Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antiviral effects of 6-diazo-5-oxo-L-norleucine (L-DON) on the replication of human parainfluenza virus type 2 (HPIV-2), mumps and vesicular stomatitis viruses were studied. L-DON suppressed growth of these viruses and, in particular, HPIV-2 in four cell types. L-DON was not toxic to the cells at the active dose and did not significantly inhibit cellular macromolecular synthesis. The L-DON-sensitive step of HPIV-2 replication was considered to be relatively early. The NP, P and M proteins were, although at a low level, clearly detectable in HPIV-2-infected Vero cells treated with L-DON, whereas the HN and F proteins were scarcely detected by either immunostaining or immunoprecipitation, indicating that L-DON mainly decreased the amounts of viral glycoproteins. Furthermore, Northern blot hybridization showed that secondary transcription of virus RNA was also inhibited.
J Gen Virol 1990 Jan
PMID:Antiviral effect of 6-diazo-5-oxo-L-norleucine, antagonist of gamma-glutamyl transpeptidase, on replication of human parainfluenza virus type 2. 196 85

Six temperature-sensitive mutants of vesicular stomatitis virus (VSV) were isolated from the central nervous system (CNS) of athymic nude mice. The nude mice had been reconstituted with syngeneic T lymphocytes and then infected with a temperature-sensitive mutant of VSV, tsG31-KS5 VSV, for 20 days. In BHK-21 cells incubated at 38 degrees C, the normal body temperature of mice, all six CNS virus clones had diminished RNA synthesis, when compared to RNA production in BHK-21 cells incubated at 31 degrees C. In contrast, the original tsG31-KS5 VSV mutant synthesized more RNA at 38 degrees C than it did at 31 degrees C. In vitro transcription assays were exploited to discern which viral protein(s) was functionally accountable for the abated synthesis of RNA of the CNS VSV isolates. The ribonucleoprotein complexes from the CNS VSV isolates were disrupted and template (N protein and RNA) and enzyme (L and NS proteins) fractions were purified. In vitro transcription assays were performed with template fractions of the brain isolates, added to enzyme fractions either wild-type wt VSV or tsG31-KS5 VSV, or with template fractions of wt VSV or tsG31-KS5 VSV mixed with enzyme fractions of the CNS isolates. The template fraction was responsible for the decrease in RNA synthesis in all six of the brain-isolated clones. When the template fractions of wt or tsG31-KS5 VSV were mixed with enzyme fractions of all the CNS-derived VSV, except BP5A VSV, leader sequence RNA and large Mr transcripts were transcribed. One clone, BP5A VSV, did not synthesize RNA when mixed with either template or enzyme of wt VSV, and probably had more than one functional mutation that influenced viral RNA synthesis.
J Gen Virol 1990 Jan
PMID:The nucleocapsid protein of vesicular stomatitis virus isolated from the brains of nude mice is responsible for abated viral RNA synthesis at the normal body temperature of mice. 215 37

An activity found in bovine brain microtubule-associated proteins (MAPs) which stimulated vesicular stomatitis virus (VSV) transcription in vitro co-eluted from a gel filtration column (Sepharose CL-6B) with a minor MAP subset of an apparent Mr of 100,000 to 250,000. The activity did not appear to be closely associated with MAPs 1, MAPs 2, tau or tubulin. Anti-MAPs 1 and anti-MAPs 2 IgG did not reduce or abolish the stimulatory activity. The bovine brain MAPs stimulatory activity was similar to that found in HeLa cell extracts: both were heat-resistant, and both co-purified with the MAPs fraction of cell extracts; also amounts of each which gave maximum stimulation when used separately did not give additional stimulation when combined. Fractions from the Sepharose CL-6B column that contained the greatest amount of stimulatory activity exhibited little or no cAMP-dependent or -independent kinase activity. The MAPs stimulatory activity required the presence of both L and NS polymerase subunits.
J Gen Virol 1990 Feb
PMID:A minor microtubule-associated protein is responsible for the stimulation of vesicular stomatitis virus transcription in vitro. 215 85

The pH dependence of early steps in the infection of human and other cells by mammalian retroviruses and retroviral pseudotype particles of vesicular stomatitis virus (VSV) was investigated for 10 strains of retrovirus, including C-type and D-type oncoviruses and human lentiviruses. When cells were treated with weak bases (NH4Cl and amantadine) to raise the pH of endocytic vesicles, only ecotropic murine leukaemia virus (MLV-E) and VSV showed pH-dependent entry. Pretreatment of retrovirus stocks in media below pH 5.0 did not reduce their titres but inactivated VSV to less than 10(-8) of the initial titre. VSV (MLV-E) pseudotype infection in five out of six mouse and rat cell lines was inhibited by NH4Cl, indicating that infection proceeds via receptor-mediated endocytosis. In contrast, NH4Cl treatment has no effect on the infection of XC cells in which MLV-E induces syncytia. It is postulated that the pH-independent entry and cell fusion of XC cells by MLV-E may result from the activity of a cell surface proteinase that cleaves viral gp70 at neutral pH.
J Gen Virol 1990 Apr
PMID:The pH independence of mammalian retrovirus infection. 215 95

TsO82, a spontaneous temperature-sensitive (ts) mutant of vesicular stomatitis virus (VSV) isolated in chick embryo fibroblasts (CEFs), complements the five prototype ts mutants of the virus. The data presented here indicate that the defect in tsO82 is localized in the M gene. The mutation changed a methionine to an arginine at position 51 of the M protein. Only true revertants could be isolated, and their frequency was low, perhaps due to the type of substitution required to return to the wild-type phenotype. TsO82 does not exhibit hypertranscription, in contrast to the data reported for all of the other ts mutants affected in the M protein. Moreover, tsO82 is conditionally ts, since it grows normally in BHK-21 cells at all temperatures. It exhibits no c.p.e. at the non-permissive temperature in CEFs. Our data argue for multiple functions of the M protein of VSV, the domain affected by the tsO82 mutation possibly being implicated both in the shut-off of cellular RNA synthesis, and for the recognition of a cellular factor required for efficient viral RNA synthesis.
J Gen Virol 1990 Apr
PMID:Genetic evidence for multiple functions of the matrix protein of vesicular stomatitis virus. 215 8

The large (L) protein subunit of unsegmented negative-strand RNA virus polymerases is thought to be responsible for the majority of enzymic activities involved in viral transcription and replication. In order to gain insight into this multifunctional role we compared the deduced amino acid sequences of five L proteins of rhabdoviruses (vesicular stomatitis virus and rabies virus) or paramyxoviruses (Sendai virus, Newcastle disease virus and measles virus). Statistical analysis showed that they share an atypical amino acid usage, outlining the uniqueness of the negative-strand virus life style. Similarity studies between L proteins traced evolutionary relationships in partial disagreement with the present taxonomic arrangement of this group of viruses. The five L proteins exhibit a high degree of homology along most of their length, with strongly invariant amino acids embedded in conserved blocks separated by variable regions, suggesting a structure of concatenated functional domains. The most highly conserved central block contains the probable active site for RNA synthesis. We tentatively identified some other functional sites, distributed around this central core, that would naturally work together to assure the polymerase activity. This provides detailed guidelines for the future study of L proteins by site-directed mutagenesis.
J Gen Virol 1990 May
PMID:Sequence comparison of five polymerases (L proteins) of unsegmented negative-strand RNA viruses: theoretical assignment of functional domains. 216 Oct 49

Prostaglandin A (PGA) exhibits antiviral activity against RNA and DNA viruses. The effect of PGA1 on vesicular stomatitis virus (VSV) was investigated. When VSV-infected L-1210 cells were kept in the presence of PGA1 the amount of all five viral proteins and their respective mRNAs was dose-dependently decreased. To determine whether the effect was on viral transcription or translation, the temperature-sensitive VSV mutant tsG 41 was employed. This is a good model system for the investigation of primary transcription; at the restrictive temperature of 39 degrees C, tsG 41 is unable to replicate but can transcribe viral mRNA. Mutant mRNA synthesis was strongly inhibited by PGA1 at this temperature, indicating that the major effect is on primary transcription. This conclusion is supported by data demonstrating that in vitro transcription of viral genomic RNA was also inhibited by PGA1.
J Gen Virol 1990 Dec
PMID:Inhibition of primary transcription of vesicular stomatitis virus by prostaglandin A1. 217 81

Theiler's murine encephalomyelitis virus (TMEV) induces demyelinating disease which is associated with persistent virus infection of the central nervous system. To study the interaction between TMEV and host cells, we infected the G26-20 glioma cell line in vitro, and this resulted in a lytic infection in which most, but not all, cells were killed. Surviving cells divided and formed a viable monolayer in which a small proportion of cells displayed viral cytopathic effects. Levels of virus produced by these cultures over a 6 month period fluctuated between 6 and 8 log10 p.f.u./ml as measured by viral plaque assay. Similarly, the percentage of cells producing both viral antigen and viral RNA, as measured by a simultaneous immunoperoxidase/in situ hybridization technique, varied between 5 and 30%. Although persistently infected cultures were susceptible to challenge by both vesicular stomatitis virus and herpes simplex virus, they were resistant to infection by homologous viruses. Interferon activity was not identified. TMEV isolated from passage 12 produced smaller plaques than wild-type Daniels strain virus (wt-DAV) on L-2 cell monolayers. In contrast to demyelination induced in SJL/J mice after intracerebral inoculation with wt-DAV, mice infected with the small plaque variant virus failed to develop viral persistence or chronic demyelination. However, following immunosuppression by total body irradiation, SJL/J mice infected with the small plaque variant developed viral persistence but no demyelination. Characterization of the biochemical and molecular determinants of the variant will lead to a better understanding of determinants important in viral persistence.
J Gen Virol 1990 Sep
PMID:Persistent infection of a glioma cell line generates a Theiler's virus variant which fails to induce demyelinating disease in SJL/J mice. 221 94

To quantify the antiviral effect of interferon (IFN) we applied a mixture of two horseradish peroxidase-labelled monoclonal antibodies, specific for the E1 glycoprotein of Semliki Forest virus, in a direct enzyme immunoassay. This assay is suitable for detection of virus replication in L-cells, seeded as monolayers in 96-well plates. Inhibition of absorbance values caused by IFN was determined in a Flow Titertek Multiskan. Three IFN samples from different sources were titrated simultaneously in the enzyme immunoassay and in the vesicular stomatitis virus plaque reduction test in five consecutive experiments. Titres were calculated as the inverse value of the dilution of IFN causing 25% inhibition of absorbance values and 50% reduction of plaque counts respectively. The results show equality of precision and reproducibility between and within the two assays. However, the enzyme immunoassay is more convenient and objective than the plaque reduction assay.
J Gen Virol 1985 Jun
PMID:Enzyme immunoassay of interferon with peroxidase-labelled virus-specific monoclonal antibodies. 240 24

Antiviral effects of prostaglandins of the A series (PGAs) on Sendai, vaccinia and vesicular stomatitis viruses have previously been reported and a relationship between the antiviral actions of PGAs and interferons has been suggested. We have investigated the antiviral activity of PGAs on encephalomyocarditis (EMC) virus. Using single-cycle assays of virus replication our results indicate that PGAs only inhibit when present in the culture medium after the cells are infected, and that they are most effective during incubation periods including from 3 to 5 h post-infection. Furthermore, viral RNA synthesis is blocked in infected cells treated with PGA and, as a result, viral antigens are greatly reduced in the cytoplasm of the cells 5 h post-infection. Since the antiviral effect of PGAs is unperturbed by actinomycin D, when cellular RNA synthesis is greatly reduced, it appears unlikely that induction of new cellular proteins is the reason for the antiviral activity of PGAs. In separate experiments we were unable to demonstrate directly the induction of interferon, or of the two dsRNA-dependent enzymes, 2',5'-oligoadenylate synthetase and protein kinase, which are greatly increased in interferon-treated cells. Thus, we conclude that the antiviral activity of PGAs is unrelated to the antiviral action of interferons and involves a unique mechanism independent of cellular protein synthesis.
J Gen Virol 1985 Nov
PMID:Antiviral activity of prostaglandin A on encephalomyocarditis virus-infected cells: a unique effect unrelated to interferon. 241 95


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