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 CD8 T cell response to vesicular stomatitis virus infection was characterized in the spleen and intestinal mucosa using MHC tetramers. Surprisingly, the primary response persisted in the lamina propria long after the splenic response had declined. Furthermore, the response was characterized by a protracted effector phase in which cytolytic activity in the lamina propria, but not in the spleen, was maintained. The appearance of Ag-specific cells in the intestinal mucosa was largely, though not exclusively, a result of beta(7) integrin-mediated migration. Infection with Listeria monocytogenes or with vaccinia virus also led to sustained mucosal responses. After reinfection of vesicular stomatitis virus-primed mice with a serotypically distinct virus, a sustained recall response was detected in all tissues. In CD40(-/-) mice, the mucosal, but not the splenic, response was compromised, resulting in diminished mucosal memory. The recall response was CD40 independent and correlated with memory levels, indicating that the mucosal and systemic responses operated independently. These findings illustrated the integrated yet distinct nature of systemic vs mucosal immune responses.
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PMID:Direct analysis of the dynamics of the intestinal mucosa CD8 T cell response to systemic virus infection. 1116 Feb 92

Infection with a newly described endotheliotropic adenovirus was the cause of a 1993 epizootic reminiscent of hemorrhagic disease in California mule deer (Odocoileus hemionus columbianus and O. hemionus hemionus). Pulmonary edema and intestinal luminal hemorrhage, or necrotizing stomatitis associated with systemic or localized vasculitis, respectively, were common lesions seen in animals that died during the epizootic. In order to determine if white-tailed deer (Odocoileus virginianus) also are susceptible to infection and fatal disease with the deer adenovirus, eight white-tailed deer fawns (4- to 6-mo-old) were inoculated with purified deer adenovirus. Four were inoculated intravenously and four were inoculated through the mucous membranes. Seven days post-inoculation, one of the fawns inoculated intravenously died. Pulmonary edema and hemorrhagic enteropathy were associated with pulmonary and intestinal vasculitis with systemic multiorgan distribution of endotheliotropic adenovirus as demonstrated by transmission electron microscopy and immunohistochemistry. Adenovirus was reisolated from lung homogenates of the fawn that died of adenovirus hemorrhagic disease.
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PMID:Experimental adenovirus hemorrhagic disease in white-tailed deer fawns. 1127 90

Conventional phenotypic analysis of resistance of the human immunodeficiency virus (HIV) to antiviral therapy is time-consuming and requires culture of infectious virus. Although phenotypic analyses may be desirable, rapid generation of test results and decentralized availability of the test system will be important to achieve utility in the clinical practice. This study describes the design of an alternative phenotypic resistance test using replication incompetent viral vectors. Chimeric HIV vectors containing a marker gene were generated. The env and most of the regulatory and accessory genes of HIV were removed. In addition, the 3'U3 region was deleted to obtain a self-inactivating construct. Cotransfection of the plasmid with a plasmid that provided the vesicular stomatitis virus glycoprotein resulted in the production of replication-incompetent virus vectors. Infection of susceptible cells with the vectors led to marker gene expression. Vector production in the presence of protease (PR) inhibitors, or infection in the presence of reverse transcriptase (RT) or integrase (IN) inhibitors reduced marker gene expression in a dose-dependent manner. Marker gene activity was preserved at higher drug levels if vectors contained RT and PR genes from resistant virus isolates. Sensitivity to nucleoside and non-nucleoside RT inhibitors, protease and integrase inhibitors could be determined in 10 working days. The phenotypic drug resistance test using replication-incompetent HIV vectors significantly speeds up drug resistance measurements and allows testing at reduced biosafety levels. This will make clinical use of phenotypic assessment of antiviral resistance more feasible.
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PMID:Phenotypic analysis of the sensitivity of HIV-1 to inhibitors of the reverse transcriptase, protease, and integrase using a self-inactivating virus vector system. 1142 8

Human astrocytes can be infected with human immunodeficiency virus type 1 (HIV-1) in vitro and in vivo, but, in contrast to T lymphocytes and macrophages, virus expression is inefficient. To investigate the HIV-1 life cycle in human fetal astrocytes, we infected cells with HIV-1 pseudotyped with envelope glycoproteins of either amphotropic murine leukemia virus or vesicular stomatitis virus. Infection by both pseudotypes was productive and long lasting and reached a peak of 68% infected cells and 1.7 microg of viral p24 per ml of culture supernatant 7 days after virus inoculation and then continued with gradually declining levels of virus expression through 7 weeks of follow-up. This contrasted with less than 0.1% HIV-1 antigen-positive cells and 400 pg of extracellular p24 per ml at the peak of astrocyte infection with native HIV-1. Cell viability and growth kinetics were similar in infected and control cells. Northern blot analysis revealed the presence of major HIV-1 RNA species of 9, 4, and 2 kb in astrocytes exposed to pseudotyped (but not wild-type) HIV-1 at 2, 14, and 28 days after infection. Consistent with productive infection, the 9- and 4-kb viral transcripts in astrocytes infected by pseudotyped HIV-1 were as abundant as the 2-kb mRNA during 4 weeks of follow-up, and both structural and regulatory viral proteins were detected in infected cells by immunoblotting or cell staining. The progeny virus released by these cells was infectious. These results indicate that the major barrier to HIV-1 infection of primary astrocytes is at virus entry and that astrocytes have no intrinsic intracellular restriction to efficient HIV-1 replication.
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PMID:Highly productive infection with pseudotyped human immunodeficiency virus type 1 (HIV-1) indicates no intracellular restrictions to HIV-1 replication in primary human astrocytes. 1148 37

Infection with vesicular stomatitis virus (VSV), the prototype rhabdovirus, causes apoptotic DNA fragmentation, but the role of apoptosis in the VSV-host interaction remains unclear. Apoptosis is the gene-regulated mechanism triggered by a wide variety of stimuli that lead to cell death in a choreographed manner. In the present study, infection of the Jurkat T cell line with VSV led to activation of caspase-3 and caspase-7, with subsequent apoptotic events involving poly (ADP ribose) polymerase (PARP) cleavage, DNA fragmentation, and membrane damage. Caspase activation was correlated with viral protein expression suggesting a link between viral replication and apoptosis. We hypothesized that VSV replication might depend on apoptosis and that the inhibition of apoptosis would lead to significant decreases in viral titers. When various inhibitors of apoptosis in VSV-infected cells were used, PARP cleavage and DNA fragmentation were inhibited but the production of infectious progeny was not affected. In addition, we demonstrated that the activation of caspase-3-like proteases is required for VSV-induced apoptosis but not in vitro viral replication. Apoptosis following VSV infection is likely to be either a host-cell attempt to control viral replication or may be a ploy used by the virus to facilitate its in vivo replication and spread.
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PMID:Caspase-3-like proteases are activated by infection but are not required for replication of vesicular stomatitis virus. 1159 48

Infection of cells by vesicular stomatitis virus (VSV) results in the inhibition of host transcription. We show in this study that infection of HeLa cells with VSV leads to a strongly diminished activation of STAT3 and STAT1 by the inflammatory cytokine IL-6. This effect was mimicked by forced expression of a single viral protein, the matrix (M)-protein of VSV, which blocked STAT activation via chimeric receptors containing the cytoplasmic domain of the IL-6 signal transducer gp130. Western blot analysis revealed that VSV M-protein did not inhibit the nuclear translocation of activated STAT3 but did inhibit its tyrosine phosphorylation. Inhibition of STAT activation was not dependent on tyrosine 759 of the IL-6 signal transducer gp130, suggesting that the inhibitory action of VSV M-protein is not mediated by the induction of the suppressor of cytokine signaling 3. VSV M-protein inhibited gene transcription from cotransfected alpha(2)-macroglobulin or antichymotrypsin promoter/luciferase reporter constructs which contain STAT3-binding sites. However, transcription from a STAT5-dependent construct was not negatively affected. In conclusion, our data suggest that infection by VSV and specifically overexpression of the viral M-protein interferes with an important signaling pathway necessary for triggering antiviral and inflammatory responses.
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PMID:The vesicular stomatitis virus matrix protein inhibits glycoprotein 130-dependent STAT activation. 1167 34

The oral and gastrointestinal mucosa acts as an important mechanical barrier that prevents local or systemic invasion by microorganisms. Cytotoxic chemotherapy-induced mucosal injury (MI) of oral cavity and intestinal epithelium occurs in many patients treated for malignancy. Compromise of the mucosal barrier can contribute to local invasion by colonizing microorganisms and, subsequently, to systemic infection. Historically, gram-negative bacteremia has been the most problematic bacterial infection in neutropenic patients, but its incidence has reduced over time because of the use of prophylactic antibiotics. There has been a shift in the type of infecting organisms responsible for bacteremia in these patients, from predominantly gram-negative organisms to gram-positive cocci. The viridans group of streptococci is composed of the most frequent bacterial pathogens associated with MI. When speciated, oral colonizers such as Streptococcus mitis, Streptococcus oralis, and Streptococcus sangulis II are the most frequently identified pathogens. Other systemic infections caused by vancomycin-resistant enterococci, Stenotrophomonas maltophilia, and Candida species have also been associated with MI after cancer treatment. Infection can also exacerbate MI after cancer treatment. The best recognized example is herpes simplex virus type 1 (HSV-1). Latent virus is frequently reactivated in HSV-seropositive patients; this reactivation leads to stomatitis, which can be indistinguishable from MI caused by cytoreductive therapies. Antiviral prophylaxis or treatment can control the virus-induced MI and bring about overall amelioration of MI. Recognition of this infectious cause of MI is important in order for clinicians to anticipate and minimize oral toxicity and to facilitate optimal delivery of the antineoplastic regimen.
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PMID:Infection and mucosal injury in cancer treatment. 1169 63

Infection with HSV or EBV was studied by measuring serum antiviral antibody titers in adults with acute tonsillitis, and results were compared to light and electron microscopy findings of tonsil biopsy specimens. The clinical and laboratory features of acute tonsillitis caused by HSV or EBV were also studied. Subjiects were 42 patients with acute tonsillitis treated at the Department of Otorhinolaryngology at Tokyo Women's Medical University Daini Hospital between August 1997 and March 2000. They had failed to respond to antimicrobial agents prescribed by a physician, and had severe oropharyngeal mucosal lesions, liver dysfunction, skin eruptions, or cervical lymphadenopathy, with hospitalization required because of impaired food intake due to sore throat or deterioration in general condition. Subjects were 24 men (mean age: 30.8 years) and 18 women (mean age: 28.3 years) aged 16 to 78 years (mean: 29.8 years). A underwent, bacteriological and hematology tests and palatine tonsil biopsy specimens were obtained to examine tissue changes by light microscopy and electron microscopy due to detect HSV antigen by immunohistochemistry and EBV nucleic acids by EBV-encoded small nuclear RNA 1 and 2 (EBER) in situ hybridization (ISH). Among patients, the serum antiviral antibody profile indicated that 4 (9.5%) had acute tonsillitis due to primary HSV infection and 5 (11.9%) had acute tonsillitis due to primary EBV infection. The findings characteristic of acute tonsillitis due to primary HSV infection included stomatitis, skin eruptions, atypical lymphocytes, and liver dysfunction. Findings characteristic of acute tonsillitis due to primary EBV infection included petechiae of the soft palate, an increase of lymphocytes, atypical lymphocytes, and liver dysfunction. At the initial test, serum anti-HSV antibody was positive in 14 patients (33.3%), and more than half had no history of prior infection. Anti-EBNA antibody was positive in 32 (76.2%), and many had been infected previously. It should be noted that a decrease in positive HSV antibody means that acute tonsillitis due to primary HSV infection is not uncommon in adults and is expected to increase steadily. Light microscopy revealed histological changes in 2 patients. HSV antigen was positive in 2 (50%) with acute tonsillitis due to primary HSV infection, while EBER cells were positive in 5 (100%) with acute tonsillitis due to primary EBV infection, so special staining of the tissues was found to be useful. Electron microscopy failed to detect viral particles in ultrathin sections and no differences were seen in morphological changes or tissue damage between patients with positivity for HSV antigen and with EBER-positive cells. Detection of HSV antigen and EBV nucleic acids in pathological specimens from patients with acute tonsillitis requires careful judgment, but is considered useful for making an early diagnosis and for making a diagnosis in patients without an increase of the antiviral antibody titer and in those with reinfection or reactivation. Pathological examination (including special staining) and careful observation of clinical features may help to identify HSV or EBV infection and allow decisions to be made with regard to the therapeutic strategy and prevention of complications.
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PMID:[Infection of herpes simplex virus (HSV) and Epstein-Barr virus (EBV) in acute tonsillitis--histopathological assessment by optical and electron microscopic observation of biopsy specimens of tonsils]. 1176 95

Infection with hepatitis C virus (HCV) generally progresses to chronic disease, although a minority of patients appear to clear viremia spontaneously. In this investigation, serum samples were analyzed for virological parameters, serum alanine aminotransferase (ALT) levels, and neutralizing antibody response against pseudotyped vesicular stomatitis virus (VSV) generated using chimeric envelope glycoprotein 1 (E1) or 2 (E2) of HCV. Testing of sequential serum samples that were collected beginning at the onset of acute-phase disease demonstrated intermittent viremia, elevated ALT levels, and detectable neutralization activity against VSV in 9 of 10 patients. Serum neutralization activity did not exhibit a correlation with the genotype of the infecting HCV or with virus load. On the other hand, patients with chronic HCV infection consistently had detectable amounts of virus present but no significant variation in ALT levels, and serum samples from a majority (>90%) of patients failed to show detectable neutralization activity.
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PMID:Neutralization of pseudotyped vesicular stomatitis virus expressing hepatitis C virus envelope glycoprotein 1 or 2 by serum from patients. 1193 Mar 27

The effective establishment of antiviral protection requires a coordinated interplay between the innate and adaptive immune system. Using osteopetrotic (op(-/-)) mice, this study investigated the influence of marginal zone macrophages in controlling and initiating a protective immune response against a cytopathic vs a non- or low-cytopathic virus. Despite the generation of potent adaptive immune responses, antiviral protection against cytopathic vesicular stomatitis virus critically depended on the presence of marginal zone macrophages. Infection with low doses (100 PFU) of non- or low-cytopathic lymphocytic choriomeningitis virus was rarely cleared and usually resulted in a carrier state in the majority of mice. This shows that the early innate immune system provides an important preparatory phase to the adaptive immune system and is particularly important for antiviral protection.
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PMID:Marginal zone macrophages and immune responses against viruses. 1213 71


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