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

When the sensitivities to interferon of Newcastle disease virus (NDV) and vesicular stomatitis virus (VSV) were compared by the plaque reduction method in chick embryo cell cultures, NDV was found to be 45-fold more resistant than VSV. This difference was exaggerated when a multiple-cycle yield inhibition method was employed. In marked contrast, when the same viruses were tested by a single-cycle yield inhibition method, the difference in sensitivity to interferon of the two viruses was virtually eliminated. Further investigation showed that, in chick embryo cells exposed to interferon, the resistance to NDV decayed more rapidly than resistance to VSV. This finding explained the divergent results obtained with the two viruses when single- or multiple-cycle replication techniques were employed. Experiments carried out with L cells showed that cellular antiviral resistance decayed much more slowly in these cells than in chick embryo cells. Consequently, when measured by the plaque reduction method in L cells, no difference was observed in the sensitivity to interferon of VSV and NDV(pi), a mutant of NDV which replicates efficiently in L cells. A procedure is suggested for determining the relative sensitivities to interferon of different viruses under conditions which minimize the role of decay of antiviral resistance in the host cells.
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PMID:Factors affecting the sensitivity of different viruses to interferon. 432 69

The virions of Newcastle disease virus (NDV) contained an enzyme that catalyzed the incorporation of ribonucleotides into ribonucleic acid (RNA). Optimal conditions for this polymerase activity were identical to the conditions for the vesicular stomatitis virus (VSV) polymerase, and both enzymes were active for longer times at 32 C than at 37 C. However, the specific activity of the NDV polymerase was less than 3% that of the VSV polymerase. Product RNA species from the NDV and VSV polymerase reactions annealed specifically to the homologous virion RNA species. Transcriptive intermediates containing product RNA attached to the respective virion RNA could be identified in both systems.
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PMID:Ribonucleic acid polymerase in virions of Newcastle disease virus: comparison with the vesicular stomatitis virus polymerase. 432 12

A general method is described for enumerating antigen-sensitive lymphocytes obtained from individuals having delayed hypersensitivity, in this case from highly tuberculin-sensitive guinea pigs. The method is based on the observation that resting lymphocytes are generally unable to support replication of RNA viruses, whereas antigen-"activated" lymphocytes can. Lymph node lymphocytes from individual animals were cultured in the presence or absence of tuberculin purified protein derivatives (PPD). After various periods of time, the cells were infected either with Newcastle disease virus or vesicular stomatitis virus, and plated in agar over a monolayer of cells susceptible to the virus. Wherever a lymphocyte yielded infectious virus, a discrete plaque in the monolayer could be seen. The increase in plaques of the antigen-stimulated cells over the background of the control sample was taken as the number of antigen-sensitive cells in the population. When lymphocytes from normal guinea pigs or from guinea pigs immunized to produce only circulating antibody to PPD were similarly tested, no increase in plaque-forming units (PFU) was observed. The average increase in PFU due to antigenic stimulation varied from 1 per 1000 lymphocytes at 24 hr to 16 per 1000 lymphocytes at 96 hr. By employing inhibitors of mitosis (colchicine, vinblastine, and thymidine) it was evident that the increase in PFU at least up to 48 hr was primarily due to initial antigen-reactive cells and not their progeny.
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PMID:A plaque assay for enumerating antigen-sensitive cells in delayed-type hypersensitivity. 432 47

Five nonionic detergents (Tweens 20, 40, 60, and 80, and Triton WR-1339) were tested for their ability to inactivate four Mycoplasma species which are common contaminants of animal cell cultures. Tween 20 was found to be the most effective, in that a concentration of 2.5 mg/ml completely inactivated cultures of M. hominis, M. hyorhinis, and Acholeplasma laidlawii within 1 hr and a culture of M. orale within 3 hr. The other detergents exhibited various degree of activity against the different mycoplasmas, with Triton WR-1339 being the least effective. The virucidal activity of the detergents was determined for six viruses. All four Tween compounds were highly virucidal for herpes simplex virus. Tween 20 also exhibited virucidal effects against vesicular stomatitis virus, California encephalitis virus, and Newcastle disease virus, and Tween 80 was found to be active against California encephalitis and Newcastle disease viruses. Detergent treatment procedures were effective in two instances in eliminating mycoplasma contaminants from virus preparations while the preparations retained most of the viral infectivity. The limitations of this technique for routine use are discussed.
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PMID:Elimination of Mycoplasma contaminants from virus stocks by treatment with nonionic detergents. 434 21

It was determined that KB-R cell strains, isolated from the KB cell line and resistant to diphtheria toxin, also resist infection by poliovirus, Mengo virus, vesicular stomatitis virus, and Newcastle disease virus. This resistance manifests itself by reduction in yields of progeny virus (a reduction of more than 2 logs in some cases), reduced production of viral-specific ribonucleic acid (RNA), and delayed cytopathic effect. In three KB-R strains tested, resistance was related to a step which falls between adsorption of virus and uncoating or release of viral messenger RNA. In two of these three strains, a second resistance mechanism was also active, causing a reduced production of viral-specific RNA. A relationship between the resistance to diphtheria toxin and the resistance to viral infection of the KB-R strains is considered. It has been postulated that the native diphtheria toxin molecule must be "activated" at the surface of a susceptible cell by a proteolytic process before it can enter the cell and inhibit protein synthesis. It is also known that the eclipse of some viruses occurs at or near the cell membrane and involves proteolytic activity. Resistance to viruses and toxin in the KB-R strains may result from the loss or modification of related labilizing or activating principles associated with the surface receptors for these agents.
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PMID:Response of cultured mammalian cells to diphtheria toxin. V. Concurrent resistance to ribonucleic acid viruses in diphtheria toxin-resistant KB cell strains. 434 25

Virus-infected mice were significantly more susceptible to the toxic effects of double-stranded ribonucleic acid (RNA) than uninfected mice. A dramatic increase in mortality was observed after injection of either synthetic (polyriboinosinic.polyribocytidylic acid) or natural (mycophage) double-stranded RNA in mice infected with Newcastle disease virus (NDV) or vesicular stomatitis virus (VSV). With the exception of endotoxin, interferon inducers other than double-stranded RNA, such as tilorone-hydrochloride and chlorite-oxidized oxyamylose, did not show this increased toxicity in virus-infected animals. The increased susceptibility of virus-infected animals to the toxic effects of double-stranded RNA appears to be related to the levels of interferon induced by the virus infection, either systemically, in the blood stream (after inoculation of NDV), or locally, in the brain (after infection with VSV).
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PMID:Increased toxicity of double-stranded ribonucleic acid in virus-infected animals. 434 63

The production of infectious vesicular stomatitis (VSV) and Newcastle disease virus can be completely inhibited by 2-deoxy-d-glucose in pyruvate-containing medium, if virus either grown in pyruvate-containing medium or dialyzed against phosphate-buffered saline is used for infection. Under these conditions, the synthesis of all VSV proteins is reduced. VSV RNA, which is synthesized at reduced rates, seems to be unstable. The effect is completely reversible. If virus grown in glucose-containing medium is used for infection, the production of both viruses is not significantly inhibited by 2-deoxy-d-glucose. Under these conditions the production of the VSV glycoprotein is specifically impaired, but does not lead to a marked reduction of the yield of infectious virus.
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PMID:Inhibition of the multiplication of vesicular stomatitis and Newcastle disease virus by 2-deoxy-d-glucose. 436 95

Heterologous viral interference is induced by Sindbis virus against vesicular stomatitis virus (VSV) in a manner analogous to intrinsic interference with Newcastle disease virus replication. Interference in both systems (i) depends upon early expression of the inducing virus genome, (ii) shows similar kinetics of induction, (iii) does not involve interferon action, and (iv) appears to be manifest as an all-or-none effect. VSV can be added to the list of viruses blocked by intrinsic interference. Sindbis virus-induced intrinsic interference with VSV replication is not mediated through homotypic interference by defective interfering particles; rather, T-particle and B-particle synthesis is inhibited. Significantly, intrinsic interference has no effect on primary transcription directed by the virion-associated transcriptase in VSV-challenged cells. However, Sindbis virus appears to induce interference with the VSV-RNA synthesized subsequent to primary transcription, namely, that which is dependent on protein synthesis. Thus, the target of intrinsic interference appears to be a reaction subsequent to primary transcription but prior to the appearance of protein synthesis-dependent VSV RNA, secondary transcription.
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PMID:Mechanism of Sindbis virus-induced intrinsic interference with vesicular stomatitis virus replication. 436 26

Peritoneal macrophages recovered from chickens 15 to 20 days after inoculation with fowlpox virus and showing a delayed hypersensitivity reaction against fowlpox antigens demonstrated an enhanced antimicrobial effect against fowlpox virus as well as unrelated viruses and bacteria. Inoculation of normal chicken macrophage cultures with fowlpox virus resulted in approximately a 200-fold increase in virus titer by 96 h, whereas the virus showed less than a fourfold increase in macrophage cultures from fowlpox-immune chickens. Similarly, the titer of Newcastle disease virus increased by more than 1 log in cultures of normal macrophages, whereas the titer decreased by approximately 1 log after infection of fowlpox-immune macrophages. Vaccinia, vesicular stomatitis, and herpes simplex viruses, which are not natural pathogens of chickens, failed to replicate in cultures of either normal or fowlpox-immune macrophages. By using Salmonella gallinarum, it was further demonstrated that the antimicrobial activity of fowlpox-immune macrophages encompassed not only nonspecific viruses but also bacteria. Infection of normal macrophages with Salmonella resulted in intracellular replication of the organism between 0 and 24 h as determined by microscope examination and viable bacteria counts. In contrast, cultures of fowlpox-immune macrophages failed to show an increase in intracellular organisms and showed a marked decrease in viable bacteria. In conclusion, these studies clearly showed that cellular immunity, previously demonstrated in mammalian species, develops in chickens after infection with fowlpox virus.
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PMID:In vitro cellular immunity to unrelated pathogens in chickens infected with fowlpox virus. 436 15

Newcastle disease virus (NDV) California strain reportedly grows poorly in L cells but replicates very well in chicken embryo cells. NDV-infected L cell cultures show a characteristic virus growth curve with respect to uridine incorporation, but plaque assays of the virus produced 24 h postinfection (PI) show no infectious particles when assayed on L cell monolayers and only a very low titer on chick cell monolayers. Plasma membranes isolated and purified from infected L cells 8 h PI contain all of the major virion proteins. In addition, NDV-infected L cells show a 50% loss of H-2 antigenic activity, a phenomenon previously observed in cells productively infected with vesicular stomatitis virus. These results suggest that at least part of the normal process of NDV maturation occurs in NDV-infected L cells. Sodium dodecyl sulfate-polyacrylamide gel patterns of supernatant virus purified from cells radiolabeled with amino acids from 3 to 24 h PI in the presence of actinomycin D show that all the major NDV structural proteins are present. Electron micrographs of NDV-infected L cells show extensive virus maturation at cell membranes. It can be concluded that infection of L cells with NDV results in a normal production of virus-specific RNA, synthesis of all the major structural proteins, association of the viral envelope proteins with the L cell plasma membrane, and the loss of cell surface H-2 antigenic activity. However, most of the virus particles produced are noninfectious.
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PMID:Newcastle disease virus infection of L cells. 483


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