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 studies show that Shope fibroma virus facilitates replication of vesicular stomatitis virus (VSV) in some rabbit cells grown in vitro. In the present investigation, the possibility that these two viruses can also interact in vivo was determined. Rabbits inoculated intradermally with both viruses together, or each separately, were examined for the formation of lesions or tumors and for the production of infectious virus. The presence of VSV interfered with tumorigenesis by Shope fibroma virus. In tumors already formed, production of infectious VSV was greater than in normal skin. Hence, each virus affected the other. Sera and tissues of normal rabbits were found to contain a substance which inhibits VSV; this may act to limit replication of VSV in rabbit skin. In addition, cultured rabbit skin cells appeared to adsorb VSV inefficiently. When persistently infected by Shope fibroma virus, however, adsorption of VSV was markedly improved. Our results suggest that in vivo Shope fibroma virus may facilitate adsorption of VSV to reduce the effect of a natural inhibitor and consequently enhance production of infectious virus.
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PMID:Replication of vesicular stomatitis virus facilitated by Shope fibroma virus in vivo. 22 73

Shope fibroma virus establishes a persistent cytoplasmic infection in primary (RK) and serially cultivated (DRK(3)) rabbit kidney cells which is accompanied by a morphological alteration of the cells. The response of such cells to superinfection by other viruses was compared with that of control cells by determining plaque production and virus yield of superinfecting viruses. It was found that the growth of other poxviruses, myxoma and vaccinia, was greatly inhibited in the fibroma virus-infected cells, but that of pseudorabies and herpes simplex viruses, which are unrelated deoxyribonucleic acid viruses, was virtually unaffected. The ribonucleic acid (RNA) viruses, poliovirus 1 and coxsackievirus B1, did not produce plaques on either RK or fibroma virus-infected (F-RK) monolayers. However, the growth of several other RNA viruses, vesicular stomatitis virus, encephalomyocarditis virus, Sindbis virus, and Newcastle disease virus, was enhanced in F-RK cells. None of these latter RNA viruses produced any infectious progeny in DRK(3) cells, but they all plaqued on and produced good yields in DRK(3) cells persistently infected with fibroma virus. This phenomenon is termed facilitation. Facilitation results from the infection of DRK(3) cells by fibroma virus. Neither interference nor facilitation were due to changes in the adsorption or eclipse of the superinfecting virus.
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PMID:Effect of persistent fibroma virus infection on susceptibility of cells to other viruses. 431 46