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 production and effect of interferon in the virus-transformed cell line TGk1, originating from kidney cells of Testudo gracea were studied and compared to those in the primary cell culture. West Nile virus and Newcastle disease virus were used as inducers. Interferon production in TGk1 cells began 6 hr later than in the primary cell culture and reached the maximum 64 IU, 18 hr after virus inoculation. In the primary culture, interferon production increased till the 48th hr reaching a fourfold level (256 IU). A significant reduction of the antiviral effect of interferon against vesicular stomatitis virus but not against vaccinia virus was observed in the transformed cells. The decreased interferon production and effect in TGk1 cells is regarded as a consequence of the disturbance of the interferon regulatory mechanism taking place as a result of the virus-induced transformation.
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PMID:Interferon induction and action in transformed poikilothermic cells. 16 42

Treatment of L cells with 3 to 10 mM 3':5'-cyclic adenosine monophosphate (cAMP) in the presence of interferon was found to potentiate the development of antiviral activity. The dose response of interferon activity at various time periods in the presence and absence of cAMP indicated that potentiation of interferon activity by cAMP occurred at an early stage in the development of antiviral activity. Among the analogues of cAMP tested for interferon-potentiating activity, only the acylated derivatives were found to be active. Combined L-epinephrine and theophylline treatment of cells elevated cellular cAMP levels and also potentiated interferon-mediated antiviral activity. Interferon was also found to elevate cAMP levels in L cells. This activity was limited to biologically active interferon and antagonized the depression of cAMP associated with vesicular stomatitis virus (VSV) infection of L cells. These observations suggest that some aspects of interferon's biological activity is associated with an alteration in cellular levels of cAMP.
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PMID:Cyclic AMP potentiation of interferon antiviral activity and effect of interferon on cellular cyclic AMP levels. 17 Mar 77

Peripheral blood leukocyte and spleen cell cultures derived from adult sheep and from third-trimester (107 to 145 days of gestation) and second-trimester (70 to 98 days of gestation) fetal lambs were examined for their ability to support viral replication and to produce interferon. Bluetongue virus, Herpesvirus hominis type 2, and Chikungunya virus failed to replicate in either leukocyte or spleen cell cultures derived from adult ewes or in cultures from second- or third-trimester fetal lambs. Similarly, peripheral blood leukocytes from adult sheep or third-trimester fetal lambs did not support the replication of Semliki Forest virus, vesicular stomatitis virus, Newcastle disease virus, or vaccinia virus. No major differences were observed in the ability of fetal and adult leukocytes to produce interferon in response to viral infection. In contrast, mean interferon titers induced by bluetongue virus, H. hominis type 2, and Chikungunya virus in spleen cells from second-trimester fetuses were 4- to 10-fold greater than those induced in spleen cells from adult ewes. Variations in interferon levels induced on separate occasions with cells from the same donor age group were observed. The antiviral substance induced in both the fetal and adult cell cultures fulfilled the usual criteria for characterization as interferon.
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PMID:Viral replication and interferon production in fetal and adult ovine leukocytes and spleen cells. 17 52

A fraction of mouse RNA containing messenger RNA coding for mouse interferon was translated with high efficiency in a wheat germ system into a fully active product. This product fulfills the criteria for mouse interferon, namely: (1) it was active against vesicular stomatitis virus and herpes simplex virus in mouse cells; (2) its antiviral activity was species specific; (3) its activity was completely neutralized by mouse anti-interferon serum. The synthesis of interferon in this cell-free system requires the presence of spermine.
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PMID:Biosynthesis of mouse interferon by translation of its messenger RNA in a cell-free system. 17 90

The effect of theophylline and adrenaline on the synthesis of interferon induced by the influenza B virus, strain Lee, in a chick embryo tissue culture was studied. Both preparation were found to decrease interferon synthesis when 5-day-old cultures were used; the inhibitory effect was increased when the two drugs were used together. The degree of inhibition of interferon production depended on a dose of the preparation; the inhibition was still present even when the drugs ere introduced several hours after the cells were infected with interferonogen. The treatment of one-day-old cultures with theophylline resulted in increase of interferon synthesis, whereas administration of adrenaline alone or together with theophylline did not affect the level of interferon synthesis. The drugs used produced no effect on the reproduction of the test-virus of vesicular stomatitis, Newcastle disease and Chickungunya viruses in chick embryo cells and influenza B virus in the developing chick embryos. The results obtained are discussed from the point of view of a possible influence of the intracellular adenosine 3',5-cyclic monophosphate level on the synthesis of virus-induced interferon.
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PMID:[Effect on drugs changing the intracellular level of adenosine 3',5'-cyclic monophosphate on interferon formation in chick embryo cells of different ages]. 17 23

Interferon-treated cultures of Ly cells survived initial infection with high multiplicities of vesicular stomatitis (VSV) or herpes simplex virus (HSV). In the case of HSV, infectious virus and intracellular viral antigen were rapidly eliminated from the interferon-treated cultures, and the cells grew out to form apparently normal monolayers that could be cultured indefinitely. In the VSV-infected Ly cultures, virus titers remained at low levels in interferon-treated cells but after about 14 days rapidly rose and the culture was destroyed. If interferon was added to the medium on days 4 and 6 after infection, virus titers rapidly declined but again recovered and the cells were destroyed. If, however, interferon treatment was resumed 9 days after initial infection, detectable infectious VSV was eliminated from the medium. Several methods, including cocultivation and molecular hybridization, failed to demonstrate persistence of a significant portion of the VSV genome in these cultures.
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PMID:Fate of interferon-treated cells. 17 68

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.
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PMID:Effect of ammonium 5-tungsto-2-antimoniate on encephalomyocarditis and vesicular stomatitis virus infections in mice. 17 29

Purified defective interfering (DI) particles of vesicular stomatitis virus (VSV) inhibit the replication of a heterologous virus, pseudorabies virus (PSR), in hamster (BHK-21) and rabbit (RC-60) cell lines. In contrast to infectious B particles of VSV, UV irradiation of DI particles does not reduce their ability to inhibit PSR replication. However, UV irradiation progressively reduces the ability of DI particles to cause homologous interference with B particle replication. Pretreatment with interferon does not affect the ability of DI particles to inhibit PSR replication in a rabbit cell line (RC-60) in which RNA, but not DNA, viruses are sensitive to the action of interferon. Under similar conditions of interferon pretreatment, the inhibition of PSR by B particles is blocked. These data suggest that de novo VSV RNA or protein synthesis is not required for the inhibition of PSR replication by DI particles. DI particles that inhibit PSR replication also inhibit host RNA and protein synthesis in BHK-21 and RC-60 cells. Based on the results described and data in the literature, it is proposed that the same component of VSV B and DI particles is responsible for most, if not all, of the inhibitory activities of VSV, except homologous interference.
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PMID:Inhibition of pseudorabies virus replication by vesicular stomatitis virus. II Activity of defective interfering particles. 17 95

Mouse serum interferons induced by polyI:C, vesicular stomatitis virus (VSV), reovirus, and Mengo virus were assayed in monolayers of mouse L-929 cells by the plaque-reduction method using both VSV and Mengo as challenge viruses. Titers obtained with Mengo virus as challenge were all lower than with VSV. With the interferons induced by VSV, reovirus, and ployI:C, the reductions were of the order of two- to three-fold. With Mengo virus-induced interferon the reduction was much greater (about 17-fold). This offers an explanation for the observation that, unit for unit (measured by the plaque reduction of VSV), Mengo virus-induced interferon is only about 1/10 as effective as polyI:C-induced interferon in protecting mice against lethal infection with Mengo virus. The data are consistent with the hypothesis that an interferon antagonist is produced in the serum of mice infected with Mengo virus. This antagonist, which is not produced in mice inoculated with polyI:C, or reovirus, effectively blocks the antiviral action of interferon during Mengo virus infections, both in vivo and in vitro.
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PMID:Further studies on the relative antiviral efficacies of interferons induced by poly I:C and Mengo virus. 17 87

In AKR mouse cells chronically infected with a murine leukemia virus, treatment with interferon for nine days resulted in sustained inhibition of extracellular production of murine leukemia virus but no inhibition of viral intracellular p30 antigen or of reverse transcriptase. Removal of interferon resulted in rapid reversal of these effects. Interferon-treated mouse L-cells were infected with high multiplicities of vesicular stomatitis virus or herpes simplex virus type 1. Infectious virus and intracellular viral antigen were rapidly eliminated from the interferon-treated cultures infected with herpes simplex virus. In cultures infected with vesicular stomatitis virus, titers of virus remained low in interferon-treated cells, but after about two weeks they rose rapidly and the cultures were destroyed. If treatment with interferon was reinstituted as late as nine days after primary infection, infectious vesicular stomatitis virus was eliminated, and there was no evidence for survival of the viral genome in these cultures. In the cultures infected with murine leukemia virus, inhibition of production of virus by treatment with interferon was possible, but the viral genome was not eliminated. In cells acutely infected with vesicular stomatitis virus or herpes simplex virus, however, the viral genomes were apparently eliminated from cultures treated with interferon.
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PMID:Persistence of the viral genome in interferon-treated cells infected with oncogneic or nononcogenic viruses. 18 Feb 9


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