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

A temperature-sensitive (ts) mutant of vesicular stomatitis virus (VSV), tsG31, produces a prolonged central nervous system disease in mice with pathological features similar to those of slow viral diseases. tsG31 and the subsequent virus recovered from the central nervous system (tsG31BP) of mice infected with tsG31 were compared with the parental wild-type (WT) VSV for plaque morphology, growth kinetics, thermal sensitivity of the virions, and viral protein synthesis and maturation. Several properties of the central nervous system isolate distinguished this virus from the original tsG31 and the WT VSV. The WT VSV produced clear plaques with complete cell lysis, and the tsG31 produced diffuse plaques and incomplete cell lysis, whereas the tsG31BP had clear plaques similar to those of the WT VSV. Although plaque morphology suggested that tsG31BP virus was a revertant to the WT, growth kinetics in either BHK-21 or neuroblastoma (N-18) cells indicated that this virus was similar to tsG31, with a productive cycle at 31 degrees C and no infectious virus at 39 degrees C. At 37 degrees C, however, the tsG31BP matured much slower than did the original tsG31 (and produced only 1% of the yield measured at 31 degrees C). WT VSV produced similar quantities of infectious virions at 31, 37, and 39 degrees C. The lack of infectious virions at 39 degrees C for the ts mutants was presumably not due to a greater rate of inactivation at 39 degrees C. Unlike WT VSV, which synthesized viral proteins equally well at all three temperatures, tsG31 had a reduced synthesis of all the structural proteins at 37 and 39 degrees C, compared with that at 31 degrees C; the formation of the M protein was most temperature sensitive. In addition, fractionation of the infected cells indicated that the incorporation of the M and N proteins into the cellular membranes was also disrupted at the higher, nonpermissive temperatures. Several characteristics of protein synthesis during tsG31BP infection at 39 degrees C distinguished this virus from tsG31: (i) no mature viral proteins were detected at 39 degrees C; (ii) several host proteins were [ill], suggesting that the virus was incapable of completely depressing host macromolecular synthesis; and (iii) a great proportion of the incorporated radioactivity was found in unusually high-molecular-weight proteins. In addition, at 37 degrees C, the tsG31BP virus showed a decreased synthesis of viral proteins and reduced assembly of the viral structural proteins.
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PMID:Growth and maturation of a vesicular stomatitis virus temperature-sensitive mutant and its central nervous system isolate. 21 25

Four methods for the assay of human interferon in Vero cells were compared based on the inhibition of viral cytopathic effect (CPE) in tubes, the inhibition of CPE in microplates, the reduction of plaques, and the inhibition of quantitative hemadsorption. For inhibition of CPE, Sindbis virus, vesicular stomatitis virus, poliovirus type 2, and vaccinia virus were used for challenge. In the plaque reduction method, Sindbis virus, vesicular stomatitis virus, and poliovirus were employed, and Newcastle disease virus was used in the quantitative hemadsorption assay. Sindbis virus was most susceptible to interferon in those tests measuring inhibition of CPE, but vesicular stomatitis virus was as sensitive in the plaque reduction method. Highest titers of interferon were recorded in microplates, especially with Sindbis virus as the challenge agent, followed by the quantitative inhibition assay. The CPE inhibition method was the simplest, and the quantitative hemadsorption assay was the most rapid to perform. Reproducibilities, as shown by the coefficient of variation, were 15, 39, and 59% for plaque reduction, CPE inhibition in tubes, and CPE inhibition in microplates, respectively.
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PMID:Assay of human interferon in Vero cells by several methods. 22 3

Cultures of bovine kidney (BK) cells infected with temperature-sensitive (ts) mutants of foot-and-mouth disease virus (FMDV) were incubated at 38.5 degrees C, a temperature nonpermissive for mutant virus growth and RNA synthesis. The cells were subsequently resistant to viral growth and RNA synthesis when superinfected with wild-type FMDV and with heterologous fowl plague virus. The extent of interference was proportional to the multiplicity of infection of the ts mutant. It increased with time elapsed between infection with mutant and challenge infection, becoming greater than 99 percent after 24 hours. Interference was not proportional to decreased levels of cellular protein synthesis. The interference could be produced in the presence of actinomycin D, and thus was apparently mostly caused by the ts mutant itself rather than by interferon. The interference could not be produced in other less susceptible cell lines. Supernatant fluids from the BK cells infected with ts mutant virus interfered with wild-type FMD viral growth and RNA synthesis in fresh BK cells, and also showed low levels of activity in a vesicular stomatitis virus-plaque reduction assay. The properties of the supernatant fluid-interfering agent resembled to some extent those of an interferon. The ts mutant-mediated interference factor was apparently not able to diffuse into the supernatant fluid.
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PMID:Viral interference phenomena induced by foot-and-mouth disease temperature-sensitive mutants in bovine kidney cells. 22 87

Four strains of vesicular stomatitis virus--New Jersey (Hazelhurst, Guatemala, Panama, and Concan) were compared by cross-neutralization and complement-fixation tests. They were indistinguishable by complement-fixation test; however, by plaque-reduction neutralization method, slight antigenic differences were observed between the Hazelhurst and the three other strains. It is concluded that these antigenic differences are insufficient to warrant reclassification of vesicular stomatitis virus--New Jersey into two distinct subtypes, as has been recently proposed.
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PMID:Antigenic variation among strains of the New Jersey serotype of vesicular stomatitis virus. 23 Jul 69

It was the purpose of the study to test the efficiency of dextranase, mutanase, and protease in removing denture plaque. The study group comprised 100 denture-wearers with denture stomatitis. The enzymes were dispensed as dissolvent tablets either in pure or in mixed preparations. Placebo tablets and Steradent, a commercial denture cleanser, were used as control tablets. The following parameters were studied: the amount of denture plaque, the degree of palatal erythema, and the concentration of yeast cells and inflammatory cells in mucosal and denture smears. The study was designed and carried out as a double-blind study. The dissolvent tablets containing the enzymes in mixed preparations were more effective than the tablets containing the pure enzymes, the placebo tablets, or the Steradent tablets. The beneficial effect of the mixed enzyme preparations included a significant reduction of the amount of denture plaque and an improvement of the clinical condition of the palatal mucosa.
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PMID:Enzymes as denture cleansers. 32 51

It was the purpose of the study to test the efficacy of brushing with a 1% chlorhexidine gel or a commercial solution cleanser (Steradent) in preventing formation of plaque on the fitting surface of new dentures. The study group consisted of 74 denture wearers with denture stomatitis who were assigned randomly to one of four treatment groups, testing either the chlorhexidine gel, a placebo gel, Steradent, or a placebo solution. The experiment was started immediately after denture treatment was completed. The experimental period was 1 month. The amount of denture plaque, the clinical condition of the palatal mucosa, and the concentration of yeasts in mucosal and denture smears were recorded while the patients used their original dentures and after the experimental period. Plaque had formed on all new dentures but to a smaller extent in the groups testing the chlorhexidine gel or the placebo gel. The study does not provide any obvious evidence of a chemical effect of chlorhexidine gel or Steradent as a means to prevent formation of microbial plaque on the mucosal surface of maxillary complete dentures.
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PMID:Chlorhexidine gel and Steradent employed in cleaning dentures. 34 70

Periodontal disease and dental plaque may predispose patients receiving antineoplastic drugs to stomatitis. Dental evaluation and appropriate treatment including oral hygiene are proposed to reduce the incidence and severity of stomatitis.
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PMID:Periodontal disease: predisposing factor to chemotherapy-induced stomatitis. 47 1

Wild type Eastern equine encephalitis virus (E) was compared with a mutant (Em) derived from it. The latter was tested as an attenuated vaccine in mice. They differed in the following properties: Em formed smaller plaques on chick embryo (CE) cell monolayers and, unlike E, did not plaque on mouse embryo (ME) monolayers. Futher, Em had a longer latent period and attained a lower peak titer than E after infection of CE cells, was more senssitive than E to chick interferon, and was less virulent for mice (SC and IP routes) and hamsters (IP route) than E. Both viruses were similar in several other properties tested. The mutant was found to induce a gradient in the specificity of protection in mice against challenge by selected viruses after a single subcutaneous injection of living virus. The protection was best against autologous (Em) challenge, was next best against challenge by the virulent parent (E) virus, but was not demonstrable against cross challenge by Venezuelan encephalitis (V) virus. Conventional hemagglutination-inhibiting (HI), complement-fixing (F), and neutralizing (N) antibodies could not be detected in Em-immunized mice even when fresh monkey or guinea pig serum was included in Ntests to provide complement and/or accessory factor(s). However, N antibodies were detected in protected mice by an indirect antiglobulin test. Passive protection by serum or ascites fluids (a.f.) was characterized by a lower but otherwise similar protection gradient like that found after active immunization with virus as described above. Interferon was not detected in the a.f. used for passive protection, nor was heterologous interference evident in Em immunized mice challenged 18 days later with vaccinia or vesicular stomatitis virus. Immunized mice that survived autologous (Em) challenge showed broadened protection against a second challenge by parent E virus, and cross protection against V virus. This typical protection was associated with the presence of HI and conventional N antibodies, except for V which showed no detectable neutralizing antibodies by either a standard or antiglobulin technique.
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PMID:An attenuated variant of Eastern encephalitis virus: biological properties and protection induced in mice. 111 39

Transovarial transmission of La Crosse virus by experimentally infected Aedes albopictus females to 2.7% of their F1 generation offspring was demonstrated. Progeny of both sexes were infected. Mean virus titers in parent mosquitoes and infected F1 generation adults were 10(4.6) and 10(3.4) plaque forming units/insect, respectively. The La Crosse-infected offspring were randomly distributed among the female parents. After two serial passages in A. albopictus, a marked change occurred in the plaque morphology of the virus but this had no apparent effect on the subsequent vertical transmission rate. In contrast, transovarial transmission did not occur in La Crosse-infected Culex fatigans or in A. albopictus and C. fatigans infected with vesicular stomatitis-Indiana, Cache Valley, Batai, Arumowot, and Itaporanga viruses. Results of this experiment suggest that the La Crosse model might be useful in studying the mechanism of transovarial transmission in additional mosquito species.
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PMID:Laboratory studies of transovarial transmission of La Crosse and other arboviruses by Aedes albopictus and Culex fatigans. 119 Mar 73

In this study, we have analysed the effects of cAMP inducers on the multiplication of vesicular stomatitis virus (VSV) and herpes simplex virus type 1 (HSV-1) in mouse macrophage-like cells. The addition of dibutyryl cAMP (dB-cAMP) or cholera toxin to resting peritoneal macrophages aged in vitro or P388D1 cells resulted in a 10- to 100-fold reduction of VSV yield compared to control cultures. In contrast, no cAMP-dependent inhibition was found in VSV-infected L929 cells. In macrophage-like cells, the dB-cAMP-induced antiviral state was not inhibited by antibodies to interferon (IFN)-alpha/beta and did not correlate with any increase in the intracellular levels of 2-5 oligo(A) synthetase. Dibutyryl cAMP did not inhibit virus yields in mouse macrophages infected with encephalomyocarditis virus. In P388D1 cells, the addition of dB-cAMP resulted in an approximately 10-fold inhibition of HSV-1 replication with respect to control cultures, as evaluated both by TCID50 and plaque assays on Vero cells. Dibutyryl cAMP did not affect VSV binding or entry into mouse macrophages and the cAMP-mediated anti-VSV state was significantly reduced by inhibitors of protein kinase C (i.e. staurosporine and H7). These data suggest that macrophages may acquire resistance to infection by VSV and HSV-1 after treatment with cAMP inducers. This cAMP-mediated antiviral activity does not depend on the modulation of the endogenous IFN system, suggesting that macrophages exhibit multiple resistance mechanisms (i.e. IFN-dependent and IFN-independent) to maintain their intrinsic antiviral activity.
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PMID:Cyclic AMP-mediated inhibition of vesicular stomatitis virus and herpes simplex virus replication in mouse macrophage-like cells. 127 3


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