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 aims of this study were to define the T-cell subpopulation(s) detected by the virus plaque assay, and particularly to determine whether the virus plaque assay could be used to enumerate cytotoxic T lymphocytes. In addition, studies were undertaken to ascertain whether cell proliferation was required for development of cytotoxic effector function and virus plaque formation by these subpopulations. The results of experiments with a secondary mouse mixed lymphocyte culture (MLC) model indicated that 70 percent of virus plaque-forming cells bore the Ly 1 phenotype and 30 percent the Ly 2,3 phenotype. Three lines of evidence suggested that cytotoxic T lymphocytes (CTL) can be detected by this assay: the fact that some virus plaque-forming cells (V-PFC) bear the same Ly phenotype as CTL; the use of an inhibitor of DNA synthesis indicated that proliferating cells could be eliminated with no effect on V-PFC production and cytotoxic activity of the Ly 2,3 cell population; and that infection of primed lymphocyteswith vesicular stomatitis virus before (MLC) stimulation eliminated cytotoxic activity. In primary MLC, development of V-PFC and CTL was completely abolished by cytosine arabinoside. In contrast, in secondary MLC, some CTL and V- PFC were generated by antigenic stimulation in the absence of proliferation. However, the development of both functions became progressively more susceptible to cytosine arabinoside as the time between primary immunization and in vitro boosting is increased. It is suggested that there may be a considerable disparity between the number of existing effector cells at any given time and the cytotoxic potential, i.e. the number of cells capable of being generated by antigenic stimulation.
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PMID:Differentiation of memory T cells to virus plaque-forming cells and cytotoxic T lymphocytes. 19 99

Virus plaque assay (VPA) was utilized for the quantitative evaluation of activated lymphocytes. We examined what types of cells, especially which of activated T and non-T lymphocytes, were detected as infective centres after infection with vesicular stomatitis virus. Marked increases in DNA synthesis and in virus-plaque forming cells (V-PFC) were observed not only during the activation of T lymphocytes with Con A, but also, though to a lesser extent, during the activation with lipopolysaccharide (LPS) of non-T lymphocyte preparations of nude spleen from which theta-positive lymphocytes and macrophages were completely depleted. The latter observation was further confirmed by the VPA on the populations enriched in LPS-activated non-T lymphocytes fractionated by the unit gravity sedimentation method. Fast sedimenting cells were found to be more active in DNA synthesis and contained more infective centres after infection than those sedimenting slowly and original unfractionated cells. Both the capacity for DNA synthesis and virus-replication were considered to be general properties accompanying lymphocyte activation.
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PMID:Detection of mitogen-activated T and non-T lymphocytes by virus plaque assay. Virus plaque assay on the cells fractionated by unit gravity sedimentation. 19

By employing improved techniques it has been possible to produce and characterize a representative spectrum of mammalian and primate retrovirus pseudotypes of vesicular stomatitis virus (VSV). Selection of appropriate cell lines for both the production and subsequent detection of the VSV pseudotypes has been the most important factor in permitting their demonstration. The host range for penetration of these retrovirus pseudotypes of VSV has been defined and found to differ from that reported for the replication of the corresponding retroviruses. Additionally, retroviruses having an identical host range for replication were distinguishable by differences in their host range for penetration, implying that restriction of replication may be occurring by different mechanisms. Studies of the plaque-forming efficiency of retrovirus pseudotypes of VSV in cell lines nonpermissive for replication of the corresponding retroviruses permitted a distinction to be made between the restriction of replication occurring as a consequence of postpenetration events and that occurring as a consequence of a block of penetration itself. The demonstration of primate retrovirus pseudotypes of VSV permits the use of VSV as a probe for the detection of this group of viruses.
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PMID:Pseudotypes of vesicular stomatitis virus with the envelope properties of mammalian and primate retroviruses. 19 55

Twelve cloned viruses were randomly isolated from original (uncloned) vesicular stomatitis virus (VSV), and their sensitivities to mouse and human interferons were examined. When the interferon sensitivities of these various VSVs were compared by the plaque reduction method in L cells, virus 3 was found to be sevenfold more sensitive than virus 11, and the interferon sensitivity of the original (uncloned) virus was intermediate. The present study shows that uncloned VSV Indiana strain is a mixture of viruses that have different sensitivities to interferon. The slope of the dose-response curve of original (uncloned) virus to mouse interferon was less steep than those of cloned viruses. Virus 11, which was the least sensitive to mouse interferon, was relatively sensitive to human interferon. There was no correlation between the sensitivities of virus clones to mouse interferon and their sensitivities to human interferon. When the interferon sensitivities were tested by various assay methods (plaque reduction, yield reduction, and cytopathic effect inhibition), the ranking of the interferon sensitivities of different viruses was not changed. These results indicate that the relative sensitivity of a virus to interferon is determined by the host cells in which the tests are performed, but not by assay method used.
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PMID:Heterogeneity of the sensitivity of vesicular stomatitis virus to interferons. 19 74

A simple and efficient microassay method for the titration of interferon was developed by the use of microtest plates for handling a large number of samples. L929 cells pretreated with interferon were infected with vesicular stomatitis virus (VSV) and cultured in the presence of 3H-uridine. The activity was expressed by the reduction of extracellular radioactive RNA released after destruction of the infected cells, which was measured in terms of the radioactivity incorporated into cold TCA-insoluble materials in the culture fluid. The interferon titer determined by this method was in the same order as that by the plaque reduction method. The activity by this method was parallel to, but lower than that expressed by the yield reduction of infectious viruses. This method requires only 0.025 ml of each test sample with higher than 1 NIH ref. unit/ml to detect its interferon activity and takes 2 to 3 days for assaying hundreds of samples.
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PMID:A simple and efficient microassay method for titration of interferon. 20 22

Fetal bovine serum markedly decreased the ability of mouse L-929 interferon preparations to inhibit the formation of L-929 clones, but did not affect their ability to inhibit vesicular stomatitis virus (VSV) plaque formation in these cells. This dissociation of effects by interferon preparations indicates that: 1. the mechanism of action of interferon for its anticlonal antiviral activities is different; or 2. the molecule responsible for the anticlonal activity is a separate growth inhibitory factor.
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PMID:Effect of serum on the antiviral and anticellular activities of mouse interferon. 20 96

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

Immunocytological properties of the splenic T cell (Tv) which develop into virus plaque-forming cells in response to the antigenic challenge in vitro were investigated in relation to the properties of helper T cells and suppressor T cells in antibody response. Tv was observed in spleen around 1 wk after the intravenous injection of mice with 10(7) sheep erythrocytes. This contrasted with the finding that both helper T cells and suppressor T cells developed as early as 3 days after the immunization. Tv was proliferative in response to the antigenic stimulation, whereas helper T-cell activity could be expressed without cell division. Development of Tv to virus plaque-forming cells was much more dependent on macrophages than the generation of helper activity. Tv was found in nylon wool adherent fraction, whereas helper T cell was found in both nylon adherent and nonadherent fractions. Tv belongs to the short-lived and nonrecirculating T-cell population (T1), whereas the major part of helper T cells belongs to the long-lived and recirculating T-cell population (T2). These results strongly suggest that vesicular stomatitis virus infect and replicate in the different subset(s) of T cell(s) to which the major part of helper T cells belong.
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PMID:Virus-replicating T cells in the immune response of mice. II. Characterization of T cells capable of replicating vesicular stomatitis virus. 21 7

Coinfection of cells with vesicular stomatitis virus (VSV) of Indiana and New-Jersey serotypes were performed. Thermosensitive mutants (ts) of VSV Indiana and the wild type strain (+) of New-Jersey were used. Harvests and titrations were made at permissive(PT) and nonpermissive (NPT) temperatures. It was shown that the harvest was mainly composed of one parental-like infectious particles. The dominance of one serotype over the other was shown to be a function of the relative multiplicity of the two viruses; the presence of a thermosensitive lesion imparts a disadvantage to the corresponding serotype. Non parental-like particles were also detected. As expected, these particles were detected only in two conditions. 1) Harvest performed at NPT and titrations allowed at PT.- Most of the infectious particles (i.e. twin particles) resistant to anti-Nj serum developped a plaque (i.e. mixed-plaque)containing virions of both serotypes: Indiana (ts) and New-Jersey (+). After sonication or EDTA treatment of the harvest, prior to titrations, no more mixed-plaques were formed. Examination of the harvest by electron microscopy showed that 7-17 % of the particles formed aggregates; therefore, it is likely that the twin-particles are in fact aggregates. 2) Harvest performed at PT and titrations allowed at NPT.-It has been shown that 1 % of the wild type infectious particles was resistant to anti-Nj serum even though being of Nj genotype. It was inactivated by a mixture of anti-Nj and anti-In sera and therfore behave as pseudotypes. But since twin particles, when plated at Nt, would give rise to an homogenous progeny from New-Jersey (+), they could be confused with pseudotypes. Under those conditions there is no absolute evidence that phenotypic mixing really occurs between VSV of Indiana and New-Jersey serotypes.
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PMID:Coinfection with a rhabdovirus: vesicular stomatitis virus of Indiana and New-Jersey serotypes. 21 3

We have compared the mechanisms of entry into host cells of three enveloped viruses: Sendai virus, vesicular stomatitis virus (VSV) and Sindbis virus. Virus entry by membrane fusion should antigenically modify the surface of a newly infected cell in such a way that it will be killed by anti-viral antibody and complement. On the other hand, virus entry by a mechanism involving uptake by the cell of the whole virion should not make cells sensitive to antibody and complement. As expected, cells newly infected with Sendai virus were readily and completely lysed by anti-Sendai antibody and complement. In marked contrast, however, cells newly infected with either Sindbis virus or VSV were killed by anti-viral antibody and complement only when infected at an extremely high multiplicity of infection, in excess of 1000 plaque-forming units per cell. We favor the following explanation for these results with Sindbis virus and VSV: a very large majority of the Sindbis and VSV virions entered the infected cells by some means other than membrane fusion, presumably engulfment of the whole particle. Efficient entry by way of membrane fusion may therefore not be a general characteristic of enveloped viruses.
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PMID:The entry into host cells of Sindbis virus, vesicular stomatitis virus and Sendai virus. 21 17


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