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 immunosuppressive effect of Cyclosporin A on T-cell-mediated antiviral immune responses was examined. When administered intraperitoneally CS-A abrogated anti-vaccinia virus, anti-lymphocytic choriomeningitis virus (LCMV), and anti-vesicular stomatitis virus (VSV) T-cell responses in a dose-dependent fashion. Usually 50-60 mg/kg were efficient in suppressing primary T-cell responses completely. In contrast, 10-20 mg/kg often enhanced T-cell responses significantly when compared with controls. Suppression was observed if CS-A treatment was started before virus injection and up to 12 hr after infection; CS-A given 24 hr after the virus still suppressed T-cell activity partially. A 50 mg/kg dose of CS-A suppressed secondary anti-vaccinia virus or anti-VSV T-cell responses in vivo by a factor of about 10. This dose suppressed the primary T-cell-dependent footpad swelling induced by local LCMV infection and prevented T-cell-mediated immunopathological death due to LCM when LCMV was injected intracerebrally. In addition, clearance of LCMV was delayed drastically by CS-A treatment. When added to cultures of in vivo-primed antiviral T cells that were restimulated in vitro, CS-A inhibited both proliferation as well as generation of virus-specific cytotoxic T cells in a dose-dependent way. The results show that in CS-A-treated mice primary and secondary antiviral T-cell responses are strongly inhibited; acute viral infections with cytopathic viruses may therefore be more dramatic. In contrast immunopathological T-cell-mediated disease caused by noncytopathic viruses such as LCMV may be prevented or attenuated.
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PMID:Suppression by cyclosporin A of murine T-cell-mediated immunity against viruses in vivo and in vitro. 298 41

Large numbers of VSV (LCMV) pseudotypes with the genomes of vesicular stomatitis virus (VSV) and the coat proteins of lymphocytic choriomeningitis virus (LCMV) were produced by infecting L cells first with LCMV and subsequently with VSV, the latter in the presence of tunicamycin. Separation by gradient centrifugation from the concomitantly produced LCMV genotypes, followed by polyacrylamide gel electrophoresis (PAGE), failed to reveal measurable quantities of the one glycoprotein ("G") of VSV. By serologic analysis it could be shown that anti-VSV antibody still attached, although with low efficiency. VSV (LCMV) retained its infectivity during purification. Reversal of the sequence of infection under otherwise identical conditions led to the formation of LCMV (VSV) pseudotypes. When separated from VSV genotypes, PAGE did not disclose glycoproteins of LCMV, and serologic analysis failed to detect attachment of anti-LCM virus antibody. LCMV (VSV) lost its infectivity during purification.
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PMID:Lymphocytic choriomeningitis virus. VIII. Reciprocal formation of pseudotypes with vesicular stomatitis virus. 608 20