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 alpha-chemokine SDF-1 binds CXCR4, a coreceptor for human immunodeficiency virus type 1 (HIV-1), and inhibits viral entry mediated by this receptor. Since chemokines are potent chemoattractants and activators of leukocytes, we examined whether the stimulation of HIV target cells by SDF-1 affects the replication of virus with different tropisms. We observed that SDF-1 inhibited the entry of X4 strains and increased the infectivity of particles bearing either a CCR5-tropic HIV-1 envelope or a vesicular stomatitis virus G envelope. In contrast to the inhibitory effect of SDF-1 on X4 strains, which is at the level of entry, the stimulatory effect does not involve envelope-receptor interactions or proviral DNA synthesis. Rather, we observed an increased ability of Tat to transactivate the HIV-1 long terminal repeat in the presence of the chemokine. Therefore, the effects of SDF-1 on the HIV-1 life cycle can be multiple and opposite, including both an inhibition of viral entry and a stimulation of proviral gene expression.
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PMID:Opposite effects of SDF-1 on human immunodeficiency virus type 1 replication. 1019 52

We describe a replication-competent, recombinant vesicular stomatitis virus (VSV) in which the gene encoding the single transmembrane glycoprotein (G) was deleted and replaced by an env-G hybrid gene encoding the extracellular and transmembrane domains of a human immunodeficiency virus type 1 (HIV-1) envelope protein fused to the cytoplasmic domain of VSV G. An additional gene encoding a green fluorescent protein was added to permit rapid detection of infection. This novel surrogate virus infected and propagated on cells expressing the HIV receptor CD4 and coreceptor CXCR4. Infection was blocked by SDF-1, the ligand for CXCR4, by antibody to CD4 and by HIV-neutralizing antibody. This virus, unlike VSV, entered cells by a pH-independent pathway and thus supports a pH-independent pathway of HIV entry. Additional recombinants carrying hybrid env-G genes derived from R5 or X4R5 HIV strains also showed the coreceptor specificities of the HIV strains from which they were derived. These surrogate viruses provide a simple and rapid assay for HIV-neutralizing antibodies as well as a rapid screen for molecules that would interfere with any stage of HIV binding or entry. The viruses might also be useful as HIV vaccines. Our results suggest wide applications of other surrogate viruses based on VSV.
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PMID:Replication-competent rhabdoviruses with human immunodeficiency virus type 1 coats and green fluorescent protein: entry by a pH-independent pathway. 1040 Jul 92

Plasmacytoid dendritic cells (pDCs) secrete large amounts of IFN-alpha upon exposure to virus, subsequently promoting and regulating innate and adaptive immune responses. However, little is known about the functional regulation of virus-activated pDCs after they exert functions in secondary lymph organs. Our previous studies show that splenic stromal microenvironment can down-regulate the T cell response by inducing generation of regulatory myeloid dendritic cells; therefore, we wondered whether the splenic stromal microenvironment can regulate the function of virus-activated pDCs. In this study, we provide evidences that the splenic stromal microenvironment can chemoattract vesicular stomatitis virus (VSV)-activated pDCs via stromal cell-derived factor 1 (SDF-1), inhibit the secretion of IFN-alpha, IL-12, TNF-alpha, and expression of I-Ab, CD86, CD80, and CD40 by VSV-activated pDCs, and subsequently inhibit VSV-infected pDCs to activate NK cell IFN-gamma production and cytotoxicity. Stroma-derived TGF-beta participates in the negative regulation of VSV-activated pDCs. Therefore, we demonstrate that splenic stromal microenvironment negatively regulates the virus-activated pDCs through TGF-beta, outlining an additional mechanistic explanation for maintenance of immune homeostasis.
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PMID:Splenic stromal microenvironment negatively regulates virus-activated plasmacytoid dendritic cells through TGF-beta. 1829 17