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)

Infection of two different lines of polarized epithelial cells grown as monolayers with several types of enveloped viruses results, for each virus type, in a characteristic asymmetric budding of virions. Influenza virus (WSN strain), simian virus 5, and Sendai virus bud exclusively from the free (apical) surface of the cells, while vesicular stomatitis virus acquires its envelope only from the basolateral plasma membrane. Because different viruses select specific domains of plasma membrane in the same cell type, virus-infected epithelial monolayers can provide an excellent model system for studies of the mechanisms that generate regional differences in the distribution of plasma membrane components of epithelial cells.
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PMID:Asymmetric budding of viruses in epithelial monlayers: a model system for study of epithelial polarity. 28 16

The resistance of a total of 13 different viruses to some important chemico-physical influences was studied under uniform experimental conditions. Stability in tape water, thermostability and sensitivity to anodic oxidation, gamma radiation, some virucidal substances and several commercial disinfectants were tested. In evaluating the results, an attempt is made to rank the viruses investigated according to their sensitivity. On average a bovine parvovirus, and also a reovirus and three enteroviruses, proved most stable. These were followed by infectious canine hepatitis (adenoviruses). Newcastle disease (paramyxoviruses) and vaccinia (poxviruses) demonstrating less resistance. In all the tests an orthomyxovirus (influenza A), a rhabdovirus (vesicular stomatitis), and particularly a herpesvirus (pseudorabies) and a togavirus (sindbis) proved to have relatively low resistance.
Infection 1979
PMID:[Variations in resistance of viruses from different groups to chemico-physical decontamination methods]. 51 42

Prevention and treatment of oral disease is required to maintain quality of life and to improve prognosis of patients infected with the human immunodeficiency virus (HIV). Management requires a team approach, and close collaboration with the appropriate responsible physicians and other health care workers is necessary. Oral infection is frequent and usually opportunistic, and management is based on certain principles. Infections may disseminate and can be persistent and severe; multiple concurrent or consecutive infections with different microorganisms are frequent; fungal, viral, and parasitic infections are rarely curable; and long-term antimicrobial therapy may be required. This article reviews the management of oral candidiasis, hairy leukoplakia, and infections with herpes simplex virus, varicella-zoster virus, and cytomegalovirus. The management of Kaposi's sarcoma, lymphomas, aphthous ulceration, gangrenous stomatitis, bleeding, xerostomia, and adverse drug reactions is also described. Treatment should avoid further immunosuppression and inducement of xerostomia or caries, and should be designed to avoid adverse drug reactions and possible drug interactions.
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PMID:Management of oral health in persons with HIV infection. 131 92

Infection by vesicular stomatitis virus (VSV) results in a rapid inhibition of host cell transcription and translation. To determine whether the viral matrix (M) protein was involved in this inhibition of host cell gene expression, an M protein expression vector was cotransfected with a target gene vector, encoding the target gene, encoding chloramphenicol acetyltransferase (CAT). Expression of M protein caused a decrease in CAT activity in a gene dosage-dependent manner, and inhibition was apparent by 12 h posttransfection. The inhibitory effect of M protein was quite potent. The level of M protein required for a 10-fold inhibition of CAT activity was less than 1% of the level of M protein produced during the sixth hour of VSV infection. Northern (RNA) analysis of cotransfected cells showed that expression of M protein caused a reduction in the steady-state level of the vector-encoded mRNAs. Expression of both CAT and M mRNAs was reduced in cells cotransfected with a plasmid encoding M protein, indicating that expression of small amounts of M protein from plasmid DNA inhibits further expression of both M and CAT mRNAs. Nuclear runoff transcription analysis demonstrated that expression of M protein inhibited transcription of the target genes. This is the first report of a viral gene product which is capable of inhibiting transcription in vivo in the absence of any other viral component.
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PMID:Vesicular stomatitis virus matrix protein inhibits host cell-directed transcription of target genes in vivo. 131 97

Infection with wild-type adenovirus 5, but not with a mutant lacking the E1A gene, prevented the induction by interferon (IFN) alpha of chloramphenicol acetyltransferase (CAT) activity in HeLaM cell lines that had been permanently transfected with chimeric CAT reporter genes driven by the transcriptional regulatory regions of the IFN-responsive genes 561 and 6-16. Similar inhibition of IFN-inducible CAT activity was observed in cells that were cotransfected with the same reporter genes and plasmids expressing either the E1A 289- or 243-amino acid protein. These proteins also prevented the induction of CAT activity by IFN-gamma from a cotransfected HLA-DR alpha-CAT gene. Experiments with E1A mutants mapped the inhibitory activity to amino acid residues 38-65 of these proteins. In a HeLa cell line permanently expressing the E1A 289-amino acid protein, the replication of vesicular stomatitis virus and encephalomyocarditis virus was not inhibited by IFN-alpha, suggesting a global blockade of IFN responses. In accord with this theory, induction of 561, 1-8, and (2'-5')oligoadenylate synthetase mRNAs by IFN was blocked in these cells at the transcriptional level. The observed transcriptional inhibition could be attributed to the lack of formation of the crucial IFN-stimulated gene factor 3 (ISGF3) transcriptional complex. As shown by mobility shift assays, this complex was not formed in the nuclear extracts of IFN-treated adenovirus-infected cells or IFN-treated E1A-producing cells. These nuclear extracts were deficient in both ISGF3 alpha and ISGF3 gamma subunits. However, they did not block the formation of ISGF3 complex from exogenously added components.
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PMID:Inhibition of interferon-inducible gene expression by adenovirus E1A proteins: block in transcriptional complex formation. 165 51

The denV gene from bacteriophage T4 encodes a pyrimidine dimer-specific endonuclease that has the capacity to initiate excision repair of DNA. Cells from excision repair-deficient xeroderma pigmentosum (XP) patients are able to carry out excision repair initiated by the denV gene product and introduction of the denV gene into XP cells results in the partial restoration of colony-forming ability after irradiation with UV light. In this work we have constructed a helper-independent recombinant human adenovirus, Ad5denV, which contains the denV gene. A 1.9 kb cartridge consisting of the denV gene flanked by the long terminal repeat (LTR) promoter from Rous sarcoma virus (RSV) and the simian virus 40 (SV40) polyadenylation (poly A) splice signals, was inserted into the E3 region of an E3 deletion mutant (Ad5d1E3) of adenovirus type 5. Infection of human fibroblasts and other permissive human cells with Ad5denV resulted in lytic infection and expression of the denV gene was confirmed by primer extension of infected cell RNA. The ability of the denV gene to restore the DNA repair deficiency in XP fibroblasts was examined using host cell reactivation of viral structural antigen formation for UV-irradiated adenovirus. The control virus, Ad5VSV, was also a recombinant which contained the gene for vesicular stomatitis virus glycoprotein G inserted into the E3 region of Ad5d1E3. UV survival of Ad5denV was similar to that of Ad5VSV following infection of two normal fibroblast strains and a Cockayne syndrome fibroblast strain, CS7SE, from complementation group B. In contrast, UV survival of Ad5denV was significantly greater than that for Ad5VSV after infection of three unrelated XP fibroblast strains from complementation groups A, C and E. However, UV survival of Ad5denV in the XP fibroblasts did not reach levels obtained in normal fibroblasts, indicating that restoration of the XP defect was partial.
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PMID:Construction of a recombinant adenovirus containing the denV gene from bacteriophage T4 which can partially restore the DNA repair deficiency in xeroderma pigmentosum fibroblasts. 170 21

Mixed infection of a cell by vesicular stomatitis virus (VSV) and retroviruses results in the production of progeny virions bearing the genome of one virus encapsidated by the envelope proteins of the other. The mechanism for the phenomenon of pseudotype formation is not clear, although specific recognition of a viral envelope protein by the nucleocapsid of an unrelated virus is presumably involved. In this study, we used Moloney murine leukemia virus (MoMLV)-based retroviral vectors encoding the gene for neomycin phosphotransferase to investigate the interaction between the VSV G protein and the retroviral nucleocapsid during the formation of MoMLV(VSV) pseudotypes. Our results show that VSV G protein can be incorporated into the virions of retrovirus in the absence of other VSV-encoded proteins or of retroviral envelope protein. Infection of hamster cells by MoMLV(VSV) pseudotypes gave rise to neomycin phosphotransferase-resistant colonies, and addition of anti-VSV serum to the virus preparations completely abolished the infectivity of MoMLV(VSV) pseudotypes. It should be possible to use existing mutants of VSV G protein in the system described here to identify the signals that are important for the formation of MoMLV(VSV) pseudotypes.
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PMID:Pseudotype formation of murine leukemia virus with the G protein of vesicular stomatitis virus. 184 50

The kinetic study of immunosuppression caused by infection of mice with lymphocytic choriomeningitis virus WE (LCMV-WE) was assessed in DBA/2 (H-2d) and C57BL/6 (H-2b) mice. Infection with LCMV caused suppression of the Day 4 IgM response (complete in DBA/2 and incomplete in C57BL/6) and completely suppressed IgG responses on Days 9 and 42 to vesicular stomatitis virus (VSV) injected 2-11 days after LCMV. Suppression was partial when VSV was injected 16-28 days after LCMV-WE infection. The observed suppression between Day 2 and Day 11 was complete and nonspecific as revealed by the fact that these mice could not mount a secondary response to VSV when reinjected with the same VSV 42 days later. Nonspecificity of suppression was further indicated by the finding that the kinetics of recovery from suppression of the anti-VSV response were comparable for the VSV serotype used during the 2- to 11-day period after LCMV infection as for the serologically noncross-reactive second VSV serotype; both anti-VSV responses had recovered by Days 56-82 after LCMV infection. Once an anti-VSV antibody response was established, a subsequent LCMV-WE infection had no suppressive effect on Day 2 or Day 42 after a primary VSV infection. Also, the capacity of VSV-primed mice that were LCMV infected to respond to VSV in a secondary challenge infection with the same VSV was not impaired.
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PMID:Immunosuppression in mice by lymphocytic choriomeningitis virus infection: time dependence during primary and absence of effects on secondary antibody responses. 217 31

Infection of tissue culture cells with certain viruses results in the shutoff of host cell protein synthesis. We have examined virally infected cell lysates using two-dimensional gel electrophoresis and immunoblotting to ascertain whether initiation factor protein modifications are correlated with translational repression. Moderate increases in eukaryotic initiation factor (eIF)-2 alpha phosphorylation are detected in reovirus- and adenovirus-infected cells, as reported previously (Samuel et al., 1984; O'Malley et al., 1989). Neither vesicular stomatitis virus, vaccinia virus, frog virus III, rhinovirus, nor encephalomyocarditis virus caused significantly increased 2 alpha phosphorylation. There were no reproducible, significant changes in eIF-4A, eIF-4B, or eIF-2 beta in cells infected by any of these viruses. The cleavage of eIF-4F subunit p220, such as has been previously demonstrated to occur in poliovirus (Etchison et al., 1982) and rhinovirus (Etchison and Fout, 1985), was not detected in any of the other virus infections analyzed.
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PMID:Protein synthesis initiation factor modifications during viral infections: implications for translational control. 218 34

Responsiveness to granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage CSF (M-CSF) of bone marrow cells derived from different mouse strains was investigated. There were great variations in proliferation between different strains of inbred mice. Bone marrow cells from mouse strains with a high rate of proliferation in response to GM-CSF also had a high proliferating capacity to M-CSF. The response to either CSF did not correlate with a certain H-2 haplotype. GM-CSF induced consistently higher proliferation than M-CSF. Proliferation in response to M-CSF, but not to GM-CSF, could be enhanced by the addition of antibodies against interferon (IFN). IFN is the only known inducer of (2'-5') oligoadenylate (oligo (A] synthetase. This enzyme was induced in macrophages grown in the presence of M-CSF, but not in GM-CSF promoted cells. Enzyme induction was completely abrogated by simultaneous treatment with anti-IFN alpha/beta. Infection of macrophages with herpes simplex virus type 1 (HSV) and vesicular stomatitis virus (VSV) revealed that GM-CSF-promoted cells were highly susceptible to lytic infection by these viruses. In contrast, virus titres in M-CSF-cultured cells were 100-fold lower. We conclude that, contrary to M-CSF, GM-CSF does not induce autocrine IFN during haematopoiesis. As judged from data with BALB/c mice, the sensitivity to the anti-proliferative effect of the autocrine IFN may be a factor which influences M-CSF-promoted proliferation.
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PMID:In vitro development of bone-marrow-derived macrophages. Influence of mouse genotype on response to colony-stimulating factors and autocrine interferon induction. 248 39


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