regulation of T cell ... positive regulation of T-helper 2 cell activation. • positive regulation of interleukin-4 production. • positive regulation of ...
Activation of RAF kinases requires interaction with RAS-GTPases. The three RAF kinase family members are: A-RAF B-RAF c-Raf ... The mouse sarcoma virus 3611 contains a RAF kinase-related oncogene that enhances fibrosarcoma induction. RAF is an acronym for ... Chadee DN, Yuasa T, Kyriakis JM (2002). "Direct activation of mitogen-activated protein kinase kinase kinase MEKK1 by the ...
Transcriptional activation of the integrated chromatin-associated human immunodeficiency virus type 1 promoter. . In: Mol. Cell ...
Additionally, NF-κB activation was suppressed in HeLa cells after incubation with NBD wild type peptides. Moreover, to better ... Human T-cell leukemia virus type I Tax interacts directly with IkappaB kinase gamma". The Journal of Biological Chemistry. 274 ... A drug called NEMO Binding Domain (NBD) has been designed to inhibit activation of NF-κB. NBD is a peptide that acts by binding ... Deng L, Wang C, Spencer E, Yang L, Braun A, You J, Slaughter C, Pickart C, Chen ZJ (October 2000). "Activation of the IkappaB ...
"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 ...
Cullen, Bryan R. (1986) Trans-activation of Human Immunodeficiency Virus Occurs Via a Bimodal Mechanism. Cell 46, 973-982. ... Cullen, Bryan R. (1986-09-26). "Trans-activation of human immunodeficiency virus occurs via a bimodal mechanism". Cell. 46 (7 ... Weinberg, J. B.; Matthews, T. J.; Cullen, B. R.; Malim, M. H. (1991-12-01). "Productive human immunodeficiency virus type 1 ( ... "Epitranscriptomic enhancement of influenza A virus gene expression and replication". doi:10.1016/j.chom.2017.08.004. Cite ...
Hurley EA, Thorley-Lawson DA (December 1988). "B cell activation and the establishment of Epstein-Barr virus latency". The ... van der Stappen JW, Williams AC, Maciewicz RA, Paraskeva C (August 1996). "Activation of cathepsin B, secreted by a colorectal ...
Watford WT, Wright JR, Hester CG, Jiang H, Frank MM (2001). "Surfactant Protein A Regulates Complement Activation". J Immunol ... Hartshorn KL, Sastry K, White MR, (1993). "Human Mannose-binding Protein Functions as an Opsonin for Influenza A Viruses". J. ... LeVine AM, Gwozdz J, Stark J (1998). "Surfactant protein-A enhances respiratory syncytial virus clearance in vivo". J Clin ... Již dříve bylo prokázáno, že SP-D umožňuje eliminovat anti-influenza A virus (velmi podobný mechanismus jako při eliminaci ...
... which are essential for the activation of apoptosis. Examples of viral Bcl-2 proteins include the Epstein-Barr virus BHRF1 ... "Apoptosis induced by Oropouche virus infection in HeLa cells is dependent on virus protein expression". Virus Research. 149 (1 ... Many viruses encode proteins that can inhibit apoptosis.[103] Several viruses encode viral homologs of Bcl-2. These homologs ... Whilst a number of viruses can block the effects of TNF and Fas. For example, the M-T2 protein of myxoma viruses can bind TNF ...
... which are essential for the activation of apoptosis. Examples of viral Bcl-2 proteins include the Epstein-Barr virus BHRF1 ... April 2010). "Apoptosis induced by Oropouche virus infection in HeLa cells is dependent on virus protein expression". Virus Res ... FLIP inhibits the activation of caspase-8.[33] Binding of this receptor can also indirectly lead to the activation of ... Many viruses encode proteins that can inhibit apoptosis.[94] Several viruses encode viral homologs of Bcl-2. These homologs can ...
Clausamines D-G inhibit early antigen activation of the Epstein-Barr virus. Leaf extracts have a mild effect on HIV-1 and HIV-2 ...
"Activation of MDA5 requires higher-order RNA structures generated during virus infection". Journal of Virology. 83 (20): 10761- ... "Activation of MDA5 Requires Higher-Order RNA Structures Genereated during Virus Infection". Journal of Virology. 83 (20): 10761 ... This can lead to activation of MDA5, an RNA helicase involved in the production of interferons. RNase L is present in very ... 2-5 A molecules then bind to RNase L, promoting its activation by dimerization. In its activated form RNase L cleaves all RNA ...
"The Ebola virus VP35 protein inhibits activation of interferon regulatory factor 3". J Virol. 77 (14): 7945-7956. doi:10.1128/ ... and most viruses have proteins to inhibit this activation. Coronaviruses' proteins 3b also inhibit this process. IRF3b is ... SARS-CoV-2 has appeared recently, so much is unknown about this virus and the ORF3b protein to us yet. Even so, now we know ... Studies showed that the presence of ORF3b results in an activation of both ERK and JNK signaling, followed by a boost of AP-1 ...
"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 ( ...
"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 ...
Originally, HERV-K was observed by low-stringency hybridization with probes for the mammary tumor virus of the mouse and A ... Also the association of HERV-K activation with carcinogenesis is especially interesting. Human endogenous retrovirus K ... HERV-K is called, phylogenetically, a supergroup of viruses. It is the only group that reported to contain human-specific ... Human endogenous retrovirus K (HERV-K) or Human teratocarcinoma-derived virus (HDTV) is a family of human endogenous ...
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 ...
In: W. Hardy, Jr., M. Essex, and A.J. McClelland, eds., Feline Leukemia Virus, Elsevier North-Holland Inc., NY, pps. 335-344 ( ... New Scientist 1703:51-54 (1990). Rosenberg, Z.F. and Fauci A.S. Activation of latent HIV infection. J. NIH Res. 2:41-45 (1990 ... In: W. Hardy, Jr., M. Essex, and A.J. McClelland, eds., Feline Leukemia Virus, Elsevier North-Holland Inc., NY, pps. 355-359 ( ... In: W. Hardy, Jr., M. Essex, and A.J. McClelland, eds., Feline Leukemia Virus, Elsevier North-Holland Inc., NY, pps 345-352 ( ...
... has been shown to play a role in the transcriptional activation of virus-inducible cellular genes, including the type I ... Activation by interferon snd silencing by hypermethylation". The Journal of Biological Chemistry. 275 (41): 31805-12. doi: ... response to virus. • negative regulation of transcription from RNA polymerase II promoter. • transcription from RNA polymerase ... Smith EJ, Marié I, Prakash A, García-Sastre A, Levy DE (March 2001). "IRF3 and IRF7 phosphorylation in virus-infected cells ...
In parallel, when toll-like receptors in the endocytic compartments recognize a virus the activation of the adaptor protein ... Some viruses evade this by producing molecules which interfere with IFN production. For example, the Influenza A virus produces ... Influenza A also blocks protein kinase R activation and establishment of the antiviral state.[26] The dengue virus also ... Viruses[edit]. Type I interferons (IFN), secreted mainly by dendritic cells,[22] play a central role in antiviral host defense ...
It activates on the third day of each month; the first known activation happened on February 3, 2006. On activation, the virus ... The virus visits a tracking Web page each time it infects a computer. Over 300,000 unique IPs visited that site, suggesting ... The virus removes antivirus programs from remote computers before attempting to infect them. When first installed, it copies ... It is not known how many of them remained infected long enough to trigger the virus's payload. Description of Blackworm from ...
... these virus infections trigger the expansion of adaptive NKG2C+ NK cells or whether other infections result in re-activation of ... Cytokine-induced NK and Cytotoxic T lymphocyte (CTL) activation[edit]. Cytokines play a crucial role in NK cell activation. As ... Cytokines involved in NK activation include IL-12, IL-15, IL-18, IL-2, and CCL5. NK cells are activated in response to ... The activation of NK cells and subsequent production of cytolytic effector cells impacts macrophages, dendritic cells, and ...
Hepatitis B Virus-Specific CD8+ T Cells Maintain Functional Exhaustion after Antigen Reexposure in an Acute Activation Immune ... Role of regulatory T cells during virus infection. Immunological Reviews. September 2013, 255 (1): 182-96. PMC 3748387. PMID ... Howson LJ, Salio M, Cerundolo V. MR1-Restricted Mucosal-Associated Invariant T Cells and Their Activation during Infectious ... Cell-intrinsic transforming growth factor-beta signaling mediates virus-specific CD8+ T cell deletion and viral persistence in ...
This enables the virus to evade the immune system by inhibiting early steps of neutrophil activation.[medical citation needed] ... The four are Bundibugyo virus (BDBV), Sudan virus (SUDV), Taï Forest virus (TAFV) and one simply called Ebola virus (EBOV, ... The virus responsible for the initial outbreak, first thought to be Marburg virus, was later identified as a new type of virus ... Main articles: Ebola virus cases in the United States, Ebola virus disease in Spain, and Ebola virus disease in the United ...
PML is caused by activation of JC virus, a common virus in the brain which is usually latent. Reactivation of the JC virus ... "Chronic Hepatitis After Hepatitis E Virus Infection in a Patient With Non-Hodgkin Lymphoma Taking Rituximab" (PDF). Retrieved ... myasthenia gravis and Epstein-Barr virus-positive mucocutaneous ulcers.[2][3][4][5] It is given by slow injection into a vein.[ ... suggesting the drug in combination with lymphoma may have weakened the body's immune response to the virus.[34] ...
"Neural mechanisms of respiratory syncytial virus-induced inflammation and prevention of respiratory syncytial virus sequelae". ... Their activation stimulates the vomiting reflex. Different emetic pathways exist, and substance P/NK1R appears to be within the ... Respiratory syncytial and related viruses appear to upregulate SP receptors, and rat studies suggest that NK1RAs may be useful ... and infections such as HIV/AIDS and respiratory syncytial virus,[54] as well as in cancer.[55][56] When assayed in the human, ...
PML is caused by activation of JC virus, a common virus in the brain which is usually latent. Reactivation of the JC virus ... myasthenia gravis and Epstein-Barr virus-positive mucocutaneous ulcers.[2][3][4][5] It is given by slow injection into a vein.[ ... suggesting the drug in combination with lymphoma may have weakened the body's immune response to the virus.[35] ... maintaining intracellular Ca2+ concentration and allowing activation of B cells. ...
... is a short term incentive to initiate trial or purchase. Sales promotion is one of the elements of the promotional mix. The primary elements in the promotional mix are advertising, personal selling, direct marketing and publicity/public relations. Sales promotion uses both media and non-media marketing communications for a pre-determined, limited time to increase consumer demand, stimulate market demand or improve product availability. Examples include contests, coupons, freebies, loss leaders, point of purchase displays, premiums, prizes, product samples, and rebates. Sales promotions can be directed at either the customer, sales staff, or distribution channel members (such as retailers). Sales promotions targeted at the consumer are called consumer sales promotions. Sales promotions targeted at retailers and wholesale are called trade sales promotions. Sales promotion includes several communications activities that attempt to provide added value or incentives to consumers, ...
The study used a common cold virus to deliver a normal version of the gene called RPE65 directly into the eyes of affected ... Arnott, S., Thaler, L., Milne, J., Kish, D., & Goodale, M. (n.d). Shape-specific activation of occipital cortex in an early ...
MicroRNAs also play a role in replicating viruses such as HIV-1.[44] Novel HIV-1-encoded microRNA have been found to enhance ... by the canonical TBP/TFIID-dependent basal transcription machinery has recently been documented in vivo showing the activation ... The TATA-binding protein (TBP) could also be targeted by viruses as a means of viral transcription.[6] ... the production of the virus as well as activating HIV-1 latency by targeting the TATA box region. ...
Simone C, Giordano A (2007). "Abrogation of signal-dependent activation of the cdk9/cyclin T2a complex in human RD ... and act as a negative regulator of human immunodeficiency virus type 1 (HIV-1) Tat protein. Two alternatively spliced ... "Role of the human and murine cyclin T proteins in regulating HIV-1 tat-activation". J. Mol. Biol. 288 (1): 57-69. doi:10.1006/ ... "Interactions between Tat and TAR and human immunodeficiency virus replication are facilitated by human cyclin T1 but not ...
Alternatively, the activation of host defense mechanisms may involve sequestration of virus components in aggregates to prevent ... Viroplasms have been found in the cauliflower mosaic virus, rotavirus, vaccinia virus and the rice dwarf virus. These appear ... The number and the size of viroplasms depend on the virus, the virus isolate, hosts species, and the stage of the infection. ... The viroplasm could also prevent virus degradation by proteases and nucleases. In the case of the Cauliflower mosaic virus ( ...
... activation with cellular viremia and plasma HIV RNA levels in asymptomatic patients infected by human immunodeficiency virus ... His interest in immunology has led to publications in HIV disease, cellular activation and natural killer cell function, tumor ... platelet activation in vascular disease and stem cell transplantation in cancer patients. As an endocrinologist he has an ...
Binding and activationEdit. Ligand binding is an equilibrium process. Ligands bind to receptors and dissociate from them ... or parts of the outside of a virus or microbe. The endogenously designated -molecule for a particular receptor is referred to ... In contrast to the accepted Occupation Theory, Rate Theory proposes that the activation of receptors is directly proportional ... activation of these receptors results in changes in ion movement across a membrane. They have a heteromeric structure in that ...
CD8+ cytotoxic T cells: virus-infected and tumor cells.. *γδ T cells: bridge between innate and adaptive immune responses; ... B cells: releases antibodies and assists activation of T cells. *T cells: *CD4+ Th (T helper) cells: activate and regulate T ... Natural killer cells: virus-infected and tumor cells.. Deeply staining, eccentric. NK-cells and cytotoxic (CD8+) T-cells. Years ... These cells bind antigens presented on MHC I complex of virus-infected or tumour cells and kill them. Nearly all nucleated ...
Virus-specific T-Lymphocytes (VST) therapy is used for patients who have received hematopoietic stem cell transplantation that ... as well as activation markers (HLA-DR, CD25, CD80 (B cells). Tests for T cell function: skin tests for delayed-type ... These new methods have reduced culture time to 10-12 days by using specific cytokines from adult donors or virus-naive cord ... "Adoptive immunotherapy for primary immunodeficiency disorders with virus-specific T lymphocytes". Journal of Allergy and ...
Activation and toxin release by eosinophils is therefore tightly regulated to prevent any inappropriate tissue destruction.[5] ... Instead, NK cells destroy compromised host cells, such as tumor cells or virus-infected cells. It recognises such cells by a ... enveloped viruses, fungi and even transformed or cancerous cells.[10] ... because they do not require activation in order to kill cells that are "missing self". ...
Eissmann P، Watzl C (2006). "Molecular analysis of NTB-A signaling: a role for EAT-2 in NTB-A-mediated activation of human NK ... a novel SH2D1A-associated surface molecule contributing to the inability of natural killer cells to kill Epstein-Barr virus- ... 2006). "NTB-A receptor crystal structure: insights into homophilic interactions in the signaling lymphocytic activation ... "Human T-cell leukemia virus type 1 (HTLV-1) p12I down-modulates ICAM-1 and -2 and reduces adherence of natural killer cells, ...
Interaction of CLEC5A and dengue virus also induces osteolytic activity.[8] Another pathogen is influenza virus and its ... Activation of MDL-1 induces production of many cytokines (TNF-α, IL-1, IL-6, IL-8 and IL-17A) and chemokines (MIP-1α, RANTES, ... virus receptor activity. • GO:0001948 protein binding. Cellular component. • integral component of membrane. • integral ... May 2008). "CLEC5A is critical for dengue-virus-induced lethal disease". Nature. 453 (7195): 672-6. Bibcode:2008Natur.453..672C ...
... certain Epstein-Barr virus gene products bearing this sequence can stall the proteasome, helping the virus propagate by ... The proteasomal activation of NF-κB by processing p105 into p50 via internal proteolysis is one major example.[69] Some ... This activity is usually attributed to the role of proteasomes in the activation of NF-κB which further regulates the ... Zhang M, Coffino P (March 2004). "Repeat sequence of Epstein-Barr virus-encoded nuclear antigen 1 protein interrupts proteasome ...
However, studies are suggesting that the so-called toxic effects are actually the result of chronic activation of the immune ... and synergistically with Hepatitis B virus) induce liver cancer.[49] Mycotoxin-contaminated grain and other food products have ...
1986). "Transactivation of the human immunodeficiency virus long terminal repeat sequences by DNA viruses". Proc. Natl. Acad. ... Appay V, Sauce D (January 2008). "Immune activation and inflammation in HIV-1 infection: causes and consequences". J. Pathol. ... Pollok RC (2001). "Viruses causing diarrhoea in AIDS". Novartis Found. Symp. 238: 276-83; discussion 283-8. doi:10.1002/ ... Laurence J (2006). "Hepatitis A and B virus immunization in HIV-infected persons". AIDS Reader 16 (1): 15-17. பப்மெட் 16433468. ...
Vesicular stomatitis virus is believed to be taken up by the autophagosome from the cytosol and translocated to the endosomes ... Prolonged autophagy activation leads to a high turnover rate of proteins and organelles. A high rate above the survival ... A subset of viruses and bacteria subvert the autophagic pathway to promote their own replication.[63] Galectin-8 has recently ... The study in mice fed with olive oil resulted in an increase in nerve cell autophagy activation compared to controls that had ...
Superantigen - A class of antigens that cause non-specific activation of T-cells, resulting in polyclonal T-cell activation and ... For virus-associated tumors, such as cervical cancer and a subset of head and neck cancers, epitopes derived from viral open ... Furthermore, for a peptide to induce an immune response (activation of T-cells by antigen-presenting cells) it must be a large ... This includes parts (coats, capsules, cell walls, flagella, fimbriae, and toxins) of bacteria, viruses, and other ...
Though PDGF is synthesized,[3] stored (in the alpha granules of platelets),[4] and released by platelets upon activation, it is ... "Serum factor requirements of normal and simian virus 40-transformed 3T3 mouse fibroplasts". Proc Natl Acad Sci U S A. 68 (3): ... PDGF-BB is the highest-affinity ligand for the PDGFR-beta; PDGFR-beta is a key marker of hepatic stellate cell activation in ... ROS)-mediated activation of the STAT3 pathway.[11] Downstream effects of this include regulation of gene expression and the ...
O grupo de Montagnier denominou o seu novo virus illado virus asociado á linfadenopatía (LAV).[181] Como estes dous virus se ... Appay V, Sauce D (2008). "Immune activation and inflammation in HIV-1 infection: causes and consequences". J. Pathol. 214 (2): ... Despois de que o virus entra no corpo hai un período de rápida replicación viral, que fai que o virus sexa abondoso no sangue ... O grupo de Gallo chamou o seu novo virus illado HTLV-III. Ao mesmo tempo, o grupo de Montagnier illou un virus dun paciente que ...
Activation of the MAPK pathways: Of the three major MAPK cascades, TNF induces a strong activation of the stress-related JNK ... response to virus. • positive regulation of osteoclast differentiation. • negative regulation of cytokine secretion involved in ... Activation of NF-κB: TRADD recruits TRAF2 and RIP. TRAF2 in turn recruits the multicomponent protein kinase IKK, enabling the ... activation of MAPK activity. • immune response. • leukocyte tethering or rolling. • positive regulation of chemokine production ...
Mast Cell Activation Syndrome»։ Clinical Reviews in Allergy & Immunology 54 (3): 353-365։ June 2018։ PMID 25944644։ doi:10.1007 ... "Exposure to foodborne and orofecal microbes versus airborne viruses in relation to atopy and allergic asthma: epidemiological ... Basophil activation test compared to skin prick test and fluorescence enzyme immunoassay for aeroallergen-specific ...
Vesicular stomatitis virus is believed to be taken up by the autophagosome from the cytosol and translocated to the endosomes ... Prolonged autophagy activation leads to a high turnover rate of proteins and organelles. A high rate above the survival ... A subset of viruses and bacteria subvert the autophagic pathway to promote their own replication.[72] Galectin-8 has recently ... Following activation of the toll-like receptor, intracellular signaling cascades are initiated, leading to induction of ...
Esté JA (2004). „Virus entry as a target for anti-HIV intervention". Curr. Med. Chem. 10 (17): 1617-32. PMID 12871111. doi: ... 2004). „Macrophage activation through CCR5- and CXCR4-mediated gp120-elicited signaling pathways". J. Leukoc. Biol. 74 (5): 676 ... 2002). „HIV-1 infection in individuals with the CCR5-Delta32/Delta32 genotype: acquisition of syncytium-inducing virus at ... 2004). „Chemokine receptor utilization and macrophage signaling by human immunodeficiency virus type 1 gp120: Implications for ...
... but have since been found in many other cells including epithelial cells and macrophages after activation by bacteria, viruses ... and viruses.[18][19] Cathelicidin rapidly destroys the lipoprotein membranes of microbes enveloped in phagosomes after fusion ...
We noted robust T- and B-cell activation during Ebola virus infection in these four patients. Ebola virus has been believed to ... Immune activation in human Ebola virus infection. Anita K. McElroy, Rama S. Akondy, Carl W. Davis, Ali H. Ellebedy, Aneesh K. ... Immune activation in human Ebola virus infection. Anita K. McElroy, Rama S. Akondy, Carl W. Davis, Ali H. Ellebedy, Aneesh K. ... Human Ebola virus infection results in substantial immune activation. Anita K. McElroy, Rama S. Akondy, Carl W. Davis, Ali H. ...
activation by virus of host NF-kappaB transcription factor activity [ GO:0039652 ]. ... Several viruses have developed strategies to activate the NF-kappa-B pathway in order to promote viral replication and prevent ... Viral protein involved in the activation of host NF-kappa-B. This protein is a pleiotropic transcription factor which is ...
Activation of anti-hepatitis C virus responses via Toll-like receptor 7. Jongdae Lee, Christina C. N. Wu, Ki Jeong Lee, Tsung- ... Activation of anti-hepatitis C virus responses via Toll-like receptor 7 ... Activation of anti-hepatitis C virus responses via Toll-like receptor 7 ... Activation of anti-hepatitis C virus responses via Toll-like receptor 7 ...
... Mariana Gandini,1,2 Fabienne Petitinga-Paiva ... R. Hamel, O. Dejarnac, S. Wichit et al., "Biology of Zika virus infection in human skin cells," Journal of Virology, vol. 89, ... Y. T. Tsai, S. Y. Chang, C. N. Lee, and C. L. Kao, "Human TLR3 recognizes dengue virus and modulates viral replication in vitro ... R. S. Lanciotti, C. H. Calisher, D. J. Gubler, G. J. Chang, and A. V. Vorndam, "Rapid detection and typing of dengue viruses ...
... of influenza viruses is activated by proteolytic cleavage. Cleavage which is necessary for the fusion activity of the ... Influenza Virus Cleavage Site MDCK Cell Avian Influenza Virus H5N2 Influenza Virus These keywords were added by machine and not ... Proteolytic activation is therefore indispensable for effective virus spread in the infected host and has been found to be a ... H.-D. Klenk and R. Rott, The molecular biology of influenza virus pathogenicity, Adv. Virus Res. 34:247 (1988).PubMedCrossRef ...
Virus Res. 2000 Sep 25;69(2):83-93.. The cleavage activation and sites of glycosylation in the fusion protein of Hendra virus. ... Hendra virus (HeV) is an unclassified member of the Paramyxoviridae family that causes systemic infections in humans, horses, ...
Viruses have evolved various strategies to evade the recognition and destruction by NK cells through the downregulation of the ... Ma, Y.; Li, X.; Kuang, E. Viral Evasion of Natural Killer Cell Activation. Viruses 2016, 8, 95. ... Ma Y, Li X, Kuang E. Viral Evasion of Natural Killer Cell Activation. Viruses. 2016; 8(4):95. ... "Viral Evasion of Natural Killer Cell Activation." Viruses 8, no. 4: 95. ...
Influenza A virus nucleoprotein exploits Hsp40 to inhibit PKR activation.. [Kulbhushan Sharma, Shashank Tripathi, Priya Ranjan ... However the influenza virus component responsible for PKR inhibition through P58(IPK) activation was hitherto unknown. Human ... In case of influenza A virus (IAV) infection, P58(IPK) is known to dissociate from Hsp40 and inhibit PKR activation. ... Furthermore, inhibition of NP expression during influenza virus replication led to PKR activation and concomitant increase in ...
Several factors, both intrinsic to the virus and external, have been proposed to influence the activation of HIV in the lung. ... Full Text HL-96-008 REGULATION OF HUMAN IMMUNODEFICIENCY VIRUS (HIV) ACTIVATION IN THE LUNG NIH GUIDE, Volume 25, Number 4, ... This Request for Applications (RFA), Regulation of Human Immunodeficiency Virus (HIV) Activation in the Lung, is related to the ... o examine genetic factors within the host lung cells that control activation of virus; o elucidate specific pathways whereby co ...
Activation of interferon regulatory factor 3 is inhibited by the influenza A virus NS1 protein.. Talon J1, Horvath CM, Polley R ... influenza virus-infected cells but not in cells infected with an isogenic virus lacking the NS1 gene (delNS1 virus). ... not only in delNS1 virus-infected cells but also in cells infected with a heterologous RNA virus (Newcastle disease virus). We ... Activation of Interferon Regulatory Factor 3 Is Inhibited by the Influenza A Virus NS1 Protein ...
These findings suggest that IPNV uses PKR activation to promote virus replication in infected cells. ... We investigated the involvement of PKR during infectious pancreatic necrosis virus (IPNV) infection using a custom-made rabbit ... PKR inhibitor pre-treatment resulted in decreased virus titers, extra- and intracellularly, concomitant with reduction of cells ... PKR Activation Favors Infectious Pancreatic Necrosis Virus Replication in Infected Cells. Viruses 2016, 8, 173. ...
... enveloped virus and subviral particles. This is the first report showing that HBV activates the ERAD pathway, which, in turn, ... it remained obscure whether or not this activation had any functional consequences on the target genes of the UPR pathway. Of ... reduces the amount of envelope proteins, possibly as a mechanism to control the level of virus particles in infected cells and ... belongs to the Hepadnaviridae family of enveloped DNA viruses. It was previously shown that HBV can induce endoplasmic ...
Here we report the crystal structures of a dengue NS2B-NS3pro complex and a West Nile virus NS2B-NS3pro complex with a ... These structures identify key residues for NS3pro substrate recognition and clarify the mechanism of NS3pro activation. ... Essential for the activation of NS3pro is a 47-residue region of NS2B. ... Structural basis for the activation of flaviviral NS3 proteases from dengue and West Nile virus. *Paul Erbel1. na1, ...
... and virus treated at 100°C (Figure 3). We found that virus treated at 56°C behaved similarly to active virus in that both virus ... Toll-like receptor-mediated activation of neutrophils by influenza A virus. Jennifer P. Wang, Glennice N. Bowen, Carolyn Padden ... Toll-like receptor-mediated activation of neutrophils by influenza A virus. Jennifer P. Wang, Glennice N. Bowen, Carolyn Padden ... Toll-like receptor-mediated activation of neutrophils by influenza A virus. Jennifer P. Wang, Glennice N. Bowen, Carolyn Padden ...
Herpes simplex virus 1 (HSV-1) induces major reprogramming of the host cell environment. Here, the authors profile the ... Consequently, Bardoxolone methyl and Sulforaphane, two known NRF2 agonists, impair virus production, suggesting that NRF2 ... activation restricts viral infection. Our study provides insights into early stages of HSV-1 infection and serves as a general ... of individual HSV-1-infected human fibroblasts and provide evidence of an antiviral program mediated by the activation of the ...
Natural Killer T Cell Activation Inhibits Hepatitis B Virus Replication in Vivo. Kazuhiro Kakimi, Luca G. Guidotti, Yasuhiko ... 2000) Relative sensitivity of hepatitis B virus and other hepatotropic viruses to the antiviral effects of cytokines. J. Virol. ... Natural Killer T Cell Activation Inhibits Hepatitis B Virus Replication in Vivo ... Indirect mechanisms could include activation of NKT cells by virus-induced cytokines (6)(22). Additional studies will be needed ...
The host tolerance mechanisms to avian influenza virus (H5N1) infection that limit tissue injury remain unknown. Emerging ... H5N1 Virus Hemagglutinin Inhibition of cAMP-Dependent CFTR via TLR4-Mediated Janus Tyrosine Kinase 3 Activation Exacerbates ... JAK3 activation, which is after activation of TLR4 by H5N1 HA, results in impaired cAMP-dependent CFTR regulation and CFTR gene ... Ramos I, Fernandez-Sesma A. (2012) Innate immunity to H5N1 influenza viruses in humans. Viruses. 4:3363-88.CrossRefGoogle ...
Hepatic enrichment and activation of myeloid dendritic cells during chronic hepatitis C virus infection†‡. ... Hepatitis C virus infection involves CD34(+) hematopoietic progenitor cells in hepatitis C virus chronic carriers. Blood 1998; ... Hepatic enrichment and activation of myeloid dendritic cells during chronic hepatitis C virus infection. Hepatology, 56: 2071- ... Hepatitis C virus versus innate and adaptive immune responses: a tale of coevolution and coexistence. J Clin Invest 2009; 119: ...
Mechanism of activation of the BNLF2a immune evasion gene of Epstein-Barr virus by Zta. Download Prime PubMed App to iPhone, ... GeneticTrans-ActivatorsTranscriptional ActivationViral Matrix ProteinsVirus LatencyVirus Replication ... Mechanism of activation of the BNLF2a immune evasion gene of Epstein-Barr virus by Zta.. J Gen Virol. 2018 06; 99(6):805-817.JG ... "Mechanism of Activation of the BNLF2a Immune Evasion Gene of Epstein-Barr Virus By Zta." The Journal of General Virology, vol. ...
Other hemorrhagic fever viruses, such as Crimean-Congo hemorrhagic fever virus (11) and dengue virus (12), have also been ... Macrophage Activation Marker Soluble CD163 Associated with Fatal and Severe Ebola Virus Disease in Humans1 On This Page ... Infection and activation of monocytes by Marburg and Ebola viruses. J Virol. 2001;75:11025-33. DOIPubMed ... Macrophage Activation Marker Soluble CD163 Associated with Fatal and Severe Ebola Virus Disease in Humans. Emerging Infectious ...
Virus Diseases. Enterovirus Infections. Picornaviridae Infections. RNA Virus Infections. Hepadnaviridae Infections. DNA Virus ... Activation of Hepatitis B Virus (HBV) in Hepatitis B Surface Antigen (HBsAg) - Negative But Hepatitis B Core Antibody (Anti-HBc ... Activation of HBV Under Immunosuppression in HBsAg-negative But Anti-HBc-positive Patients With Hematological Malignancies. ... have latent hepatitis B virus (HBV) infection in their liver tissue. Cytotoxic chemotherapy and hematopoietic stem cell ...
An evaluation of 2 cohorts of patients with EVD revealed that a marker of macrophage activation (sCD163) but not T-cell ... This type of hyperinflammatory state is reminiscent of 2 rheumatologic disorders known as macrophage activation syndrome and ... These data suggest that host macrophage activation contributes to EVD pathogenesis and that directed antiinflammatory therapies ... predominantly in areas of extensive immunostaining for Ebola virus antigens, was observed in fatal cases. ...
... ... "Receptor interacting protein kinase 2-mediated mitophagy regulates inflammasome activation during virus infection." Nature ... We demonstrate that Nod2−/− and Ripk2−/− mice are hypersusceptible to influenza A virus infection. Ripk2−/− cells displayed ... Accordingly, Ulk1−/− cells displayed enhanced mitochondrial superoxide production and caspase-1 activation. These results ...
Recruitment and activation of a lipid kinase by hepatitis C virus NS5A is essential for integrity of the membranous replication ... title = {Recruitment and activation of a lipid kinase by hepatitis C virus NS5A is essential for integrity of the membranous ... TI - Recruitment and activation of a lipid kinase by hepatitis C virus NS5A is essential for integrity of the membranous ... textit{Recruitment and activation of a lipid kinase by hepatitis C virus NS5A is essential for integrity of the membranous ...
However the role of shed GP in virus replication and pathogenicity is not yet clearly defined. Here we show that shed GP ... released from virus-infected cells binds and activates non-infected DCs and macrophages causing the massive release of pro- and ... Author Summary Ebola virus, a member of the Filoviridae family, causes lethal hemorrhagic fever in man and primates, displaying ... be at the heart of the excessive and dysregulated inflammatory host reactions to infection and thus contribute to high virus ...
Induction of microglia activation after infection with the non-neurotropic A/CA/04/2009 H1N1 influenza virus.. [Shankar ... H1N1 virus. Based on previous studies showing that the highly pathogenic avian influenza (HPAI) A/Vietnam/1203/2004 H5N1 virus ... Following intranasal inoculation, we found no evidence for CA/09 H1N1 virus neurotropism in the enteric, peripheral or central ... possibility that influenza and perhaps other non-neurotropic viruses can initiate inflammatory signals via microglia activation ...
The hepatitis C virus protein NS3 suppresses TNF-α-stimulated activation of NF-κB by targeting LUBAC ... The hepatitis C virus protein NS3 suppresses TNF-α-stimulated activation of NF-κB by targeting LUBAC ... The hepatitis C virus protein NS3 suppresses TNF-α-stimulated activation of NF-κB by targeting LUBAC ... The hepatitis C virus protein NS3 suppresses TNF-α-stimulated activation of NF-κB by targeting LUBAC ...
... and this proteolytic processing event is critical to the virus... ... Activation of the Hemagglutinin of Influenza Viruses. *Authors ... glycoprotein of influenza viruses is posttranslationally cleaved into the disulfide-linked subunits HA1 and HA2, ... Boycott R, Klenk HD, Ohuchi M. Cell tropism of influenza virus mediated by hemagglutinin activation at the stage of virus entry ... Activation of the Hemagglutinin of Influenza Viruses. In: Böttcher-Friebertshäuser E., Garten W., Klenk H. (eds) Activation of ...
Influenza A virus (IAV) triggers a contagious and potentially lethal respiratory disease. A protective IL-1β response is ... Type I IFN triggers RIG-I/TLR3/NLRP3-dependent inflammasome activation in influenza A virus infected cells PLoS Pathog. 2013;9( ... Influenza A virus (IAV) triggers a contagious and potentially lethal respiratory disease. A protective IL-1β response is ... in increased interaction with RIG-I and inhibited type I IFN and IL-1β responses compared to the least pathogenic virus strains ...
We have analyzed lung cytokine responses as well as the activation, interferon (IFN)-γ production and cytotoxicity of lung and ... We have analyzed lung cytokine responses as well as the activation, interferon (IFN)-γ production and cytotoxicity of lung and ... Despite the known decisive role of TLR7 for NK cell activation by therapeutic immuno-stimulatory RNAs, the contribution of TLR7 ... Despite the known decisive role of TLR7 for NK cell activation by therapeutic immuno-stimulatory RNAs, the contribution of TLR7 ...
  • Very little is known about the human cellular immune response to Ebola virus infection, and this lack of knowledge has hindered development of effective therapies and vaccines. (
  • In this study, we characterize the human immune response to Ebola virus infection in four patients. (
  • Four Ebola patients received care at Emory University Hospital, presenting a unique opportunity to examine the cellular immune responses during acute Ebola virus infection. (
  • These results raise the possibility that high-affinity TLR7 stimulants may be able to control chronic HCV infection in vivo , both by induction of IFN and by direct activation of antiviral mechanisms in infected hepatocytes. (
  • The pathogenic strains of these viruses are activated by ubiquitous proteases and cause therefore systemic infection mostly leading to rapid death of the animal, whereas activation of the apathogenic strains occurs only in epithelial cells of the respiratory or the enteric tract resulting in local infection of these organs. (
  • The mammalian influenza viruses, including the human ones, resemble the apathogenic avian strains in possessing also hemagglutinins of restricted cleavability and in causing usually local infection of the respiratory tract. (
  • In case of influenza A virus (IAV) infection, P58(IPK) is known to dissociate from Hsp40 and inhibit PKR activation. (
  • Taken together our data suggest that NP is the viral factor responsible for P58(IPK) activation and subsequent inhibition of PKR-mediated host response during IAV infection. (
  • We investigated the involvement of PKR during infectious pancreatic necrosis virus (IPNV) infection using a custom-made rabbit antiserum and the PKR inhibitor C16. (
  • Influenza virus infection of the respiratory tract is characterized by a neutrophil infiltrate accompanied by inflammatory cytokine and chemokine production. (
  • Neutrophils are highly recruited to sites of infection and are a significant source of tissue injury during the innate immune response to viral infection, including that by influenza A virus. (
  • 1 In an animal model of infection with influenza virus, bronchoalveolar lavage samples showed a predominance of neutrophils over monocytes and macrophages. (
  • 2 Neutrophil activation may contribute to the pathogenesis of severe or fatal viral infection. (
  • 3 Notably, infection of macaque monkeys with the 1918 influenza virus produced a pathological immune response characterized by uncontrolled and aberrant activation of the innate immune system. (
  • 6 Notably, fatal outcome following human infection with avian influenza A virus (H5N1) is associated with high levels of inflammatory cytokines in the peripheral blood including IP-10, MCP-1 (CCL2), MIG (CXCL9), and IL-8 (CXCL8). (
  • Consequently, Bardoxolone methyl and Sulforaphane, two known NRF2 agonists, impair virus production, suggesting that NRF2 activation restricts viral infection. (
  • Our study provides insights into early stages of HSV-1 infection and serves as a general blueprint for the investigation of heterogeneous cell states in virus infection. (
  • The characterization of cellular heterogeneity due to the activation of different host pathways and the progression of viral infection is of great interest. (
  • In addition, the data suggest that therapeutic activation of NKT cells may represent a new strategy for the treatment of chronic HBV infection. (
  • The host tolerance mechanisms to avian influenza virus (H5N1) infection that limit tissue injury remain unknown. (
  • Our findings provide novel insight into the pathogenesis of acute lung injury via the inhibition of cAMP-dependent CFTR channels, indicating that the administration of cAMP-elevating agents and targeting JAK3 may activate host tolerance to infection for the management of influenza virus-induced fatal pneumonia. (
  • Secondary, virus-associated HLH is most commonly reported after Epstein-Barr virus (EBV) infection, and even though EBV infection is exceedingly common (seroprevalence in adults 80%-90%) ( 10 ), development of EBV-associated HLH is still a rare event, estimated at 0.4 cases/1 million population ( 9 ). (
  • Individuals with resolved hepatitis B, characterized as hepatitis B surface antigen (HBsAg)-negative and hepatitis B core antibody-positive, have latent hepatitis B virus (HBV) infection in their liver tissue. (
  • We demonstrate that Nod2−/− and Ripk2−/− mice are hypersusceptible to influenza A virus infection. (
  • Induction of microglia activation after infection with the non-neurotropic A/CA/04/2009 H1N1 influenza virus. (
  • Despite the known decisive role of TLR7 for NK cell activation by therapeutic immunostimulatory RNAs, the contribution of TLR7 to the NK cell response following IAV infection has not been addressed. (
  • We have analyzed lung cytokine responses as well as the activation, interferon (IFN)-γ production, and cytotoxicity of lung and splenic NK cells following sublethal respiratory IAV infection in wild-type and TLR7ko mice. (
  • At the same time, lung type I IFN levels were significantly reduced in TLR7ko mice early following IAV infection, displaying a potential upstream mechanism of the attenuated NK cell activation observed. (
  • Taken together, our data clearly demonstrate a specific role for TLR7 signaling in local and systemic NK cell activation following respiratory IAV infection despite the presence of redundant innate IAV-recognition pathways. (
  • Chronically SIVagm-infected African green monkeys (AGMs) have a remarkably stable nonpathogenic disease course, with levels of immune activation in chronic SIVagm infection similar to those observed in uninfected monkeys and with stable viral loads for long periods of time. (
  • Activation of endothelial cells via antibody-enhanced dengue virus infection of peripheral blood monocytes. (
  • Although endothelial cells have been speculated to be a target in the pathogenesis of dengue hemorrhagic fever (DHF), there has been little evidence linking dengue virus infection to any alteration in endothelial cell function. (
  • Maximum activation was achieved with culture fluids from monocytes in which virus infection was enhanced by the addition of dengue virus-immune serum, thus correlating with epidemiological evidence that prior immunity to dengue virus is a major risk factor for DHF. (
  • Epstein-Barr virus (EBV) nuclear proteins EBNA-LP and EBNA-2 are the first two proteins expressed in latent infection of primary B lymphocytes. (
  • Hepatitis C virus (HCV) causes chronic infection in humans leading to liver cirrhosis and hepatocellular carcinoma. (
  • Thus, we conclude that in this model of infection, site-specific virus persistence develops as a consequence of potent immune activation coupled with reductions in virus-specific neutralizing antibodies. (
  • Dendritic cells (DCs) are targets for dengue virus (DENV) and yellow fever virus (YF) replication and are the first cell population to interact with these viruses during a natural infection, which leads to an induction of protective immunity in humans. (
  • The mechanism of CD4 + T-cell depletion during chronic human immunodeficiency virus type 1 (HIV-1) infection remains unknown. (
  • Human immunodeficiency virus type 1 (HIV-1) is the etiologic agent of AIDS, which is a manifestation of the progressive CD4 + T-cell depletion that occurs in the setting of HIV-1 infection ( 19 , 59 ). (
  • Furthermore, the frequency of HIV-1-infected CD4 + T cells in humans is, on average, very low ( 14 ) and likely is too low if virus-induced death subsequent to infection is solely responsible for HIV-1-mediated CD4 + T-cell depletion ( 20 ), given known parameters of CD4 + T-cell dynamics in the setting of HIV-1 infection ( 2 ). (
  • Several studies focus on understanding the pathogenic mechanisms of the prototype lyssavirus rabies virus (RABV) infection, and little is known about the pathogenesis of rabies caused by other lyssaviruses. (
  • We sought to characterize the host response to Duvenhage virus infection and compare it with responses observed during RABV infection by gene expression profiling of brains of mice with the respective infections. (
  • An unresolved question regarding the physiopathology of hepatitis C virus (HCV) infection is the remarkable efficiency with which host defenses are neutralized to establish chronic infection. (
  • Cells express multiple molecules aimed at detecting incoming virus and infection. (
  • Recognition of virus infection leads to the production of cytokines, chemokines and restriction factors that limit virus replication and activate an adaptive immune response offering long-term protection. (
  • TLR ligand-dependent activation of naive CD4 T cells by plasmacytoid dendritic cells is impaired in hepatitis C virus infection. (
  • Chronic hepatitis C virus (HCV) infection is characterized by diminished numbers and function of HCV-reactive T cells and impaired responses to immunization. (
  • Despite the prevalence of dengue virus infection and the heavy economic burden it puts on the endemic countries, the immunopathogenesis of dengue virus infection remains unclear. (
  • In addition, the interaction of viral factor with TLR6 was found to play an important role in the manifestation of dengue virus infection. (
  • Our study provides new insights into the involvement of TLR6 in dengue virus infection and the potential of using TLR6 anatagonist in therapeutic treatment for DV infection. (
  • Up-regulation of proinflammatory cytokines and immune cells during dengue virus infection could lead to increased vascular permeability and leakage [ 17 - 20 ]. (
  • In addition to acute infection, these viruses cause asymptomatic infection in up to 60% of exposed people, and may lead to late-onset disease or relapse of encephalitis years after initial infection [24] , as well as persistent or delayed neurological sequelae. (
  • Immune activation in HIV infection: what can the natural hosts of simian immunodeficiency virus teach us? (
  • AIDS resistance in natural hosts is characterized by a rapid control of inflammatory processes in response to simian immunodeficiency virus infection despite persistent viremia. (
  • The airway inflammation that results from respiratory syncytial virus infection is associated with a marked increase in interleukin 8 and neutrophils in the infected sites of the lung. (
  • In this study, the relationship between production of interleukin 8, infection of A549 cells by the virus, and activation of mitogen-activated protein kinases (MAPKs) was investigated. (
  • Decapping protein 1 phosphorylation modulates IL-8 expression during respiratory syncytial virus infection. (
  • Marked induction of matrix metalloproteinase-10 by respiratory syncytial virus infection in human nasal epithelial cells. (
  • Nuclear polyhedrosis virus infection ofPseudoplusia includens [Lep. (
  • Activation of invariant NKT cells enhances the innate immune response and improves the disease course in influenza A virus infection. (
  • We show that activation of iNKT cells with alpha-galactosylceramide (alpha-GC) during influenza virus infection transiently enhanced early innate immune response without affecting T cell immunity, and reduced early viral titres in lungs of C57BL/6 mice. (
  • We conclude that activation of iNKT cells enhances early innate immune response in the lungs and contribute to antiviral immunity and improved disease course in influenza A virus infection. (
  • A role of AGO2 in pathogen-induced SAR is suggested by the enhanced activation of AGO2 after infiltrating systemic leaves of plants expressing a localized hypersensitive response upon CMV(Y) infection. (
  • Mathematical Models for Immunodeficiency Virus, Post-treatment and Memory Activation by Alejandra Donaji Herrera Reyes A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE in The Faculty of Graduate Studies (Mathematics) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) August 2012 c Alejandra Donaji Herrera Reyes 2012 Abstract Nowdays, HIV infection can be controlled by anti-retroviral drug therapy (ART). (
  • Here, using a Drosophila loss-of-function ERK ( rolled ) mutant we demonstrated that ERK is important for fly survival during virus infection. (
  • ERK mutant flies subjected to Drosophila C virus (DCV) oral and systemic infection were more susceptible to virus-induced mortality as compared with wild-type flies. (
  • We have demonstrated experimentally that ERK activation is important for fly survival during oral and systemic virus infection. (
  • The results indicate that ERK activation is increased in the presence of Wolbachia but this does not appear to influence Wolbachia -mediated antiviral protection, at least during systemic infection. (
  • Drosophila C virus systemic infection leads to intestinal obstruction. (
  • Here, we sought to determine if exposure to select stimuli can improve LC permissiveness to infection, if specific components of the mLC cocktail are responsible for lowering viral yields, if this is due to defects in progeny production or release, and if these restrictions are also effective against reactivated virus. (
  • In this study, we found that ectopically expressed UL24 could inhibit cGAS-STING-mediated promoter activation of IFN-β and interleukin-6 (IL-6), and UL24 also inhibited interferon-stimulatory DNA-mediated IFN-β and IL-6 production during HSV-1 infection. (
  • To establish persistent infection, viruses have evolved various mechanisms to counteract the host NF-κB pathway. (
  • It has been reported that the severe complication of dengue virus infection, dengue hemorrhagic fever (DHF) is much more commonly observed during secondary dengue virus infections than primary infections. (
  • Through in vitro studies, we show that virus infection up-regulated RANTES production at both mRNA and protein levels in human brain-derived cell lines and primary progenitor-derived astrocytes. (
  • Moreover, IRF-3 was activated upon TBEV infection as evidenced by phosphorylation of TBK1 and IRF-3, while blockade of IRF-3 activation drastically reduced virus-induced RANTES expression. (
  • Bronchiolitis is the result of common viral infection in young children, usually caused by respiratory syncytial virus (RSV) and rhinovirus. (
  • Nef appears to lower the threshold required for T cell activation, which may increase the permissiveness of cells for productive infection. (
  • the interferon response can thus dictate the outcome of a virus infection and it is therefore important to understand how viruses induce interferon. (
  • When transmission of the virus from mother to child duringpossible delivery complications such as encephalitis, eye damage, skin rash and mucous membrane of the mouth, disseminated herpes infection, leading to death in 80% of cases. (
  • If the result of the presence of IgM positive IgGi- There are two options: the infection occurred recently or long ago, but at the moment the virus intensified. (
  • Some viruses, including those that cause AIDS, HPV infection, and viral hepatitis, evade these immune responses and result in chronic infections. (
  • Viral protein involved in the activation of host autophagy. (
  • Viral protein involved in the activation of host NF-kappa-B. This protein is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. (
  • The cleavage activation and sites of glycosylation in the fusion protein of Hendra virus. (
  • Human heat shock 40 protein (Hsp40) was identified as an interacting partner of Influenza A virus nucleoprotein (IAV NP) using a yeast two-hybrid screen. (
  • Activation of interferon regulatory factor 3 is inhibited by the influenza A virus NS1 protein. (
  • The double-stranded RNA (dsRNA) binding protein NS1 of influenza virus is shown to prevent the potent antiviral interferon response by inhibiting the activation of interferon regulatory factor 3 (IRF-3), a key regulator of IFN-alpha/beta gene expression. (
  • We propose that inhibition of IRF-3 activation by a dsRNA binding protein significantly contributes to the virulence of influenza A viruses and possibly to that of other viruses. (
  • The NEP is a second protein normally produced by alternative splicing from the influenza A virus NS gene. (
  • This activation induces the interaction between TLR4 and Gαi protein, which blocks ACs. (
  • found that the HCV protein NS3 blocked TNF-α-stimulated NF-κB activation in a human hepatocyte cell line. (
  • Through competitive binding, NS3 blocked the interaction between the adaptor protein NEMO and the multiprotein complex LUBAC, which is required for the ubiquitylation of NEMO and the activation of NF-κB. (
  • The transcription factor nuclear factor κB (NF-κB) is crucial for innate immune defense against viral infections, and its activation requires the ubiquitylation of upstream proteins, including the adaptor protein NEMO (NF-κB essential modulator). (
  • The NS1 protein derived from a highly pathogenic strain resulted in increased interaction with RIG-I and inhibited type I IFN and IL-1β responses compared to the least pathogenic virus strains. (
  • In vivo administration of LPS or an IL-2/diphtheria toxin fusion protein (Ontak) to chronically SIVagm-infected AGMs triggered increases in immune activation and subsequently of viral replication and depletion of intestinal CD4 + T cells. (
  • Epstein-Barr virus nuclear protein LP stimulates EBNA-2 acidic domain-mediated transcriptional activation. (
  • Since both viral regulatory elements can bind the EBNA-2-associated cell protein RBPJ kappa, consensus RBPJ kappa binding sites were positioned upstream of the herpes simplex virus type 1 thymidine kinase promoter and were found to be sufficient for EBNA-LP and EBNA-2 coactivation. (
  • EBNA-LP strongly stimulated activation of an adenovirus E1b promoter with upstream Gal4 binding sites by a Gal4 DNA binding domain/ EBNA-2 acidic domain fusion protein, indicating that EBNA-LP coactivation requires only the EBNA-2 acidic domain to be localized near a promoter. (
  • The regulation of human immunodeficiency virus type 1 (HIV-1) gene expression involves a complex interplay between cellular transcription factors, chromatin-associated proviral DNA, and the virus-encoded transactivator protein, Tat. (
  • Further analysis revealed that HCV nonstructural protein 5A (NS5A) was responsible for activation of rRNA transcription. (
  • Expression of human immunodeficiency virus type 1 (HIV-1) structural proteins requires the presence of the viral trans-activator protein Rev. Rev is localized in the nucleus and binds specifically to the Rev response element (RRE) sequence in viral RNA. (
  • During the endosomal journey, acidification triggers a conformational change of the virus spike protein hemagglutinin (HA) that results in escape of the viral genome from the endosome into the cytoplasm. (
  • The non-structural protein 1 (NS1) of different influenza A virus (IAV) strains can differentially regulate the activity of c-Jun terminal kinase (JNK) and PI-3 kinase (PI3K). (
  • We demonstrate here that DIs of paramyxoviruses, including parainfluenza virus 5, mumps virus and Sendai virus, can activate the IFN-induction cascade and the IFN-β promoter in the absence of virus protein synthesis. (
  • As virus protein synthesis is an absolute requirement for paramyxovirus genome replication, our results indicate that these DI viruses do not require replication to activate the IFN-induction cascade. (
  • The results demonstrate that tight complementarity of the protein sequences is necessary for NS2B-dependent activation of NS3. (
  • This virus differs from the fully virulent wild-type IC-B strain by a single arginine-to-alanine substitution at amino acid 533 of the attachment protein hemagglutinin and infects cells through SLAM about 40 times less efficiently than the isogenic wild-type strain. (
  • We have used site-directed mutagenesis to delineate sequence specific domains within the human immunodeficiency virus type 1 (HIV-1) trans-acting-responsive (TAR) RNA element that are required for trans activation by the viral Tat protein. (
  • Cross-trans-activation studies of mutant HIV-1 TAR elements with the HIV-2 Tat protein suggest that a similar recognition event(s) forms the basis for trans activation of HIV-1 and HIV-2. (
  • DRibbles or cell lysates derived from HEK293T or UbiLT3 cell lines expressing cytomegalovirus (CMV) pp65 protein or transfected with a plasmid encoding dominant HLA-A2 restricted CMV, Epstein-Barr virus (EBV), and Influenza (Flu) epitopes (CEF) were loaded onto human monocytes or PBMCs and the response of human CMV pp65 or CEF antigen-specific CD4 + and CD8 + memory T cells was detected by intracellular staining. (
  • The latent membrane protein (LMP) 2A of Epstein-Barr virus (EBV) is expressed during different latency stages of EBV-infected B cells in which it triggers activation of cytoplasmic protein tyrosine kinases. (
  • We show that mere expression of LMP2A not only stimulated protein tyrosine kinases but also induced phospholipase C-γ2-mediated Ca 2+ oscillations followed by activation of the extracellular signal-regulated kinase (Erk) mitogen-activated protein kinase pathway and induction of the lytic EBV gene bzlf1 . (
  • Using IRF3 phosphorylation as a marker of activation of the IFN induction cascade that occurs upstream of the IFN-β promoter, we demonstrate strong activation of the IFN induction cascade in A549 cells infected with a range of influenza A viruses in the presence of cycloheximide or NP siRNA, which inhibit viral protein synthesis and thus cRNP and progeny vRNP synthesis. (
  • Although autophagy is clearly important for antiviral immune response, it can also be activated by viruses and serves as platform for viral replication. (
  • Human hepatocyte line Huh-7 carrying an HCV replicon expressed TLR7, and activation of the receptor induced several antiviral genes including IFN regulatory factor-7. (
  • Herpes simplex virus (HSV) type I keratitis remains a leading cause of corneal morbidity, despite the availability of effective antiviral drugs. (
  • In addition several genes of the IFN signaling pathway are up-regulated, indicating a strong antiviral response and activation of the negative feedback mechanism to limit type I IFN responses. (
  • We recently showed that the addition of a cholesterol group to HRC peptides active against Nipah virus targets these peptides to the membrane where fusion occurs, dramatically increasing their antiviral effect. (
  • The viral RNA encodes a serine protease (NS2B-NS3), essential for virus replication in infected cells, that constitutes an attractive target for antiviral compounds. (
  • Dengue virus activates membrane TRAIL relocalization and IFN-alpha production by human plasmacytoid dendritic cells in vitro and in vivo," PLoS Neglected Tropical Diseases , vol. 7, no. 6, article e2257, 2013. (
  • In vivo studies of gene activation have revealed that changes in chromatin are often associated with transcriptional activation (reviewed in references 21 , 30 , and 44 ). (
  • Furthermore, the interaction of the Rev activation domain with a cellular cofactor is essential for Rev function in vivo. (
  • The failure of HAART to completely shut down virus replication in vivo is a function of both the intrinsic potency of the drug regimen and its distribution to the cellular sites of virus replication. (
  • In vivo activation of human immunodeficiency virus type 1 long termina" by John D. Morrey, S M. Bourn et al. (
  • Ex vivo, this virus infects primary lymphocytes at low levels regardless of SLAM expression. (
  • In order to elucidate the role of T lymphocytes in the pathogenesis of DHF, we attempted to determine whether T lymphocytes are activated in vivo during dengue virus infections, by examining the levels of soluble IL-2 receptor (sIL-2R), soluble CD4 (sCD4), soluble CD8 (sCD8), interleukin-2 (IL-2) and interferon-gamma (IFN gamma) in the sera of 59 patients with DHF and 41 patients with dengue fever (DF). (
  • These results indicate (a) T lymphocytes are activated and produce IL-2 and IFN gamma in vivo during DHF and DF, (b) CD4+ T lymphocytes are activated in DHF and DF, and the level of activation is higher in DHF than in DF, and (c) activation of CD8+ T lymphocytes is evident in DHF, but not in DF. (
  • PAK2 is likely to play a role in Nef-mediated enhancement of viral replication and immune activation in vivo . (
  • Some viruses such as poliovirus, use the autophagic pathway as a nonlytic mechanism for viral release. (
  • Several viruses have developed strategies to activate the NF-kappa-B pathway in order to promote viral replication and prevent virus-induced apoptosis. (
  • Using a hepatitis B virus (HBV) transgenic mouse model, we have previously shown that the intrahepatic induction of IFN-γ inhibits HBV replication in the liver ( 23 )( 24 ) by a nitric oxide (NO)-dependent pathway ( 25 ). (
  • Pathway analysis of gene expression changes during TLR3 activation highlighted 41 genes also related to neuronal development, suggesting a mechanistic connection to disrupted neurogenesis. (
  • Wolbachia induces reactive oxygen species (ROS)-dependent activation of the Toll pathway to control dengue virus in the mosquito Aedes aegypti. (
  • Reactive oxygen species elevation is linked to the activation of the Toll pathway, which is essential in mediating the expression of antioxidants to counterbalance oxidative stress. (
  • This immune pathway also is responsible for activation of antimicrobial peptides-defensins and cecropins. (
  • H5N1 virus activated JNK but inhibited the PI-3 kinase pathway. (
  • whereas H1N1 virus activated the PI-3 kinase pathway but did not activate JNK. (
  • Conserved herpesvirus kinases target the DNA damage response pathway and TIP60 histone acetyltransferase to promote virus replication. (
  • Herpes Simplex Virus 1 UL24 Abrogates the DNA Sensing Signal Pathway by Inhibiting NF-κB Activation. (
  • In the present study, for the first time, HSV-1 UL24 was demonstrated to inhibit the activation of NF-κB in the DNA sensing signal pathway via binding to the RHDs of the NF-κB subunits p65 and p50 and abolishing their nuclear translocation. (
  • Hepatitis C virus is a poor inducer of interferon (IFN), although its structured viral RNA can bind the RNA helicase RIG-I, and activate the IFN-induction pathway. (
  • We present a novel mechanism by which viruses may inhibit the alpha/beta interferon (IFN-alpha/beta) cascade. (
  • 11 , 12 Similarly, the induction of interferon-α (IFN-α) by influenza virus in murine plasmacytoid dendritic cells is dependent on the presence TLR7 and endosomal acidification. (
  • We have previously reported that hepatitis B virus (HBV)-specific CD8 + cytotoxic T lymphocytes and CD4 + helper T lymphocytes can inhibit HBV replication in the liver of HBV transgenic mice by secreting interferon (IFN)-γ when they recognize viral antigen. (
  • Expression and activation of STAT1 (a factor activated by both interferon (IFN)-alpha and IFN-gamma) were increased in HCV infected livers, particularly in those with high inflammatory activity. (
  • The differential cytokine production indicates that DENV2 results in TNF induction, which discriminates it from vaccine viruses that preferentially stimulate interferon expression. (
  • Conflicting reports exist regarding the requirement for virus replication in interferon (IFN) induction by paramyxoviruses. (
  • Hepatitis C virus controls interferon production through PKR activation. (
  • Both input and progeny genomes have been linked to interferon induction by influenza viruses. (
  • We have previously reported that hepatitis B virus (HBV)-specific CD8(+) cytotoxic T lymphocytes and CD4(+) helper T lymphocytes can inhibit HBV replication in the liver of HBV transgenic mice by secreting interferon (IFN)-gamma when they recognize viral antigen. (
  • On the other hand, virus entry affects a range of cellular pathways, which may in turn lead to transcriptional activation or repression of downstream target genes 9 . (
  • We now show that EBNA-LP stimulates EBNA-2 activation of the LMP1 promoter and of the LMP1/LMP2B bidirectional transcriptional regulatory element. (
  • These results indicate that EBNA-LP's critical role in EBV-mediated cell growth transformation is in stimulating (and probably regulating) EBNA-2-mediated transcriptional activation. (
  • Here we show that Tat transactivates the integrated HIV-1 long terminal repeat (LTR), even in the absence of detectable basal promoter activity, and this transcriptional activation is accompanied by chromatin remodeling downstream of the transcription initiation site, as monitored by increased accessibility to restriction endonucleases. (
  • Histone acetylation renders the inactive HIV-1 LTR responsive to NF-κB, indicating that a suppressive chromatin structure must be remodeled prior to transcriptional activation by NF-κB. (
  • We assumed that the pathogenic process of excessive CD4 + T-cell activation would be reflected in the transcriptional profiles of activated CD4 + T cells. (
  • IRF-3 activation and, as a consequence, IFN-beta mRNA induction are inhibited in wild-type (PR8) influenza virus-infected cells but not in cells infected with an isogenic virus lacking the NS1 gene (delNS1 virus). (
  • Using heat inactivation of influenza virus, we show that viral entry but not replication is required for cytokine induction. (
  • Because retroviruses such as human immunodeficiency virus type 1 (HIV-1) must integrate a DNA copy of their genome into the chromosomal DNA of newly infected cells, it is necessary to characterize the nucleosomal organization of the integrated viral promoter to understand the mechanism(s) associated with the induction of viral transcription. (
  • Monocytes, macrophages and dendritic cells (DCs) are the main targets for viruses involved in vascular permeability induction (Schnittler & Feldmann 2003, Clyde et al. (
  • Our previous work has demonstrated that pathogen-associated molecular patterns capable of activating the IFN-induction cascade are not normally generated during virus replication, but are associated instead with the presence of defective interfering (DI) viruses. (
  • In contrast, activation of the IFN induction cascade by influenza viruses was very effectively abrogated by treatment with actinomycin D and other transcription inhibitors, which correlated with the inhibition of the synthesis of all viral RNA species. (
  • thus, both viral RNA synthesis and nuclear export are required for IFN induction by influenza A viruses. (
  • The study of viruses is known as virology, a subspeciality of microbiology. (
  • Our analysis suggests that the direct activation of a lipid kinase by HCV NS5A contributes critically to the integrity of the membranous viral replication complex. (
  • Our study indicates that circulating microbial products can increase viral replication by inducing immune activation and increasing the number of viral target cells, thus demonstrating that immune activation and T cell proliferation are key factors in AIDS pathogenesis. (
  • Nef-mediated enhancement of cellular activation and viral replication in primary T cells is dependent on PAK2 and on the strength of the activating stimuli, and correlates with the ability of Nef to associate with PAK2. (
  • A recent report suggested that ribavirin could induce IRF-7 in cells infected with respiratory syncitial virus ( 21 ). (
  • Influenza A virus is a negative stranded RNA virus that infects epithelial cells of the upper respiratory tract and bronchi. (
  • H5N1 HA is detected by TLR4 expressed on respiratory epithelial cells, facilitating JAK3 activation. (
  • Although influenza is primarily a respiratory disease, it has been shown, in some cases, to induce encephalitis, including people acutely infected with the pandemic A/California/04/2009 (CA/09) H1N1 virus. (
  • Influenza A virus (IAV) triggers a contagious and potentially lethal respiratory disease. (
  • Activation of ERK2 by respiratory syncytial virus in A549 cells is linked to the production of interleukin 8. (
  • Respiratory syncytial virus represses glucocorticoid receptor-mediated gene activation. (
  • Respiratory syncytial virus (RSV) is the most common cause of bronchiolitis in the pediatric population worldwide and an important cause of death in developing countries. (
  • We define the kinetics of T- and B-cell activation, and determine which viral proteins are targets of the Ebola virus-specific T-cell response in humans. (
  • Hendra virus (HeV) is an unclassified member of the Paramyxoviridae family that causes systemic infections in humans, horses, cats, guinea pigs and flying foxes. (
  • Herpes simplex virus-1 (HSV-1) is one of nine known herpes viruses that affect humans. (
  • Ebola virus (EBOV) disease (EVD) in humans is frequently severe and accompanied by fever, signs of endothelial dysfunction, coagulopathy, shock, and multisystem organ dysfunction. (
  • N2 - Hepatitis C virus (HCV) is a major causative agent of chronic liver disease in humans. (
  • Herpes simplex virus 1 (HSV-1) is one of the eight herpesviruses that can infect humans and is prevalent worldwide. (
  • NiV and Hendra (HeV) viruses are emerging zoonotic paramyxoviruses [14] that are lethal to humans. (
  • With the emerging importance of high-pathogenicity influenza A virus infections in humans, we questioned whether iNKT cells contribute to immune defence against influenza A virus and whether activation of these cells influences outcome. (
  • Tick-borne encephalitis virus (TBEV) is one of the most important flaviviruses that targets the central nervous system (CNS) and causes encephalitides in humans. (
  • Herpesviridae is a large family of DNA viruses that cause infections and certain diseases in animals, including humans. (
  • More than 90% of adults have been infected with at least one of these, and a latent form of the virus remains in almost all humans who have been infected. (
  • We have also shown that IFN-α/β produced in the liver of HBV transgenic mice during various virus infections or after poly-inosinic-polycytidylic acid (Poly-I/C) injection inhibits HBV replication via NO-independent pathways ( 24 )( 26 )( 27 ). (
  • Influenza A virus (IAV) is an Orthomyxovirus carrying a segmented, single-stranded RNA genome, and IAV infections remain a serious burden for human health during seasonal outbreaks. (
  • While antisense transcription from viral genomes has been described previously, e.g., in HIV-1 [ 17 ], and was also observed in our sequencing data from the HSV-1 genome, to our knowledge, modulation of host cell antisense transcription by virus infections has not been studied so far. (
  • Activation of T lymphocytes in dengue virus infections. (
  • and Ennis, Francis A., "Activation of T lymphocytes in dengue virus infections. (
  • A common feature of herpes viruses is their ability to maintain latent infections during which no virus particles are produced. (
  • Viral infections in animals provoke an immune response that usually eliminates the infecting virus. (
  • Infected cells are able to recognize the virus through Toll-like receptor (TLR) 3, TLR7, RIG-I, MDA5, and the NLRP3 inflammasome, most of which sense the viral genome or replication intermediates ( 2 ) and contribute to the anti-IAV host defense in a cell-type-specific manner ( 3 , 4 ). (
  • We show for the first time that a virus induces widespread antisense transcription of the host cell genome. (
  • As a poxvirus, VACV is an unusual virus that replicates its large DNA genome exclusively in the cytoplasm of infected cells. (
  • Dengue virus genome encodes for a single polyprotein that consists of 3 structural proteins (capsid, premembrane and envelope) that form the physical structure of the virus particle and 7 non-structural proteins (NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5) which are necessary for the replication of the virus. (
  • West Nile virus (WNV) has a positive sense RNA genome with conserved structural elements in the 5′ and 3′ -untranslated regions required for polyprotein production. (
  • Here we report that the region at the 5′-end of the WNV genome comprising both the 5′-UTR and initial coding region is capable of OAS1 activation in vitro. (
  • Cyclic GMP-AMP synthase (cGAS) is a newly identified DNA sensor that recognizes foreign DNA, including the genome of herpes simplex virus 1 (HSV-1). (
  • The primary objectives of this special grant program are to understand the cellular and molecular mechanisms involved in activation of HIV in lung cells and the subsequent effects this has on the course of HIV disease, especially in the lung. (
  • The human gamma herpes virus Epstein-Barr virus (EBV) exploits multiple routes to evade the cellular immune response. (
  • High-resolution structures are available for the HA precursor (HA0), the cleaved neutral pH conformation of HA, and the low pH conformation that the HA assumes when triggered by acidification of endosomes to mediate fusion of viral and cellular membrane during virus entry. (
  • Eukaryotic initiation factor 5A is a cellular target of the human immunodeficiency virus type 1 Rev activation domain mediating trans-activation. (
  • Using cross-linking experiments and Biospecific Interaction Analysis (BIA) we identify eukaryotic initiation factor 5A (eIF-5A) as a cellular factor binding specifically to the HIV-1 Rev activation domain. (
  • Such events may involve interaction with a cellular coreceptor or other factors but do not require cathepsins B and L, late endosomal proteases that activate Ebola virus and reovirus for entry. (
  • Our data establish that LMP2A expression has a function beyond the putative inhibition of the BCR by generating a ligand-independent cellular activation signal that may provide a molecular switch for different EBV life cycle stages and most probably contributes to EBV-associated lymphoproliferative disorders. (
  • We identify five potential Zta-response elements (ZREs) in the promoter that are highly conserved between virus isolates. (
  • We show that this can be DNA methylated during EBV latency and that both Zta binding and promoter activation are enhanced by its methylation. (
  • In summary, we find that the BNLF2a promoter is directly targeted by Zta and that DNA methylation within the proximal ZRE aids activation. (
  • EBNA-LP also stimulates EBNA-2 activation of a multimerized regulatory element from the BamC EBNA promoter. (
  • Indeed, when Tax is coexpressed with the E2F-1 transcription factor in CEM T-cells, which lack expression of p16(INK4A), it strongly potentiates the E2F-dependent activation of a reporter construct driven by a promoter containing E2F binding sites. (
  • In the context of immunosuppression in kidney transplant patients, reactivation of the viral early promoter (BKV E ) results in production of T antigen, enabling virus replication and transition from latency to the lytic phase, causing polyomavirus-associated nephropathy. (
  • A Tat-induced auto-up-regulatory loop for superactivation of the human immunodeficiency virus type 1 promoter. (
  • Furthermore, UL24 selectively blocked nuclear factor κB (NF-κB) but not IFN-regulatory factor 3 promoter activation. (
  • Site mutation of an IRF-3-binding motif abrogated the RANTES promoter activity in virus-infected brain cells. (
  • Viruses bearing wild-type Nefs, but not Nef mutants defective for PAK2 association, enhanced NFAT and IL2 receptor promoter activity in Jurkat cells. (
  • The YF17DD vaccine induces long-lasting immunity, similar to wild viruses (Monath 2001, Halstead 2007). (
  • If the result of the presence of IgG positive, andIgM negative - in the body of the virus is present, but there is immunity. (
  • Effect on delNS1 virus-induced nuclear accumulation of hIRF-3 in HEC-1b cells by transient transfection of influenza virus NS1 proteins. (
  • In an attempt to identify residues and motifs on NS2B that are necessary for protease activity of the ALKV NS2B-NS3 complex, a series of modified NS2B-NS3 proteins was constructed, with point mutations on particular residues or with the NS2B domain derived from two different viruses. (
  • 7 Thus, understanding the mechanisms of chemokine and cytokine responses to influenza virus is of high priority, as excessive cytokine production may contribute to viral pathogenesis. (
  • These data suggest that host macrophage activation contributes to EVD pathogenesis and that directed antiinflammatory therapies could be beneficial in the treatment of EVD. (
  • CD150) is the immune cell receptor for measles virus (MV). To assess the importance of the SLAM-MV interactions for virus spread and pathogenesis, we generated a wild-type IC-B MV selectively unable to recognize human SLAM (SLAM-blind). (
  • Based on previous studies showing that the highly pathogenic avian influenza (HPAI) A/Vietnam/1203/2004 H5N1 virus was neurotropic, induced CNS inflammation and a transient parkinsonism, we examined the neurotropic and inflammatory potential of the CA/09 H1N1 virus in mice. (
  • Since inflammation can reduce neurogenesis, we tested whether Theiler's murine encephalomyelitis virus (TMEV) induces inflammation and reduces neurogenesis in the SVZ. (
  • CD45+ activation (inflammation) occurred early in the forebrain and preceded cerebellar and spinal cord inflammation. (
  • S. B. Halstead and N. J. Marchette, "Biologic properties of dengue viruses following serial passage in primary dog kidney cells: studies at the University of Hawaii," The American Journal of Tropical Medicine and Hygiene , vol. 69, Supplement, no. 6, pp. 5-11, 2003. (
  • R. Rott, M. Orlich, H.-D. Klenk, M.L. Wang, J.J. Skehel, and D.C. Wiley, Studies on the adaptation of influenza viruses to MDCK cells, EMBO J . 3:3328 (1984). (
  • Viruses have evolved various strategies to evade the recognition and destruction by NK cells through the downregulation of the NK cell activating receptors. (
  • Further, the IAV NP-Hsp40 interaction was validated in mammalian cells infected with various seasonal and pandemic strains of influenza viruses. (
  • In this study, we examined expression from the promoters of Maize streak virus (MSV) in transgenic maize plants and cells to determine whether they showed cell-cycle specificity. (
  • Inhibition of IRF-3 activation can be achieved by the expression of wild-type NS1 in trans, not only in delNS1 virus-infected cells but also in cells infected with a heterologous RNA virus (Newcastle disease virus). (
  • Nuclear accumulation of hIRF-3 in delNS1 virus-infected cells. (
  • A) Coverslips coated with Hec-1b cells were mock infected or infected with delNS1 or wild-type influenza A virus (PR8) at an MOI of 1. (
  • B) HEC-1b cells were infected with delNS1 or PR8 virus for 2, 4, or 8 h. (
  • C) 293T cells were transfected with pCAGGS-hIRF-3 and infected 24 h later with either Sendai, PR8, or delNS1 virus or were mock infected. (
  • PKR inhibitor pre-treatment resulted in decreased virus titers, extra- and intracellularly, concomitant with reduction of cells with compromised membranes in IPNV-permissive cell lines. (
  • These findings suggest that IPNV uses PKR activation to promote virus replication in infected cells. (
  • Both of these events were temporally associated with the rapid disappearance of NKT cells from the liver, presumably reflecting activation-induced cell death, and by the recruitment of activated NK cells into the organ. (
  • Ripk2−/− cells displayed defective mitophagy leading to enhanced mitochondrial superoxide production and accumulation of damaged mitochondria resulting in increased NLRP3 inflammasome activation and IL-18 production. (
  • Accordingly, Ulk1−/− cells displayed enhanced mitochondrial superoxide production and caspase-1 activation. (
  • Many infectious pathogens, including hepatitis C virus (HCV), inhibit NF-κB signaling in host cells, which promotes pathogen survival. (
  • Bottcher E, Freuer C, Steinmetzer T, Klenk HD, Garten W. MDCK cells that express proteases TMPRSS2 and HAT provide a cell system to propagate influenza viruses in the absence of trypsin and to study cleavage of HA and its inhibition. (
  • In this study, we show that human umbilical vein endothelial cells become activated when exposed to culture fluids from dengue virus-infected peripheral blood monocytes. (
  • Endothelial cells inoculated directly with dengue virus or with virus-antibody combinations were poorly infectable (compared to Vero cells or peripheral blood monocytes), and virus-inoculated endothelial cells showed no increased expression of VCAM-1, ICAM-1, or E-selectin. (
  • T helper cells can support the functions of CD8(+) T cells against persistently infecting viruses such as murine lymphocytic choriomeningitis virus (LCMV), cytomegalovirus, hepatitis C virus and HIV. (
  • Transfer of virus-specific B cells but not virus-specific T cells augmented virus clearance from persistent sites. (
  • Virus elimination from the kidneys was associated with the formation of IgG deposits in the interstitial space, presumably from kidney-infiltrating B cells. (
  • CD8(+) T cells in the kidneys of mice that did not clear virus from this site were activated but showed evidence of exhaustion. (
  • We analysed the status of STATs in hepatitis C virus (HCV) infected livers and the relationship between expression and activation of STATs and HCV replication in Huh7 cells transfected with HCV genomic replicon. (
  • HCV replication in Huh7 cells also inhibited STAT1 and STAT2 activation by IFN-alpha while there was no impairment of STAT1 phosphorylation by the proinflammatory cytokine IFN-gamma. (
  • Consistent with the idea of increased destruction, CD4 + T cells from simian immunodeficiency virus (SIV)-infected macaques have been shown to have a substantially higher turnover rate than CD4 + T cells from uninfected macaques ( 30 , 41 , 52 , 65 ). (
  • The 50% effective concentration (EC 50 ) of GS 7340 against human immunodeficiency virus type 1 in MT-2 cells was 0.005 μM compared to an EC 50 of 5 μM for the parent drug, tenofovir. (
  • The lymphatic tissues and the peripheral blood mononuclear cells (PBMCs) are the primary sites of virus replication and potential virus latency ( 9 , 19 ). (
  • TLR ligand was observed to enhance both MDC and PDC activation of naive CD4 T cells. (
  • In contrast, PDC from HCV-infected persons had reduced activation marker (HLA-DR) and cytokine (IFN-alpha) expression upon R-848 stimulation, and these were associated with impaired activation of naive CD4 T cells. (
  • Here we report that H5N1 (A/mallard/Huadong/S/2005) influenza A virus induced functional autophagy, as evidenced by increased LC3 lipidation and decreased p62 levels, and the presence of autolysosomes in chicken fibroblast cells. (
  • Temporal changes in iNKT cells in the liver, blood and lungs suggest activation and migration of iNKT cells from the liver to the lungs in mice that were administered alpha-GC. (
  • Improvement in viral titres appears dependent on activation of iNKT cells via the intraperitoneal route since intranasal administration of alpha-GC did not have the same effect. (
  • The drug Auranofin has been shown to accelerate the activation rate of latent cells and also alters the kinetics of viral rebound when drug treatment is interrupted. (
  • Polyomavirus BK (BKV) is a serious problem for immunocompromised patients, where latent virus can enter into the lytic cycle causing cytolytic destruction of host cells. (
  • The first TBEV replication usually occurs in dendritic cells of the skin following tick bites, later in regional lymph nodes, and then virus can be detected in plasma [ 5 , 6 ]. (
  • During the stage of active viremia, virus may cross the blood-brain barrier (BBB) and invade the CNS where it causes profound destruction of nerve cells [ 2 ]. (
  • siRNA knockdown of PAK2 in Jurkat cells reduced NFAT activation induced by anti-CD3/CD28 stimulation both in the presence and absence of Nef, and expression of a PAK2 dominant mutant inhibited Nef-mediated enhancement of CD25 expression. (
  • Early studies revealed that an immunoreceptor tyrosine-based activation motif (ITAM) in the cytoplasmic N-terminus of LMP2A can trigger a transient increase of the cytosolic Ca 2+ concentration similar to that observed in antigen-activated B cells when expressed as a chimeric transmembrane receptor. (
  • A virus is a submicroscopic infectious agent that replicates only inside the living cells of an organism. (
  • The origins of viruses in the evolutionary history of life are unclear: some may have evolved from plasmids-pieces of DNA that can move between cells-while others may have evolved from bacteria. (
  • 8 The potential contribution of TLR7 and TLR8 to inflammatory cytokine production by neutrophils in response to viral pathogens such as influenza virus has not been explored. (
  • Ebola virus disease (EVD) is associated with elevated cytokine levels, and hypercytokinemia is more pronounced in fatal cases. (
  • We studied the infectivity of DENV2 (strain 16681), a YF vaccine (YF17DD) and a chimeric YF17D/DENV2 vaccine in monocyte-derived DCs in vitro with regard to cell maturation, activation and cytokine production. (
  • Influenza A virus nucleoprotein exploits Hsp40 to inhibit PKR activation. (
  • R. Ohuchi, M. Ohuchi, W. Garten, and H.-D. Klenk, Human influenza virus hemagglutinin with high sensitivity to proteolytic activation, J. Virol . (
  • This Request for Applications (RFA), Regulation of Human Immunodeficiency Virus (HIV) Activation in the Lung, is related to the priority area of immunization and infectious diseases. (
  • We demonstrate that influenza virus can induce IL-8 and other inflammatory cytokines from GM-CSF-primed human neutrophils. (
  • Bottcher E, Matrosovich T, Beyerle M, Klenk HD, Garten W, Matrosovich M. Proteolytic activation of influenza viruses by serine proteases TMPRSS2 and HAT from human airway epithelium. (
  • When introduced to nonnative mosquito hosts, Wolbachia induce resistance to a number of human pathogens, including dengue virus (DENV), Plasmodium, and filarial nematodes, but the molecular mechanism involved is unclear. (
  • Herpes simplex virus type 1 (HSV-1) is a human pathogen, together with seven other viruses from the alpha, beta, and gammaherpesvirinae. (
  • Highly active antiretroviral therapy (HAART) for the treatment of human immunodeficiency virus is effective in reducing plasma viral loads below current assay detection limits and is responsible for significant reductions in AIDS-related mortality in the United States ( 13 ). (
  • 3 years, leading to the conclusion that it may not be possible to eradicate human immunodeficiency virus (HIV) from an infected individual by using current HAART ( 2 ). (
  • The human T-cell leukemia virus type I (HTLV-I) is a causative agent of adult T-cell leukemia. (
  • Alkhurma virus (ALKV) is a tick-borne class 4 flavivirus responsible for several human cases of haemorrhagic fever in Saudi Arabia, with no specific treatment currently available. (
  • BK virus-associated hemorrhagic cystitis in a human immunodeficiency virus-infected patient. (
  • A collection of activities and demonstrations focusing on various aspects of the human immunodeficiency virus (HIV) life cycle. (
  • Hepatitis C virus (HCV) is an important human pathogen associated with chronic liver disease. (
  • trans activation of human immunodeficiency virus type 1 is sequence specific for both the single-stranded bulge and loop of the trans-acting-responsive hairpin: a quantitative analysis. (
  • Several therapeutic strategies targeting Epstein-Barr virus (EBV)-associated tumors involve upregulation of viral lytic gene expression. (
  • We investigated the effects of clofoctol on an EBV-positive Burkitt lymphoma cell line and confirmed the upregulation of all three branches of the UPR and activation of EBV lytic gene expression. (
  • Some strategies for treating these cancers involve activation of lytic viral gene expression. (
  • 2010). Both dengue and YF wild viruses can induce a broad spectrum of clinical manifestations from asymptomatic to severe clinical features, the latter of which is characterised by haemorrhaic manifestations and shock syndrome, which are associated with vascular permeability and leakage. (
  • Higher viral antigen positive cell frequencies were observed for DENV2 when compared with both vaccine viruses. (
  • Like many other viral glycoproteins, the hemagglutinin (HA) of influenza viruses is activated by proteolytic cleavage. (
  • Cleavage which is necessary for the fusion activity of the hemagglutinin and thus for the infectivity of the virus is exerted by host cell proteases, and the presence of an appropriate enzyme determines whether infectious virus is made in a given cell. (
  • S. Li, M. Orlich, and R. Rott, Generation of seal influenza virus variants pathogenic for chickens because of hemagglutinin cleavage site changes. (
  • Y. Kawaoka and R.G. Webster, Interplay between carbohydrate in the stalk and the length of the connecting peptide determines the cleavability of influenza virus hemagglutinin, J. Virol . (
  • Y. Kawaoka, C.W. Naeve, and R.G. Webster, Is virulence of H5N2 influenza viruses in chickens associated with loss of carbohydrate from the hemagglutinin? (
  • therefore, this study aims to elucidate whether JAK3 activation induced by H5N1 hemagglutinin (HA) inhibits cAMP-dependent CFTR channels. (
  • The hemagglutinin (HA) glycoprotein of influenza viruses is posttranslationally cleaved into the disulfide-linked subunits HA 1 and HA 2 , and this proteolytic processing event is critical to the virus life cycle as it is required to activate membrane fusion potential and virus infectivity. (
  • Sequence relationships among the hemagglutinin genes of 12 subtypes of influenza A virus. (
  • Bertram S, Glowacka I, Steffen I, Kuhl A, Pohlmann S. Novel insights into proteolytic cleavage of influenza virus hemagglutinin. (
  • Boycott R, Klenk HD, Ohuchi M. Cell tropism of influenza virus mediated by hemagglutinin activation at the stage of virus entry. (
  • In other instances, complexes such as SWI-SNF, NURF, or RSC utilize ATP-dependent nucleosome remodeling mechanisms for efficient transcription activation (reviewed in reference 54 ). (
  • These results, along with the biochemical and genetic studies of yeast histones ( 29 , 42 ), support the conclusion that nucleosomes exert a repressor effect on a variety of genes and remodeling of chromatin structure is a part of the transcription activation process. (
  • Both the NH 2 -terminal amphipathic helix and the polyproline motifs of NS5A seem to be essential for rRNA transcription activation. (
  • The NS5A-dependent activation of rRNA transcription seems to be due to hyperphosphorylation and consequent activation of upstream binding factor (UBF), a Pol I DNA binding transcription factor. (
  • These results suggest that the endoplasmic reticulum-associated NS5A is able to transduce signals into the nucleoplasm via UBF hyperphosphorylation leading to rRNA transcription activation. (
  • UBF1 is activated during G 1 progression by phosphorylation of Ser484 by cdk4/cyclin D1 ( 7 ) and Ser388 by cdk2/cyclin E and cdk2/cyclin A ( 6 ), resulting in full activation of rRNA transcription. (
  • Our findings open new perspectives on global and specific alterations of host cell transcription by viruses. (
  • We have examined the requirements for virus transcription and replication, and thus the roles of input and progeny genomes, in the generation of IFN-inducing PAMPs by influenza A viruses using inhibitors of these processes. (
  • They have duties such as capsid transport to the nucleus and other organelles, activation of early gene transcription, and mRNA degradation. (
  • Chromatin dynamics regulate the transcription competency of entire herpes virus genomes. (
  • Ohuchi M., Ohuchi R., Stieneke-Gröber A., Vey M., Garten W. (1992) Proteolytic Activation of Influenza Viruses: Substrates and Proteases. (
  • It has been known for decades that influenza strains and subtypes can vary with regard to HA cleavage properties and that cleavage site sequences and the proteases that recognize them can represent a major determinant for virus pathogenicity. (
  • However, a number of questions remain with respect to the identity and characteristics of the proteases that activate HAs in the various natural hosts and complex ecosystems that constitute the realm of influenza viruses. (
  • Proteolytic activation is therefore indispensable for effective virus spread in the infected host and has been found to be a prime determinant for virus pathogenicity. (
  • Flaviviruses are arthropod-borne viruses that may cause severe acute infectious diseases, such as dengue fever and yellow fever (YF). (
  • Recently, based on a genotype 2a isolate, tissue culture systems supporting complete replication and infectious virus production have been developed. (
  • A meaning of "agent that causes infectious disease" is first recorded in 1728, long before the discovery of viruses by Dmitri Ivanovsky in 1892. (
  • In 1892, the Russian biologist Dmitri Ivanovsky used this filter to study what is now known as the tobacco mosaic virus: crushed leaf extracts from infected tobacco plants remained infectious even after filtration to remove bacteria. (
  • Among the animal herpesviruses are pseudorabies virus, the causative agent of Aujeszky's disease in pigs, and bovine herpesvirus 1, the causative agent of bovine infectious rhinotracheitis and pustular vulvovaginitis. (
  • PURPOSE The National Heart, Lung, and Blood Institute (NHLBI) invites research grant applications for support of research on the regulation of activation of HIV in the lung and mechanisms by which co-factors may lead to increased HIV-associated pulmonary disease. (
  • These results demonstrate a role for NOD2-RIPK2 signaling in protection against virally triggered immunopathology by negatively regulating NLRP3 inflammasome activation and IL-18 production via ULK1-dependent mitophagy. (
  • 15 In addition, we showed that influenza A virus (H3N2) can induce cytokines in a manner dependent on TLR7 and that influenza viral RNA is a potent inducer of TLR7 in several cell systems. (
  • In this work, we report that unlike the untagged HRC peptides, which bind to the postulated extended intermediate state bridging the viral and cell membranes, the cholesterol tagged HRC-derived peptides interact with F before the fusion peptide inserts into the target cell membrane, thus capturing an earlier stage in the F-activation process. (
  • For many other enveloped viruses, acidic pH triggers an irreversible conformational change, which promotes virion-endosomal membrane fusion. (
  • In the present study, we found that ectopic expression of STAP-2 inhibited Epstein-Barr virus (EBV) LMP1-mediated NF-B signaling and interleukin-6 expression. (
  • Here we report the crystal structures of a dengue NS2B-NS3pro complex and a West Nile virus NS2B-NS3pro complex with a substrate-based inhibitor. (
  • SP600125, a JNK inhibitor, inhibited H5N1 virus-induced autophagy and virus replication in a DF-1 chicken fibroblast cell line. (
  • These structures identify key residues for NS3pro substrate recognition and clarify the mechanism of NS3pro activation. (
  • This concept has been derived mainly from studies on avian influenza viruses. (
  • Bosch FX, Garten W, Klenk HD, Rott R. Proteolytic cleavage of influenza virus hemagglutinins: primary structure of the connecting peptide between HA1 and HA2 determines proteolytic cleavability and pathogenicity of Avian influenza viruses. (
  • The activation of certain Toll-like receptors (TLRs), particularly TLR7 and TLR9, induces the production of type I IFNs, and thus primes the host for a Th1 adaptive immune response. (
  • 4 , 5 However, it was unclear from these studies whether neutrophils were among the virus-responsive instigators or only the final effectors of the immune response and tissue pathology. (
  • Toll-like receptors (TLRs) play a key role in the innate immune recognition of many viral pathogens, including influenza virus. (
  • These studies demonstrate neutrophil activation by influenza virus and highlight the importance of TLR7 and TLR8 in that response. (
  • Kuang, E. Viral Evasion of Natural Killer Cell Activation. (
  • It is believed that geminiviral DNA replication is coupled to the cell-cycle regulatory complex of the plant cell and that the virus-early (complementary or C sense) gene products REP and REPA may be able to manipulate the regulation of the cycle. (
  • NKT cell activation results in (a) rapid production of cytokines such as IL-4 and IFN-γ, (b) upregulation of activation markers such as CD69, (c) cell proliferation, and (d) increased cytotoxic capacity ( 6 )( 9 )( 12 ). (
  • This type of hyperinflammatory state is reminiscent of 2 rheumatologic disorders known as macrophage activation syndrome and hemophagocytic lymphohistiocytosis, which are characterized by macrophage and T-cell activation. (
  • An evaluation of 2 cohorts of patients with EVD revealed that a marker of macrophage activation (sCD163) but not T-cell activation (sCD25) was associated with severe and fatal EVD. (
  • SCREEN}, language = {eng}, issn = {1931-3128}, journal = {Cell Host & Microbe}, title = {Recruitment and activation of a lipid kinase by hepatitis C virus NS5A is essential for integrity of the membranous replication compartment. (
  • Activation was strongest for endothelial cell expression of VCAM-1 and ICAM-1. (
  • In contrast, activation of endothelial cell E-selectin expression appeared to be more transient, as indicated by its detection at 3 h, but not at 16 h, of treatment. (
  • Treatment of monocyte culture fluids with anti-tumor necrosis factor alpha (TNF-alpha) antibody largely abolished the activation effect (as measured by endothelial cell expression of ICAM-1), whereas treatment with IL-1beta receptor antagonist had a much smaller inhibitory effect on activation. (
  • Taken together, the results strongly indicate that dengue virus can modulate endothelial cell function by an indirect route, in which a key intermediary is TNF-alpha released from virus-infected monocytes. (
  • Together, therefore, our findings identify a link between ZIKV-mediated TLR3 activation, perturbed cell fate, and a reduction in organoid volume reminiscent of microcephaly. (
  • Here we show that mice with potent virus-specific T-cell responses have reduced levels and delayed formation of neutralizing antibodies, and these mice fail to clear LCMV from extralymphatic epithelia. (
  • Boosting T-cell responses alone may not reduce virus persistence. (
  • and CD28-mediated T cell activation. (
  • Flavivirus-infected cultures exhibited dendritic cell activation and maturation molecules. (
  • Influenza viruses enter the cell inside an endosome. (
  • Many studies suggest a significant role for chronic CD4 + T-cell activation. (
  • Fusion of enveloped viruses with the host cell is a key step in viral infectivity. (
  • We find that more than one latent cell needs to activate in order to observe the data blips, and that the net reproductive number of virus must be very close to one. (
  • We optimized the conditions for T-cell activation and IFN-γ production following direct loading of DRibbles onto PBMCs. (
  • Nef mediates diverse functions including downmodulation of cell surface CD4 and MHC Class I, enhancement of viral infectivity, and enhancement of T cell activation. (
  • When infected, a host cell is forced to rapidly produce thousands of identical copies of the original virus. (
  • Viruses are considered by some biologists to be a life form, because they carry genetic material, reproduce, and evolve through natural selection, although they lack the key characteristics, such as cell structure, that are generally considered necessary criteria for life. (
  • In this fashion, the virus can persist in the cell (and thus the host) indefinitely. (
  • Furthermore, inhibition of NP expression during influenza virus replication led to PKR activation and concomitant increase in eIF2α phosphorylation. (
  • Inhibition of NP expression also led to reduced IRF3 phosphorylation, enhanced IFN β production and concomitant reduction of virus replication. (
  • Retinoic acid inhibits IL-6-dependent but not constitutive STAT3 activation in Epstein-Barr virus-immortalized B lymphocytes. (
  • Dengue virus (DV) is a member of the Flavivirus genus of the Flaviviridae family. (
  • A subset of these is also activated by the closely related varicella zoster virus. (
  • Other hemorrhagic fever viruses, such as Crimean-Congo hemorrhagic fever virus ( 11 ) and dengue virus ( 12 ), have also been reported to trigger HLH. (
  • The innate immune system senses influenza A virus (IAV) through different pathogen-recognition receptors including Toll-like receptor 7 (TLR7). (
  • Given that neuroinflammation contributes to generation and progression of a number of neurodegenerative disorders, these findings have significant implications as they highlight the possibility that influenza and perhaps other non-neurotropic viruses can initiate inflammatory signals via microglia activation in the brain and contribute to, but not necessarily be the primary cause of, neurodegenerative disorders. (