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)

Rabies virion-associated transcriptase activity was investigated in vitro and compared with that of the New Jersey serotype of vesicular stomatitis virus. The concentration of detergent that affected [3H]GMP incoporation into acid-insoluble material was significantly different for both viruses. Vesicular stomatitis virus New Jersey required 0.05 to 0.1% nonionic detergent, whereas rabies virion could not be fully activated unless 4 to 5% detergent was used. Other optimal conditions were as follows: 40 mM NaCl, 5 mM Mg2+, 40 mM Tris-hydrochloride (pH 7.4), 5 mM dithiothreitol, and 30 degrees C. The reaction required four nucleoside triphosphates. The initial rate of RNA synthesis by rabies virion enzyme was 140 pmol of GMP incorporated/mg of viral protein per h and linearly increased until about 8 h, with a slight initial lag phase. The enzyme activity that correlated with the content of L protein was highest when rabies virions were grown at 33 degrees C. The product was single-stranded RNA, which was complementary in base sequences to rabies viral RNA. Most of the RNA synthesized sedimented at 6-16S.
J Virol 1977 Dec
PMID:Transcriptase activity associated with rabies virion. 2 66

The virulence of temperature-sensitive mutants of vesicular stomatitis virus (VSV) injected subcutaneously into newborn hamsters was positively correlated with their tendency to generate revertants and with their leakiness in cultured hamster embryo fibroblasts maintained at 37 degrees C, the measured body temperature of the animals under our experimental conditions. The complementation group of the mutants seemed important only in that it tended to determine reversion frequency and leakiness. One non-reverting group I mutant (T1026), however, was much less virulent than would be expected from its extreme leakiness at body temperature. The disease produced by the less virulent mutants was characterized by neurological symptoms and led to delayed death, unlike the rapid deatth produced by virulent mutants. Infectious virus could be found in higher titres in the brains than in peripheral organs of such animals (with ratios as high as 10(8)). This neurotropism was not correlated with the complementation group of the mutant but was shown to be the consequence of survival for more than 3 days after injection. Age was not responsible for the effect. Animals injected at birth with T1026 were completely resistant to subcutaneous superinfection with the highly virulent wildtype virus HR at 3 to 4 days, though non-T1026-protected animals were completely sensitive. When HR was injected intracerebrally at 3 to 4 days, the T1026-protected animals allowed replication to high titres in the brain but not in peripheral organs, whereas non-T1026-protected animals allowed replication to high titres in both brain and in peripheral organs. We suggest from these results that the observed neurotropism is produced by a resistance mechanism operative in peripheral organs but not in the brain; this resistance develops rapidly in newborn animals on exposure to virus and clears virus from the peripheral organs leaving it in the brain. It is possible that our effect represents a controlled and accelerated induction of the classical peripheral resistance of animals to various viruses which normally develops with age.
J Gen Virol 1975 Dec
PMID:On the mechanism of neurotropism of vesicular stomatitis virus in newborn hamsters. Studies with temperature-sensitive mutants. 17 95

An interaction between sarcoma-180/TG cells and vesicular stomatitis virus in adult mice resulted in the rapid onset of extensive mortality. This interaction, termed lethal synergy, occurred only at early stages of ascites induction in animals with no prior virus contact. A significant sparing effect conferred by the serotonin antagonist dibenamine was reversed by the administration of serotonin. The cause of death was not determined, but a mechanism involving hypersensitivity is indicated.
Proc Soc Exp Biol Med 1975 Dec
PMID:Lethal synergy between sarcoma-180/TG cells and vesicular stomatitis virus in mice. 17 41

The association of vesicular stomatitis virus proteins with intracellular and plasma membranes was examined by pulse and pulse-chase labeling of virus-infected HeLa cells with [35S]methionine and separation of cell homogenates into three major membrane fractions in discontinuous sucrose gradients. The glycoprotein G was primarily associated with rough endoplasmic reticulum-like membranes after short radioactive pulses (2 to 4 min) but accumulated in the plasma membrane-enriched fraction and the smooth internal membrane fraction with longer pulse or chase periods. The nucleocapsid protein N and the matrix protein M accumulated in the rough endoplasmic reticulum and plasma membrane-like fractions but not in the smooth internal membrane fraction. Only a fraction (35 to 40%) of the viral protein synthesized during a short pulse in the mid-cycle of infection was apparently utilized in released virus. The newly synthesized virus proteins first appeared in released virus in the order: M, N and L, and G.
J Virol 1976 Dec
PMID:Association of vesicular stomatitis virus proteins with HeLa cell membranes and released virus. 18 39

Glycosylation of the envelope glycoprotein of vesicular stomatitis virus was examined using virus-infected HeLa cells that were pulse-labeled with radioactive sugar precursors. The intracellular sites of glycosylation and the stepwise elongation of the carbohydrate side chains of the G protein were monitored by membrane fractionation and gel filtration of Pronase-digested glycopeptides. The results with short pulses of sugar label (5 to 10 mtein linkage (glucosamine and mannose) are added to G which was associated with the rough endoplasmic reticulum-enriched membrane fraction, whereas the more distal sugars (galactose, sialic acid, fucose, and possibly more glucosamine) are added in the light-density internal membrane fraction. Accumulation of mature G was observed in the plasma membrane-enriched fraction. The gel filtration studies indicated that the initial glycosylation event may be the en bloc addition of a mannose and glucosamine oligomer, followed by the stepwise addition of the more distal sugars.
J Virol 1976 Dec
PMID:Glycosylation of vesicular stomatitis virus glycoprotein in virus-infected HeLa cells. 18 40

The membrane-impermeable reagent trinitrobenzenesulfonate has been shown to react only with the surface components of vesicular stomatitis virus (VSV) membranes. When the amount of phosphatidylethanolamine (PE) available to modification by trinitrobenzenesulfonate in intact virions was determined, it was found that 36% of the total membrane PE was converted to the trinitrophenyl derivative. The same proportion of the total membrane PE was reactive after removal of the surface glycoprotein by trypsin digestion, but disruption of the virus membrane by sonication rendered all of the PE reactive. These results indicate that PE is asymmetrically distributed in the VSV membrane; 36% is present in the outer lipid leaflet, whereas 64% is found on the inner layer.
J Virol 1976 Dec
PMID:Asymmetric distribution of phosphatidylethanolamine in the membrane of vesicular stomatitis virus. 18 41

Previous studies on vesicular stomatitis virus (VSV) maturation in infected cells have utilized in vitro cell cultures. The present study is, to our knowledge, the first in vivo analysis of VSV-cell interaction in the central nervous system of weaning outbred Swiss mice. Intracerebral inoculation of wild-type VSV resulted in rapid viral replication in brain and spinal cord. By immunoflourescence, viral antigens were first seen in ependymal cells of brain and spinal cord and soon thereafter in surrounding neurons. The large anterior horn neurons of spinal cord appeared to be in the most heavily infected. Ultrastructurally, VSV-neuron interaction evolved in three phases. The first phase consisted of viral entry into the cell by fusion and viropexis. The second phase was characterized by nucleocapsid accumulation and resulted in the appearance of large cytoplasmic inclusions. The third phase was maturation and release from the infected cell and was accomplished by viral budding from plasma membranes. Degenerative changes in infected neurons were generally absent. Cells in the area of the central canal seemed to present a different pattern of virus-cell interaction especially at the level of maturation and release. Some of these cells in advanced stages of degeneration showed viral particles free in nucleocapsid material with no virus-membrane association. Viral budding was not observed and, because these cells do eventually die, it is possible that virus was released in the intercellular space at the moment of cellular disruption. These results suggest that VSV-cell interactions may vary depending upon the nature of the infected cells.
Lab Invest 1976 Dec
PMID:In vivo assembly and maturation of vesicular stomatitis virus. 18 63

The effect of hydrocortisone on bovine interferon production in vitro was studied. Infectious bovine rhinotracheitis virus was used as an inducer. Interferon was assayed by the plaque-reduction method in bovine fetal kidney cultures, using vesicular stomatitis virus as challenge virus. Hydrocortisone decreased interferon production in bovine fetal spleen and peripheral blood leukocyte cultures. Hydrocortisone did not decrease interferon production by bovine alveolar macrophages, in 1 experiment. Properties of viral inhibitors were those of interferon.
Am J Vet Res 1976 Dec
PMID:In vitro interferon production by bovine tissues: effects of hydrocortisone. 18 92

The interferon-inducing ability of infectious bovine rhinotracheitis (IBR) virus was determined in tissue cultures of bovine origin inoculated with untreated and ultraviolet (UV) irradiated IBR viruses. Interferon was assayed by the plaque-reduction method in bovine fetal kidney (BFK) cell cultures, using vesicular stomatitis virus as challenge virus. Highest interferon concentrations were produced by cultures of bovine fetal (BF) spleen cells and aveolar macrophage cultures derived from adult cattle. Moderate interferon concentrations were produced by peripheral blood leukocyte (PBL) suspension cultures from adult cattle with serum-neutralizing antibodies against IBR virus. Cultures of PBL from 1 cow without detectable serum-neutralizing antibodies against IBR virus did not produce detectable interferon in response to IBR virus. Cultures of PBL from cattle with or without detectable serum-neutralizing antibodies against IBR virus produced interferon when stimulated with phytohemagglutinin (PHA). Low levles of viral inhibitors were detected infrequently in monolayer cultures of BFK and BF nasal mucosa inoculated with UV-irradiated IBR virus and in BF tracheal organ cultures inoculated with untreated IBR virus. Interferon was not detected in fluids collected from IBR virus-exposed monolayer cultures of primary and secondary BF lung, secondary BF tracheal mucosa, secondary BF liver, secondary BF adrenal, and PBL in the 4th and 7th passages. The antiviral inhibitors from BF spleen, bovine alveolar macrophage, and PBL cultures induced with IBR virus, as well as inhibitors from PBL cultures induced with PHA, had the usual properties of interferon.
Am J Vet Res 1976 Dec
PMID:In vitro interferon production by bovine tissues: induction with infectious bovine rhinotracheitis virus. 18 93

Vesicular stomatitis virus forms discrete, microscopic plaques in stationary cultures of the WISH amnion cell line. Microplaque formation is rapid, reproducible, and easily quantitated, occurs at temperatures ranging from 33 to 40 degrees C, and does not require a semisolid overlay. WISH cells, however, are less sensitive to vesicular stomatitis virus than are chicken embryo, 3T6, or Vero cells. WISH amnion cells also are highly sensitive to the antiviral effects of human interferon, and a quantitative human interferon assay, based on vesicular stomatitis virus plaque reduction in WISH cells, is described. This interferon assay can be performed within 1 day, uses a liquid overlay medium, does not require a vital stain, is as sensitive as other methods that use diploid cell strains, and is performed in a microtiter system.
J Clin Microbiol 1976 Dec
PMID:Vesicular stomatitis virus plaque production in monolayer cultures with liquid overlay medium: description and adaptation to a one-day, human interferon-plaque. 18 19


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