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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Inhibitors of elongation steps in protein synthesis such as cycloheximide and anisomycin mimic interferon treatment in that they specifically inhibit the synthesis of certain viral proteins. These specific effects are seen only at very low concentrations of the antibiotics, under conditions where host cellular protein synthesis, as well as cell viability, are not severely reduced. A qualitatively as well as quantitatively close correlation between the effects of the two types of agents has been established for encephalomyocarditis virus, vesicular stomatitis virus and murine leukemia virus protein synthesis. It is concluded that one of the primary mechanisms of interferon action may be a nonspecific retardation of one or more elongation steps, and that this may be sufficient to account for its effects on the replication of certain viruses such as encephalomyocarditis and vesicular stomatitis viruses.
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PMID:Specificity of interferon action in protein synthesis. 21 87

A previous report (Youngner et al., J. Virol. 19:90-101, 1976) documented that noncytocidal persistent infection can be established with wild-type vesicular stomatitis virus (VSV) in mouse L cells at 37 degrees C and that a rapid selection of RNA(-), group I temperature-sensitive (ts) mutants consistently occurs in this system. To assess the selective advantage of the RNA(-)ts phenotype, evolution of the virus population was studied in persistent infections initiated in L cells by use of VSV ts 0 23 and ts 0 45, RNA(+) mutants belonging to complementation groups III and V. In L cells persistently infected with ts 0 23, the ts RNA(+) virus population was replaced gradually by viruses which had a ts RNA(-) phenotype. VSV ts 0 45 (V) has another marker in addition to reduced virus yield at 39.5 degrees C: a defective protein (G) which renders virion infectivity heat labile at 50 degrees C. Persistent infections initiated with this virus (ts, heat labile, RNA(+)) evolved into a virus population which was ts, heat resistant, and RNA(-). These findings suggest that the ts phenotype itself is not sufficient to stabilize the VSV population in persistently infected L cells and also indicate that the ts RNA(-) phenotype may have a unique selective advantage in this system. In addition to the selection of ts RNA(-) mutants, other mechanisms which also might operate in the maintenance of persistent VSV infections of L cells were explored. Whereas defective-interfering particles did not seem to mediate the carrier state, evidence was obtained that interferon may play a role in the regulation of persistent infections of L cells with VSV.
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PMID:Persistent infection of L cells with vesicular stomatitis virus: evolution of virus populations. 21 14

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

The rate of development of interferon-induced virus resistance in a mixture of two human cell types (U and WISH) is determined by the cell type (WISH) in the mixture which responds first. This phenomenon has been shown with two types of interferon assay procedure, and with both vesicular stomatitis virus and Sindbis virus. The transfer of virus resistance from one human cell (WISH) to another (U) (homospecific transfer) is much more efficient than the transfer from mouse L cells to WISH cells (heterospecific transfer), as shown by a much lower ratio of donor to recipient cells required for maximum transfer as well as a more rapid transfer. Thus, virus protection afforded by the interferon system is amplified more efficiently in mixtures of different human cells than in mixtures of mouse and human cells. These results suggest that, in a mixed population of cells such as occurs in vivo, more slowly responding cells might be influenced by cells which respond more rapidly to interferon. A defensive role is suggested for this mechanism which amplifies protection due to interferon.
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PMID:Efficient transfer of interferon-induced virus resistance between human cells. 21 20

The effect of interferons on vesicular stomatitis virus (VSV) primary transcription, amplified RNA synthesis [i.e. the sum of primary transcription RNA replication (leading to [ - ] RNA) and secondary transcription (leading to [ + ] RNA) and virus protein synthesis were studied. In a human cell line, both human and simian interferons inhibited the initiation of primary transcription and amplified RNA synthesis. In contrast, in a simian cell line tested similarly, the initiation of these activities was not affected, though they decreased as the infection progressed. Nevertheless, virus protein synthesis was completely inhibited. These results demonstrate that the action of interferon on virus transcription and/or translation may depend more on the host cell than on the particular interferon used.
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PMID:Effect of interferon on transcription and translation of vesicular stomatitis virus in human and simian cell cultures. 21 23

The rate and degree of interferon action on mouse embryo (ME), mouse L, and human amnion (WISH) cells were found to be dependent on the cell density. The most precipitous drop in interferon action occurred just below cell confluency. This effect was shown with both vesicular stomatitis virus and Sindbis virus and at both constant and variable input multiplicities of infection. At both "high" and "low" cell densities, cells attached to a surface develop viral resistance faster than suspended cells. These data indicate that either cell contact or close cell proximity is required for maximal interferon activity. These results are discussed in relation to interferon-induced transfer of viral resistance.
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PMID:Cellular interactions determine the rate and degree of interferon action. 21 33

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 enhanced phosphorylation of specific protein(s) observed in extracts from interferon-treated cells (in the presence of ATP and double-stranded [ds] RNA) was also seen in intact mouse L929 cells upon treatment with dsRNA, polyriboinosinic.polyribocytidylic acid [poly(rI.rC)] or reovirus dsRNA, using 32Pi as radiolabel. Labeling of a 65,000-dalton protein(s) with 32P was greatly increased in interferon-treated cells in the presence of added dsRNA, suggesting that the expression in vivo of the kinase activity involved is regulated by dsRNA. This was used as a test system to investigate whether the activity of interferon-induced enzyme(s) is stimulated following virus infection, possibly owing to the accumulation of dsRNA. No obvious increase in 32P-labeling of 65,000-dalton protein(s) was observed upon infection of interferon-treated cells with mengovirus or vesicular stomatitis virus. A basal level of 32P-labeling of the 65,000-dalton protein(s) was detected in interferon-treated cells in the absence of added dsRNA, indicating a basal level of expression of the kinase activity involved. The possible implications of these results are discussed.
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PMID:Specific protein phosphorylation in interferon-treated uninfected and virus-infected mouse L929 cells: enhancement by double-stranded RNA. 21 24

In the experiments performed in vitro and in vivo it has been found that the rat and rat embryo fibroblasts cultured in vitro after the induction with virus produce interferon which displays the antiviral activity not only in the homologous cells but also in the heterologous ones. When analysed by chromatography on Sephadex G-100 it was shown that the rat serum contains two interferon populations differing in the molecular weight and both active in the homologous and heterologous cells. The interferon with the heterospecific activity has been used in the experimental therapy of mice infected with Encephalomyocarditis Virus (EMC), Vesicular Stomatitis Virus (VSV) and Influenza Virus, and was found to be effective.
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PMID:Heterospecific activity of rat interferon. 21 6


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