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)

Ammonium 5-tungsto-2-antimoniate (HPA 23) protected micr partially or completely against two strains of encephalomyocarditis (EMC) virus and one strain of vesicular stomatitis (VSV) virus. The best protective effect was obtained with EMC strain VR 129 and VSV when a single i.p. injection of HPA 23 was administered shortly before virus inoculation. Mice protected by HPA 23 against EMC strain VR129 had virus titres in the blood and brain similar to those in untreated mice. A synergism between interferon and HPA 23 was observed in mice infected with EMC VR129. Our results demonstrate the in vivo activity of HPA 23 against two lethal viral infections and suggest that, at least in mice infected with EMC, death may not be related solely to virus multiplication.
J Gen Virol 1976 Apr
PMID:Effect of ammonium 5-tungsto-2-antimoniate on encephalomyocarditis and vesicular stomatitis virus infections in mice. 17 29

Preparations of human fibroblast and leukocyte interferons of similar potency show markedly different dose-response curves in an assay which measures the degree of protection of tissue cultures against virus c.p.e. The effect is observed with both vesicular stomatitis virus (VSV) and Mengovirus, and is not altered by purification of the interferons.
J Gen Virol 1976 May
PMID:Human fibroblast and leukocyte interferons show different dose-response curves in assay of cell protection. 18 Feb 44

Serial high multiplicity passage of a cloned stock of vesicular stomatitis virus was found to generate defective interfering particles containing three size classes of RNA, with sedimentaiton coefficients of 31 S, 23 S and 19 S. The 31 S and 23 S RNA species were found to be complementary to both the 12 to 18 S and 31 S size classes of VSV mRNAs. The 19 S class of RNA was found to be partially base-paired. All three RNA species were found to contain ppAp at their 5' termini.
J Gen Virol 1976 Oct
PMID:Analysis of the RNA species isolated from defective particles of vesicular stomatitis virus. 18 28

The anticellular and antiviral effects of human leukocyte interferons were studied in vitro in the transformed human embryonic cell lines. RSa and RSb. The growth of these cells was inhibited and they began to deteriorate about 48 h after treatment with 500 units/ml of interferon. When interferon was washed out within 48 h, their growth recovered gradually. The effects of interferon on cell growth depended on the amount of interferon added per cell. A subline, named IFr, was isolated which grows in the presence of 2000 units/ml of interferon, whereas growth of vesicular stomatitis virus in these cells is suppressed by 10 units/ml of interferon, just as in the parent cells. The anticellular and antiviral effects of interferon on IFr cells are discussed in relation to cell surface receptors.
J Gen Virol 1976 Oct
PMID:Effects of interferon on cell and virus growth in transformed human cell lines. 18 29

Virus-induced RNA synthesis was studied in BHK 21 cells persistently infected with vesicular stomatitis virus (VSV) and rabies virus by labelling RNA synthesized in the presence of antinomycin D. During persistent infection the species of messenger RNA synthesized were similar in size and relative proportions to those seen during acute infection, but there were some minor differences. Full-sized B virion RNA was generally not detected during persistent infection, and new species (probably DI virion RNA) appeared.
J Gen Virol 1976 Nov
PMID:RNA synthesis in BHK 21 cells persistently infected with vesicular stomatitis virus and rabies virus. 18 60

Homologous interference between a temperature-sensitive small plaque mutant (HVJ-pB) derived from an HVJ (haemagglutinating virus of Japan - the Sendai strain of parainfluenza I virus) carrier culture of BHK cells and the original wild-type virus (HVJ-W) has been investigated. Prior infection of LLCMK2, HeLa, BHK or mouse L cells with HVJ-pB, both at permissive and non-permissive temperatures, for 24 h resulted in a reduced yield of superinfecting HVJ-W, reflecting a smaller number of cells capable of producing the superinfecting virus. However, HVJ-pB did not interfere with the replication of vesicular stomatitis virus, Sindbis virus or Newcastle disease virus. Interference in this system seems to be due to inhibition of the attachment of superinfecting HVJ-W as a result of intracellular mechanisms operating at a late stage in the replication of the interfering virus. There is also blocking or destruction of cellular receptors by extra-cellular particles of the interfering virus. Protein synthesis coded for by the complete virus genome is required to establish and maintain the interference, and treatment with actinomycin D has no effect on the interference phenomenon.
J Gen Virol 1976 Nov
PMID:Homologous interference induced by a temperature-sensitive mutant derived from an HVJ (Sendai virus) carrier culture. 18 64

The L, N and M proteins of vesicular stomatitis virus (VSV) were resolved from each other by gel filtration in the presence of 6 m-guanidine hydrochloride. Amino acid analysis for purified M protein of VSV showed that its chemical composition differed from those of influenza and SV5 M proteins.
J Gen Virol 1976 Dec
PMID:Isolation of the matrix (membrane) protein of vesicular stomatitis virus by gel filtration in guanidine hydrochloride. 18 28

Recent studies on the mechanism by which the virion-associated RNA polymerase of vesicular stomatitis virus transcribes RNA have revealed several new biological features of general interest. The mode of synthesis of the 5'-terminal cap structure of the mRNAs, the sequential transcription of the genes and the presence of a transcribed "leader" RNA segment are properties which are either not shown by other viruses, or have not yet been described. These features are probably inter-related with the primary transcription process, which itself may be a useful model for future studies on mRNA biosynthesis in eukaryotic systems.
J Gen Virol 1977 Jan
PMID:Vesicular stomatitis virus: mode of transcription. 18 75

Addition of concanavalin A to BHK cell monolayers infected with vesicular stomatitis virus prevented the formation of mature virus particles. In these cells the virus glycoprotein (G) was inserted into the plasma membrane and the protein that is in close association with the ribonucleic acid, protein N, was found in the cytoplasm. At times when cells infected in the absence of the lectin were liberating virus into the supernatant medium, the M or matrix protein was found in association with the plasma membrane of the lectin-treated cells. The removal of the lectin from the cells with alpha-methyl-D-glucoside 3 h after infection was followed by the immediate release of mature virus particles. The rate of virus release from these cells was the same as that from cells infected in the absence of the lectin. Addition of cycloheximide, and inhibitor of protein synthesis, immediately after alpha-methyl-D-glucoside treatment of the cells did not alter the rate of virus production, suggesting that the proteins required for virus synthesis were available in the lectin-treated cells and that virus assembly took place without further protein synthesis on removal of the lectin.
J Gen Virol 1977 Feb
PMID:Effect of concanavalin A on vesicular stomatitis virus maturation. 19 Mar 44

The role of sialic acid in the infection of tissue culture cells and mice with vesicular stomatitis virus has been studied. No loss of infectivity of the Indiana serotype of the virus was detected by incubating with neuraminidase although the virus particles had lost sialic acid as judged by their ability to inhibit the agglutination of red blood cells by influenza virus. The results did not depend on the type of cell used for growth and assay of the virus since essentially similar findings were made in BHK cells, L cells or mice. Similar results were obtained with Brazil virus, a subtype of the Indiana serotype and with the New Jersey serotype. We consider that the sialic acid of the virus which is removed by neuraminidase does not play a major role in the infectivity of the virus.
J Gen Virol 1977 Apr
PMID:Role of sialic acid in infection with vesicular stomatitis virus. 19 44


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