Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six commonly used strains of lymphocytic choriomeningitis virus (LCMV) [Armstrong (Arm) CA 1371, Arm E-350, WE, UBC, Traub and Pasteur C1PV 76001] were examined for distinctive genetic and biological properties. Agarose gel electrophoresis yielded no detectable differences among the L or S RNAs of these six strains. The RNase T1 fingerprint patterns of LCMV Arm CA 1371 and E-350 RNAs were similar, but in contrast, those of the WE, UBC, Traub and Pasteur strains differed from each other and from the pattern of LCMV Arm CA 1371 and E-350. There were also differences among LCMV strains in their biological properties. LCMV Arm CA 1371, E-350 and Pasteur caused severe vasculitis and focal necrotizing hepatitis in the livers of neonatally infected BALB/WEHI mice in contrast to LCMV WE which caused minimal lesions. LCMV Arm CA 1371 and E-350 were lethal for neonatal C3H/St mice. In contrast, LCMV WE, Traub and Pasteur induced persistent infections in C3H/St mice. Adult guinea-pigs resisted infection by Arm CA 1371, E-350, Traub and Pasteur but succumbed to WE and UBC LCMV strains. Our results show a wide variation in the RNA genomes of LCMV strains commonly used in research laboratories, and these genomic differences are accompanied by variations in the biological properties of LCMV strains.
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PMID:Genomic and biological variation among commonly used lymphocytic choriomeningitis virus strains. 687 16

Murine F9 and PCC4 teratoma cells do not express H-2 major transplantation antigens according to virus-specific T-lymphocyte cytotoxic or serological assays. However, such cells can be infected with and readily replicate many types of viruses (coxsackie B 3, mouse hepatitis, Sindbis, Semliki Forest [SFV], lymphocytic choriomeningitis, Pichinde, vesicular stomatitis, herpes simplex type 1) to the same extent as do murine F12 teratoma cells and mouse embryo fibroblasts, all of which express the H-2 determinants. In contrast, F9 and PCC4 cells are not productively infected with murine cytomegalovirus, whereas F12 and mouse embryo fibroblast cells are. In addition to replicating in H-2-negative murine teratoma cells, SFV replicates in H-2-negative murine lymphoblastoid cells. The ability of SFV to infect cells without H-2 antigens and then to effect viral antigenic expression in the cells' cytoplasm and on their surface with similar kinetics and in equivalent amounts as cells with H-2 antigens indicates that the H-2 receptor is not needed for SFV infection. Daudi cells, which lack HLA antigens, block the replication of SFV. This occurs at some point after receptor binding, as demonstrated by diminished viral mRNA. In addition, a possible membrane defect precludes viral exit in Daudi cells transfected with SFV infectious RNA. These results indicate that a cell's possession of H-2 antigens is not a requirement for SFV infection and that major histocompatibility complex antigens are not specific receptors for this virus.
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PMID:Does the major histocompatibility complex serve as a specific receptor for Semliki Forest virus? 737 8

Callitrichid hepatitis is an arenavirus infection that recently emerged as a highly fatal disease of New World primates in the Callitrichidae family. As we previously reported, these primates develop hepatitis after contact with mice that are infected with variants of LCMV (LVMCCH), recently determined to have 86% identity with GC-P gene of the Armstrong and Western strains of LCMV. Here, we describe the histopathological lesions and tissue localization of viral antigens in confirmed cases of callitrichid hepatitis from recent outbreaks in two U.S. zoos. The liver in marmosets and tamarins with fatal infections consistently showed degeneration, necrosis, and inflammation, with variable involvement of the spleen, lymph nodes, adrenal glands, intestine, pancreas, and central nervous system. Lymphocytic choriomeningitis virus antigens were identified immunohistochemically in necrotic foci in these organs as well as in nondegenerating areas in lungs, kidney, urinary bladder, brain, and testes. The multi-organ tropism and histological pattern of LCMV infection in marmosets and tamarins are similar to those reported for the highly virulent arenavirus that causes Lassa fever in humans. Comparative studies of callitrichid hepatitis and Lassa fever would therefore be mutually beneficial for human and nonhuman primate medicine.
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PMID:Pathology and immunohistochemistry of callitrichid hepatitis, an emerging disease of captive New World primates caused by lymphocytic choriomeningitis virus. 748 6

Callitrichid hepatitis is an infection of New World primates caused by an arenavirus, currently referred to as callitrichid hepatitis virus, that is closely related to lymphocytic choriomeningitis virus (LCMV). We have cloned and sequenced the GP-C gene of callitrichid hepatitis virus and found that the cDNA sequence is 84 to 86% identical to those of the GP-C genes of LCMV strains Armstrong and WE, while the deduced amino acid sequence is 95 to 96% identical to those of the GP-C gene products of the same strains. This high degree of similarity indicates that the etiologic agent of callitrichid hepatitis is in fact LCMV. The wide geographic distribution of callitrichid hepatitis outbreaks in the United States serves as a reminder that LCMV is also a human pathogen whose public health implications are not well understood.
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PMID:cDNA sequence analysis confirms that the etiologic agent of callitrichid hepatitis is lymphocytic choriomeningitis virus. 781 20

Different biological materials were tested for murine viral contamination by using the mouse/rat antibody production test. Of 297 tumors examined, 75 (25.3%) were contaminated. Considerable differences in the contamination rate became evident when transplantable tumors from in vitro and from in vivo passages were compared. Of 186 tumors that had been propagated in animals, 36.6% were positive, whereas only 7 of 111 (6.3%) tumors propagated in vitro were contaminated. The highest rate of contamination was detected in mouse tumors. Testing of 135 specimens of mouse origin revealed 46.7% were contaminated, and 57 (70.4%) of 81 samples propagated in mice were positive for murine viruses. Moreover, 6.7% of 90 human tumors that had been passaged in athymic nude mice and 3.5% of 57 rat tumors were positive. Lymphocytic choriomeningitis virus was detected in 4 of 14 hamster tumors. The most frequent contaminant was lactic dehydrogenase elevating virus followed by reovirus 3, lymphocytic choriomeningitis virus, minute virus of mice, mouse hepatitis virus, rat coronaviruses, Kilham rat virus, and Mycoplasma pulmonis. Contamination with reovirus 3 and minute virus of mice was found in 4 (3.7%) of 109 cell lines tested, and 2 of 60 monoclonal antibody preparations or hybridoma cells contained lactic dehydrogenase virus. Contamination with two pathogens was detected in four mouse tumors and in one cell line.
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PMID:Contamination of transplantable tumors, cell lines, and monoclonal antibodies with rodent viruses. 823 Oct 85

B cells from nonimmune mice mediate the cytolysis of fibroblasts infected with the coronavirus, mouse hepatitis virus (MHV), strain A59. In this investigation, we report that splenic B cells and a B cell hybridoma induced the fragmentation of MHV-infected target cell DNA into a nucleosomal ladder pattern, characteristic of apoptosis. To determine the mechanism by which B cells mediated this killing event, we used criteria previously established for the killing of target cells by cytotoxic T lymphocytes (CTLs) and compared this B-cell-mediated killing to lymphocytic choriomeningitis virus (LCMV)-specific CTL killing of LCMV-infected target cells. Unlike CTL-mediated cytotoxicity, B cells efficiently lysed and induced the fragmentation of the DNA in their target cells in the presence of EGTA, arguing against a Ca(2+)-dependent granule exocytosis model for killing. In addition, paraformaldehyde-fixed B cells were able to kill MHV-infected targets. We were unable to detect TNF-alpha-associated cytotoxicity via bioassay with nonimmune effector B cells against the TNF-sensitive cell line, LM, or the TNF-alpha-resistant subline, L929.w, infected with MHV. Serine esterase inhibitors (benzamidine hydrochloride and N alpha-p-tosyl-L-arginine methyl ester) blocked CTL-induced 51Cr release and DNA fragmentation. In contrast, the inhibitors did not block the B-cell-induced 51Cr release, but did cause an inhibition in the fragmentation of the DNA of the target cell. These data indicate that B cells are capable of inducing the lysis and DNA fragmentation of MHV-infected target cells similar to CTL-induced apoptosis. However, we show that the mechanism(s) by which these processes are induced by B cells is distinct from CTL-mediated cytotoxicity.
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PMID:B cells induce apoptosis via a novel mechanism in fibroblasts infected with mouse hepatitis virus. 839 6

Callitrichid hepatitis (CH) is a highly fatal, emerging arenavirus disease of captive South American marmosets and tamarins (Callitrichidae), including the endangered golden lion tamarin. A common-source outbreak of CH in golden lion tamarins and pygmy marmosets at a US zoo resulted from a single feeding of the primates with newborn mice in apparently infected with lymphocytic choriomeningitis virus (LCMV). Isolates from livers of mice and primates were related to isolates from previous CH outbreaks and to laboratory strains of LCMV by serology and nucleic acid hybridization, and 2 surviving animals developed antibody to other LCMVCH isolates and to laboratory strains of LCMV. Thus, LCMV, an arenavirus prevalent in wild mice in the US, can cause sporadic fatal hepatic disease in primates. Exposure of humans to wild or laboratory mice or to marmosets and tamarins that are infected with wild-type strains of LCMV poses the danger of serious disease.
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PMID:A common-source outbreak of callitrichid hepatitis in captive tamarins and marmosets. 845 Feb 60

We have previously demonstrated that hepatitis B virus (HBV) replication and gene expression are abolished in the livers of HBV transgenic mice by cytotoxic T lymphocytes (CTLs) and during lymphocytic choriomeningitis virus (LCMV) infection, stimuli that trigger the production of alpha/beta interferon, gamma interferon, and tumor necrosis factor alpha in the liver. We now report that hepatic HBV replication and gene expression are inhibited by the local induction of these cytokines during adenovirus- and murine cytomegalovirus (MCMV)-induced hepatitis. Further, we show that MCMV also blocks HBV replication and gene expression in the proximal convoluted tubules of the kidney by causing interstitial nephritis and inducing the same cytokines in the renal parenchyma. These results suggest that inflammatory cytokines probably contribute to viral clearance during acute viral hepatitis in humans, and they imply that induction of these cytokines in the liver and other infected tissues of chronically infected patients might have therapeutic value.
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PMID:Inhibition of hepatitis B virus replication during adenovirus and cytomegalovirus infections in transgenic mice. 952 79

House mice (Mus domesticus) were recently introduced to Thevenard Island, off the northwest coast of Western Australia. This island is also habitat for an endangered native rodent, the short-tailed mouse (Leggadina lakedownensis). Concerns have been raised that house mice may pose a threat to L. lakedownensis both through competition and as a source of infection. To assess the threat to L. lakedownensis posed by viral pathogens from M. domesticus, a serological survey was conducted from 1994 to 1996 of both species for evidence of infection with 14 common murine viruses (mouse hepatitis virus, murine cytomegalovirus, lymphocytic choriomeningitis virus, ectromelia virus, mouse adenovirus strains FL and K87, minute virus of mice, mouse parvovirus, reovirus type 3, Sendai virus, Theiler's mouse encephalomyelitis virus, polyoma virus, pneumonia virus of mice, and encephalomyocarditis virus) and Mycoplasma pulmonis. Despite previous evidence that populations of free-living M. domesticus from various locations on the Australian mainland were infected with up to eight viruses, M. domesticus on Thevenard Island were seropositive only to murine cytomegalovirus (MCMV). Antibodies to MCMV were detected in this species at all times of sampling, although seroprevalence varied. Infectious MCMV could be isolated in culture of salivary gland homogenates from seropositive mice. In contrast, L. lakedownensis on Thevenard Island showed no serological evidence of infection with MCMV, any of the other murine viruses, or M. Pulmonis, and no virus could be isolated in culture from salivary gland homogenates. Although MCMV replicated to high titers in experimentally infected inbred BALB/c laboratory mice as expected, it did not replicate in the target organs of experimentally inoculated L. lakedownensis, indicating that the strict host specificity of MCMV may prevent its infection of L. lakedownensis. These results suggest that native mice on Thevenard Island are not at risk of MCMV infection from introduced house mice, and raise interesting questions about the possible selective survival of MCMV in small isolated populations of M. domesticus.
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PMID:Murine viruses in an island population of introduced house mice and endemic short-tailed mice in Western Australia. 1023 57

To study peripheral tolerance of CD8 T cells to a classically MHC-restricted peptide Ag expressed in hepatocytes, ALB1 transgenic (tg) mice expressing the CTL epitope GP33 of the lymphocytic choriomeningitis virus glycoprotein under control of the mouse albumin promoter were generated. ALB1 mice exclusively expressed the GP33 transgene in the liver and, at a 100- to 1000-fold lower level, in the thymus. TCR-tg mice specific for the GP33 epitope were used to directly follow GP33-specific T cells in vivo. These experiments revealed that 1) thymic expression of the GP33 transgene led to incomplete central deletion of TCR-tg cells; and 2) peripheral TCR-tg cells in ALB1 mice ignored the GP33 transgene expressed in hepatocytes. Ignorance of adoptively transferred TCR-tg cells in ALB1 mice was broken by infection with lymphocytic choriomeningitis virus, leading to induction of hepatitis in ALB1, but not in control, mice. Taken together, we have established a novel model of virus-induced CD8 T cell-mediated autoimmune hepatitis in mice and demonstrate that naive CD8 T cells may ignore Ags expressed in the liver.
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PMID:Break of T cell ignorance to a viral antigen in the liver induces hepatitis. 1094 66


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