Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the effects of CC-chemokines on human immunodeficiency virus type 1 (HIV-1) infection, focusing on the infectivity enhancement caused by RANTES. High RANTES concentrations increase the infectivity of HIV-1 isolates that use CXC-chemokine receptor 4 for entry. However, RANTES can have a similar enhancing effect on macrophagetropic viruses that enter via CC-chemokine receptor 5 (CCR5), despite binding to the same receptor as the virus. Furthermore, RANTES enhances the infectivity of HIV-1 pseudotyped with the envelope glycoprotein of murine leukemia virus or vesicular stomatitis virus, showing that the mechanism of enhancement is independent of the route of virus-cell fusion. The enhancing effects of RANTES are not mediated via CCR5 or other known chemokine receptors and are not mimicked by MIP-1alpha or MIP-1beta. The N-terminally modified derivative aminooxypentane RANTES (AOP-RANTES) efficiently inhibits HIV-1 infection via CCR5 but otherwise mimics RANTES by enhancing viral infectivity. There are two mechanisms of enhancement: one apparent when target cells are pretreated with RANTES (or AOP-RANTES) for several hours, and the other apparent when RANTES (or AOP-RANTES) is added during virus-cell absorption. We believe that the first mechanism is related to cellular activation by RANTES, whereas the second is an increase in virion attachment to target cells.
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PMID:Enhancement of human immunodeficiency virus type 1 infection by the CC-chemokine RANTES is independent of the mechanism of virus-cell fusion. 984 74

During acute Vesicular Stomatitis Virus (VSV) infection of the mouse central nervous system, neutrophils, natural killer (NK) cells, macrophages, and CD4+ and CD8+ T cells are recruited from the circulation in response to chemokines and cytokines. This study elucidated the production of these factors and infiltration of these peripheral cells. Chemokines that were observed included CCL1, CXCL10 (IP-10), CCL5 (RANTES), CCL3 (MIP-1alpha), CCL4 (MIP-1beta), CXCL1 (MIP-2), CCL2 (MCP-1), and CCL11 (eotaxin). Cytokines produced in response to the infection include IL-1 and interferon-gamma, but not type I interferons. Neutrophils are the first recruited cell type, appearing as early as 24 h after intranasal application of the virus. NK cells follow, but T cells are not detected until 6 days postinfection.
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PMID:Gene expression contributing to recruitment of circulating cells in response to vesicular stomatitis virus infection of the CNS. 1698 71