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)

We have compared the effects of infection with herpes simplex virus (HSV) and vesicular stomatitis virus (VSV) on the protein synthetic apparatus of Friend erythroleukemia cells. Previous studies demonstrated that infection with HSV rapidly shuts off the synthesis of globin and other cellular polypeptides (Y. Nischioka and S. Silverstein, 1977, Proc. Natl. Acad. Sci. U.S.A. 74: 2370-2374). In contrast to these findings, globin synthesis persists in Friend erythroleukemia cells infected with VSV. Physical measurements of the size of bulk-infected cell mRNA, using hybridization with polyuridylic acid, demonstrated that there was no detectable change in the size of mRNA's after infection with VSV. A comparison of the kinetics of hybridization of cytoplasmic RNA extracted from cells infected with either HSV or VSV with globin complementary DNA revealed that by 4 h postinfection with HSV only about 15% of the globin mRNA sequences remained, whereas there was no discernible change in the sequence abundance of globin mRNA in VSV-infected cells.
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PMID:Alterations in the protein synthetic apparatus of Friend erythroleukemia cells infected with vesicular stomatitis virus or herpes simplex virus. 20 53

(S)-9-(2,3-Dihydroxypropyl)adenine, a novel nucleoside analog, the sugar moiety of which is replaced by an aliphatic chain, inhibits the replication in vitro of several DNA and RNA viruses, including vaccinia, herpes simplex (types 1 and 2), measles, and vesicular stomatitis. It is also effective in vivo in reducing the mortality rate of mice inoculated intranasally with vesicular stomatitis virus.
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PMID:(S)-9-(2,3-Dihydroxypropyl)adenine: an aliphatic nucleoside analog with broad-spectrum antiviral activity. 20 46

The methyl ester of amphotericin B (AME) is water soluble, retains antifungal activity, and is significantly less toxic in mammals than amphotericin B. In contrast to amphotericin B, which is not water soluble, AME exhibits antiviral effects against vesicular stomatitis virus, herpes simplex virus types 1 and 2, Sindbis virus, and vaccinia virus in a plaque reduction assay. No antiviral effects could be demonstrated against the unenveloped adenovirus type 4 or echovirus type 11. The extent of virus inactivation was found to be dependent upon the AME concentration, contact time, and temperature. No consistent effect of the virus concentration on the probability of plaque-forming unit inactivation could be determined. The antiviral effects of AME were partially antagonized by the presence of serum. Binding of AME to vesicular stomatitis virus was demonstrated by the comigration of drug and virus in linear sucrose gradients. AME represents a new class of antiviral agents with activity at concentrations relevant to therapeutics. Sterol components of the host cell membrane that become incorporated into the viral envelope are postulated as the site of reaction with AME.
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PMID:Antiviral effects of amphotericin B methyl ester. 20 1

The replication of human cytomegalovirus (CMV) and herpes simplex virus (HSV) was studied in three human embryo cell lines (CMV-Mj-HEL-I, CMV-Mj-HEL-2, and CMV-Mj-HEL-2,T-I) transformed in vitro by human CMV. Growth studies revealed that these cells were completely resistant to infection by CMV strains ADI69 and Mj and partially resistant to HSV types I and 2. Neither virus DNA nor virus proteins were synthesized in the transformed cells infected with CMV AD169. The HSV production in CMV-transformed human embryo lung (HEL) cells was delayed when compared to the virus production in normal HEL cells and spread of HSV c.p.e. was slower in the transformed cells. The treatment of normal HEL cells with a crude extract of CMV-transformed HEL cells also resulted in inhibition of the spread of c.p.e. of HSV types I and 2. The inhibitory effect was not due to interferon since vesicular stomatitis virus replication was not affected and several experiments showed that it was not due to mycoplasma. The presence of virus inhibitor molecules in CMV-transformed cells absent in normal HEL cells is postulated.
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PMID:Replication of herpesviruses in human cells transformed by cytomegalovirus. 21 Nov 87

Visna is a slow infection of sheep caused by a retrovirus. The persistence of virus despite the immune response of the host is best explained by restricted genetic expression of the virus and consequently prolonged periods of residence inside cells. The purpose of this investigation was to determine whether the restriction in genetic expression of visna virus is mediated by interferon. Sheep interferon induced by polyriboinosinic-polyribocytidylic acid in fetal lambs inhibited the growth of herpes simplex virus, vesicular stomatitis virus, and vaccinia virus, but even highly concentrated interferon did not affect the replication of visna virus in sheep choroid plexus cells. The same results were obtained whether the effects of interferon were assessed in single of multiple cycles of growth and when interferon was added at later times in the growth cycle of the virus. This unusual resistance of visna virus to interferon suggests that restriction of viral expression by the host is probably not mediated in this way.
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PMID:Resistance of visna virus to interferon. 21 2

A cell line established from human embryonic lung, HEL-R66, was demonstrated to be highly susceptible to herpes simplex virus types 1 and 2, vaccinia virus, Newcastle disease virus (NDV), Japanese encephalitis virus (JEV), western equine encephalitis (WEE) virus, Sindbis virus, vesicular stomatitis virus (VSV), and rabies virus. The maximal yields of NDV, JEV, WEE virus, and rabies virus in this cell line exceeded by 2--4 logs those in control human embryonic lung cells. Inability of this cell line to produce interferon upon treatment with native and UV-irradiated forms of virogenic and lentogenic strains of NDV and with poly I:C was revealed. A refractory state to challenging VSV did not develop in HEL-R66 cells treated with the inducers. Furthermore, pretreatment of HEL-R66 cells with interferon did not potentiate the capacity to produce interferon in response to the addition of poly I:C, whereas the same treatment enhanced the production of interferon in normal human embryonic lung cells.
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PMID:Absence of interferon production in a newly established human cell line. 21 1

The ability of vaccinia virus to replicate in BSC-40 monkey cells whose nuclei have been functionally inactivated was examined. Exposure of cell monolayers to ultraviolet radiation at doses that did not alter the cells' capacity to support a subsequent infection by a cytoplasmic virus (vesicular stomatitis virus) caused a reduction to less than 10% in the observed yield of infectious progeny from vaccinia virus and herpes simplex virus (type 1) infections. Similarly, replication of vaccinia virus was reduced to 5% by treatment of BCS-40 cells with alpha-amanitin (10 microgram/ml), a potent inhibitor of nuclear mRNA synthesis. In both situations, ultraviolet irradiation and alpha-amanitin treatment, early and late vaccinia viral genes were expressed at high levels, but the newly synthesized virion components were not assembled into mature infectious particles. Taken together, these data suggest that the active involvement of the host cell nuclear transcriptive system is obligatory in the vaccinia virus replicative cycle.
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PMID:Vaccinia virus replication requires active participation of the host cell transcriptional apparatus. 22 9

The effects of Newcastle disease, herpes simplex, vaccinia, encephalomyocarditis, vesicular stomatitis and reoviruses on in vitro function of neutrophils were studied in Ficoll-Hypaque-separated polymorphonuclear leukocytes (PMN) employing the technique of luminol-dependent chemiluminescence. Newcastle disease, herpes simplex vaccinia, and reoviruses depressed chemiluminescence by 98, 65, 46, and 29%, respectively, while encephalomyocarditis and vesicular stomatitis viruses had no inhibitory effect. None of the viruses affected phagocytosis or PMN viability. These observations suggest significant alteration of neutrophil function by interaction with several viruses in in vitro settings. It is suggested that similar changes in PMN function may occur during in vivo viral infection.
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PMID:Effect of viruses on luminol-dependent chemiluminescence of human neutrophils. 22 82

SN11841 [4'-(9-acridinylamino)-methanesulfon-m-aniside] is an antitumor compound discovered by B.F. Cain. The LD50 for BALB/c mice with single intraperitoneal dosage is approximately 25 mg/kg. RLV-(Rauscher leukemia virus)-induced splenomegaly, a disease indicator in BALB/c mice, is inhibited at SN11841 doses not causing acute mortality. The life span of RLV-infected mice increases at some SN11841 doses. SN11841 does not have direct, or virolytic effects on RLV under conditions approximating those of antiviral effectiveness. SN11841 is cytotoxic for cells in tissue culture, as measured by inhibition of growth rate or vital dye uptake. At nontoxic concentrations SN11841 has no effect on RLV infectivity for murine cells, as determined by XC-cell induced syncytium formation. SN11841 has antiviral activity against vaccinia virus in tissue culture but is inactive against herpes simplex (Type 1), vesicular stomatitis, encephalomyocarditis, or reoviruses. SN11841 apparently does not act by inducing interferon. SN11841 is chemically labile, particularly in the presence of sulfhydryl compounds, but the degradation products resulting from prolonged storage in media are neither cytotoxic nor antiviral.
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PMID:Antiviral activities of 4'-(9-acridinylamino)-methanesulfon-M-aniside (SN11841). 28 Jan 45

Extracts of two species of marine algae, Constantinea simplex and Farlowia mollis, were tested for antiviral activity in tissue culture and in experimental infections of mice. Treatment of confluent mouse embryo fibroblast cell monolayers with either compound before viral inoculation was effective in inhibiting the replication of herpes simplex virus type 1 and type 2, vaccinia virus, and vesicular stomatitis virus, but not encephalomyocarditis virus, Semliki Forest virus, or murine cytomegalovirus. Prophylactic administration of these extracts was effective in reducing final mortality or prolonging the mean day of death of animals inoculated by the intraperitoneal, intracerebral, or intranasal routes with herpes simplex virus type 2. When therapy was initiated after viral inoculation or at a site other than that of viral inoculation, no significant effect on mortality or on mean day of death was observed. Neither preparation was effective in mice inoculated intraperitoneally with encephalomyocarditis virus, Semliki Forest virus, or murine cytomegalovirus or in animals infected intravaginally with herpes simplex virus type 2. The prophylactic but not therapeutic antiviral activity of these preparations seriously limits their potential use in human herpes simplex virus infections.
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PMID:Antiviral activity of extracts from marine algae. 68 7


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