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)

Previous work in our laboratory has demonstrated that only certain temperature-sensitive (ts) mutants of vesicular stomatitis virus (VSV) appear capable of producing central nervous system (CNS) infection in a mouse model system. Considerable effort has been devoted to studies directed at unraveling the mechanisms underlying host virulence with these tsVSV mutants. With the previous demonstration that certain neuropeptides, capable of lowering body temperature, alter avirulent into virulent infection, we explored the role of one of these neuropeptides, bombesin, in CNS infection induced by normally avirulent tsG11 VSV, as well as certain tsVSV mutants derived from persistently infected (pi) carrier cultures. Our observations indicate that bombesin dramatically alters CNS infection with either tsG11 VSV as well as tsVSV mutants derived from persistent carrier cultures. When virus alone was inoculated intracerebrally, no sign of illness was observed and no animal died. When bombesin was injected along with normally avirulent tsG11 VSV, or glioma derived tsG31 VSV, 50% of mice died within 6-8 days after inoculation. Moreover, mice infected with virus and neuropeptide demonstrated striking pathological alterations in the CNS. These studies are in agreement with previously published results from others as well as our own laboratory and strongly suggest a direct correlation between CNS temperature and the capacity of certain tsVSV mutants to induce clinical and pathological disease.
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PMID:Altered neurovirulence of temperature-sensitive vesicular stomatitis virus mutants in a murine model by inoculation of bombesin: a neuropeptide. I. Clinical, virological and pathological observations. 253 76

A single injection of the hypothermia-inducing neuropeptide bombesin resulted in an excellent recovery system for reisolating viruses from Swiss albino mice infected with vesicular stomatitis virus even up to 90 days after infection. The virus was recovered from a cell homogenate prepared from whole brain tissue 24 h after intracerebral injection of bombesin; brain cells were cocultivated with BHK-21 cell monolayers and then plaqued on BHK-21 cells at 31 degrees C. All of the recovered viruses were identified as vesicular stomatitis virus by antibody neutralization and peptide analyses of some of the structural proteins. However, some of the recovered viruses were altered with regard to tryptic peptide maps, temperature sensitivity, and central nervous system disease induced compared with the viruses used to initiate the infection. Most of the recovered viruses induced a similar disease when reinoculated intracerebrally into mice, characterized by hind-leg paralysis 4 to 6 days after infection. Two of the recovered viruses were lethal, however, resulting in a relatively rapid generalized wasting disease and death in 3 to 4 days.
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PMID:Hypothermia-inducing peptide promotes recovery of vesicular stomatitis virus from persistent animal infections. 298 89