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

Virus-induced cell fusion has been examined in a series of stable cell lines which were originally selected for resistance to the fusogenic effects of polyethylene glycol (PEG). For a wide variety of viruses, including murine hepatitis virus (a coronavirus), vesicular stomatitis virus (a rhabdovirus), and two paramyxoviruses (Sendai virus and SV5), susceptibility to virus-induced fusion was found to be inversely correlated with susceptibility to PEG-induced fusion. This phenomenon was observed both for cell fusion occurring in the course of viral infection and for fusion induced "from without" by the addition of high titers of noninfectious or inactivated virus. The fusion-altered cell lines (fusible by virus but not by PEG) are characterized by their unusual lipid composition, including marked elevation of saturated fatty acids and the presence of an unusual ether-linked neutral lipid. To test the association between lipid composition and fusion, acyl chain saturation was manipulated by supplementing the culture medium with exogenous fatty acids. In such experiments, it was possible to control the responses of these cells to both viral and chemical fusogens. Increasing the cellular content of saturated fatty acyl chains increased the susceptibility of cells to viral fusion and decreased susceptibility to PEG-induced fusion, whereas lowering fatty acid saturation had the opposite effect. Thus, parallel cultures of cells can be either driven toward the PEG-fusible/virus-fusion-resistant phenotype of the parental cells or rendered susceptible to viral fusion but resistant to PEG-induced fusion, solely by the alteration of cellular lipids. The ability of cellular lipid composition to regulate virus-induced membrane fusion suggests a possible role for lipids in viral infection and pathogenesis.
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PMID:Control of virus-induced cell fusion by host cell lipid composition. 215 79

Metabolically stable phosphorothioate tetramer analogues of (2'-5')(A)n with Rp and/or Sp chirality in the 2'-5'-phosphodiester linkages constitute a new class of antiviral agents since they mimic the effects of interferons. Three of the diastereomeric 5'-monophosphates (i.e., pRpRpRp, pSpRpRp, and pRpSpSp) bind to and activate RNase L from extracts of HeLa cells. However, the pSpSpSp (2'-5')-(A)4-phosphorothioate is unique in that it binds to, but cannot activate, RNase L to cleave rRNA. When microinjected into the cytoplasm of HeLa cells followed by virus infection, the pRpRpRp, pSpRpRp, and pRpSpSp (2'-5')(A)4-phosphorothioates demonstrate antiviral activity, as does (2'-5')(A)4ox-red, an active (2'-5')(A)n analogue. When microinjected simultaneously with (2'-5')(A)nox-red, an active the pSpSpSp (2'-5')(A)4-phosphorothioate inhibits activation of RNase L in HeLa cells, thereby blocking direct protection of vesicular stomatitis virus. The agonist and antagonist properties of pRpRpRp and pSpSpSp, respectively, are transient probably as a consequence of the hydrolysis of the 5'-monophosphate and formation of the less active (2'-5')(A)4-phosphorothioate cores. The possible use of these (2'-5')(A)4-phosphorothioates as tools for dissecting the biological significance of the (2'-5')(A)n system or in antiviral chemotherapy is discussed.
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PMID:Phosphorothioate analogues of (2'-5')(A)4: agonist and antagonist activities in intact cells. 215 24

We examined the inductive signals necessary to render B lymphocytes capable of supporting a productive vesicular stomatitis virus infection. Small murine splenic B cells in the G0 phase of the cell cycle were cultured with stimulators which allow progression through various stages in the activation and/or differentiation pathway leading to antibody secretion. We found that vesicular stomatitis virus expression is dependent on the state of B-cell activation and that three distinct phases can be defined. A nonsupportive state, which is defined by the failure to produce infection centers, viral proteins, or PFUs, is characteristic of freshly isolated small B cells, B cells cultured 48 h without further stimulation, or B cells in the G1 phase of the cell cycle induced by culture with T-cell-derived lymphokines. This refractory state was not due to a failure of virus uptake. Activation of G0 B cells with anti-immunoglobulin at doses which allow entry into the S phase rendered them capable of synthesizing viral proteins and increased the number of B cells producing infection centers, without enhancing PFU production on a per cell basis. In contrast, B cells stimulated with multiple inductive signals provided by anti-immunoglobulin and lymphokines showed increased infectious particle production (7 PFU per infection center). Lipopolysaccharide stimulation, acting through another induction pathway, caused the maximum increase in the number of infected B cells and production of infectious particles (25 PFU per infection center).
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PMID:Virus-lymphocyte interactions: inductive signals necessary to render B lymphocytes susceptible to vesicular stomatitis virus infection. 216 42

Attempts were made to demonstrate herpes simplex virus (HSV) type 1 and type 2, varicella zoster virus (VZV) and cytomegalovirus (CMV) in specimens obtained from aphthous ulceration lesions by the immunofluorescent method using fluorescein-labeled monoclonal antibodies. HSV-1 and VZV were detected in 2 and 4 out of 30 patients, respectively. Although almost all viruses that can infect the oral cavity could occasionally cause stomatitis, neither HSV-2 nor CMV was not found in this study. VZV was detected in 1 out of 8 patients with recurrent aphthous ulceration. After treatment with acyclovir, the patient's symptoms has become less severe and recurrence rates of attacks reduced, however, the patient has not been totally free of the disease. There were no differences in clinical aspects of stomatitis between the patients with and without viral isolation. Further clinical investigation is encouraged to confirm the relationship between aphthous stomatitis and viral infection.
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PMID:[Detection of herpes simplex virus, varicella zoster virus and cytomegalovirus in aphthous stomatitis]. 217 Jun 7

Treatment of cells with interferons (IFNs) induces resistance to virus infection. The 2'-5'oligo A (2-5A) synthetase/RNase L is one of the pathways leading to translation inhibition induced by IFN treatment. A murine cDNA encoding the 43-kDa 2-5A synthetase was cloned and sequenced. NIH-3T3 cell clones transfected with this cDNA expressed the enzymatic activity to various extents and exhibited resistance to encephalomyocarditis virus (EMCV) but not to vesicular stomatitis virus replication. The specific resistance to EMCV can be attributed to 2-5A synthetase.
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PMID:A full-length murine 2-5A synthetase cDNA transfected in NIH-3T3 cells impairs EMCV but not VSV replication. 217 Dec 6

Theiler's murine encephalomyelitis virus (TMEV) induces demyelinating disease which is associated with persistent virus infection of the central nervous system. To study the interaction between TMEV and host cells, we infected the G26-20 glioma cell line in vitro, and this resulted in a lytic infection in which most, but not all, cells were killed. Surviving cells divided and formed a viable monolayer in which a small proportion of cells displayed viral cytopathic effects. Levels of virus produced by these cultures over a 6 month period fluctuated between 6 and 8 log10 p.f.u./ml as measured by viral plaque assay. Similarly, the percentage of cells producing both viral antigen and viral RNA, as measured by a simultaneous immunoperoxidase/in situ hybridization technique, varied between 5 and 30%. Although persistently infected cultures were susceptible to challenge by both vesicular stomatitis virus and herpes simplex virus, they were resistant to infection by homologous viruses. Interferon activity was not identified. TMEV isolated from passage 12 produced smaller plaques than wild-type Daniels strain virus (wt-DAV) on L-2 cell monolayers. In contrast to demyelination induced in SJL/J mice after intracerebral inoculation with wt-DAV, mice infected with the small plaque variant virus failed to develop viral persistence or chronic demyelination. However, following immunosuppression by total body irradiation, SJL/J mice infected with the small plaque variant developed viral persistence but no demyelination. Characterization of the biochemical and molecular determinants of the variant will lead to a better understanding of determinants important in viral persistence.
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PMID:Persistent infection of a glioma cell line generates a Theiler's virus variant which fails to induce demyelinating disease in SJL/J mice. 221 94

From January 1988-September 1989, dental practitioners performed a comprehensive oral examination on 83 HIV positive patients at the Department of Infectious Diseases, University Clinic of Internal Medicine in Kinshasa, Zaire for a study on prevalence and clinical aspects of oral lesions associated with HIV infection. Women comprised 55.5% of these AIDS patients. They all had oral lesions: 94% fungal, 33% bacterial, 23% viral, 14% unknown origin, and 12% neoplasms. The majority of these oral lesions developed in 31-40 year olds. Further, the 21-30 year olds were more likely to have bacterial infections, especially aggressive periodontitis. Fungal infections occurred most often on the lips, palate, and tongue, while viral infections occurred mainly on the tongue. Kaposi's sarcoma only afflicted the palate. Pseudomembranous candidiasis was the leading fungal infection (32% of all oral lesions) then atrophic (22.8%) and hyperplastic (6%) types. 17% and 16% of all lesions included these bacterial infections: aggressive periodontitis and necrotizing gingivitis respectively. the leading viral infection was hairy leukoplakia (14%) followed by leukoplakia (8%), and herpetic stomatitis (4%). The unknown lesions included ulcers (12%) and a swollen salivary gland )2%). 12% of the examined AIDS patients, mostly 31-50 year olds, had oral Kaposi's sarcoma. They also had it on other parts of the body. Since HIV prevalence in Zaire ranges between 3-8%, all dentists should be cognizant of oral manifestations of HIV which may indeed be the 1st clinical indications of HIV. They should refer any patients with such lesions to a health facility with AIDS specialists for diagnosis and care.
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PMID:Oral manifestations of AIDS in a heterosexual population in a Zaire hospital. 235 42

Papaverine, an inhibitor of cAMP phosphodiesterase, reduced yields of infectious vesicular stomatitis virus in HEp-2 cells approximately 100-fold if added to cultures at a concentration of 30 microM before and after virus infection. The extent of papaverine-induced suppression of viral growth was dependent on drug dose and treatment regimen. Cells progressively recovered their viral permissive state after removal of drug. The cyclic nucleotide, cGMP, nullified the inhibitory effect of papaverine if added to cells during drug treatment. Pulse labeling experiments with [35S]methionine showed that papaverine compromises production of all virus-specific proteins in infected cells without adversely affecting host cell protein synthesis. Treatment of cells with papaverine strongly inhibited the production of viral RNA and both cellular RNA and DNA. It was found that VSV causes an immediate but transient stimulation of DNA synthesis in HEp-2 cells which is prevented by papaverine treatment. This drug also selectively blocked primary transcription of VSV in vivo and to a lesser extent in vitro RNA polymerase activity of the virion-bound transcriptase. The finding that papaverine has a strong inhibitory effect on viral biosynthesis including early transcription suggests that VSV replication may depend on host factors that regulate intracellular levels of cyclic nucleotides such as cAMP.
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PMID:Inhibitory effect of papaverine on RNA and protein synthesis of vesicular stomatitis virus. 241 Oct 62

From the NIH 3T3 clone 1 line which is normally unprotected by interferon (IFN) against lytic virus infection we have selected subclones which show high sensitivity to IFN. The selection procedure was based on encephalomyocarditis virus (EMCV) as selection agent. In the IFN-sensitive subclones thus obtained EMCV replication was inhibited by IFN to a similar degree as observed in L929 cells. Like in the original NIH 3T3 clone 1 line, however, replication of vesicular stomatitis virus (VSV) and cell multiplication were only marginally affected by IFN. We measured the levels of known IFN-induced enzymes (2-5A-synthetase, dsRNA protein kinase and 2-5A-dependent RNase) in a number of subclones and found no consistent differences to the original population. Thus, the newly acquired IFN-dependent protection against EMCV may be mediated by a different antiviral mechanism.
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PMID:Studies on interferon-sensitive cells derived from the interferon-resistant NIH 3T3 clone 1 line. 242 4

Despite many attempts to find reliable in vitro criteria for the efficacy of Biological Response Modifiers--BRMs (immunomodulators, paramunity inducers) animal challenge models are still the only way to demonstrate the totality of interlocking defense mechanisms. Challenge models with mouse pathogenic viruses provide an excellent possibility to study protective effects of BRMs against acute or chronic forms of viral diseases. For comparative studies two completely different virus challenge models--Pseudorabies PR and Stomatitis Vesicularis VSV--were developed with adult and baby NMRI mice respectively. The potency of BRMs in preventing lethal disease reveals significant differences depending upon the sort of BRM, the route of application and the time of pretreatment. Defense mechanisms important for the control of Pseudorabies virus infection in adult NMRI mice were tested in vitro (ex vivo) and correlated well with the degree of protection in vivo. Comparison of BRM efficacy in selective viral challenge models combined with screening of a variety of antiviral defense functions in infected animals in vitro provide reliable methods in demonstrating the potency of BRMs against viral infections.
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PMID:Tests on protection against viral diseases. 243 29


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