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HIV‐1 Vpr regulates expression of β chemokines in human primary lymphocytes and macrophages
Author(s) -
Muthumani Karuppiah,
Kudchodkar Sagar,
Papasavvas Emmanouil,
Montaner Luis J.,
Weiner David B.,
Ayyavoo Velpandi
Publication year - 2000
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.68.3.366
Subject(s) - chemokine , biology , proinflammatory cytokine , cytokine , macrophage inflammatory protein , transcription (linguistics) , microbiology and biotechnology , transcription factor , recombinant dna , extracellular , virology , gene , inflammation , immunology , genetics , linguistics , philosophy
The HIV‐1 vpr gene encodes a 14‐kDa virion‐packaged protein that has been implicated in viral pathogenesis. Vpr exhibits profound effects on human primary cells influencing proliferation, differentiation, apoptosis, and cytokine production, in part through NF‐κB‐mediated transcription. NF‐κB, a potent transcription factor, activates many proinflammatory cytokines/chemokines upon infection. Here, we analyzed the effect of extracellular Vpr as well as the virion‐associated Vpr on β chemokines (MIP‐1α, MIP‐1β, and RANTES) production in human macrophages and primary lymphocytes (PBLs). Macrophages and PBLs exposed to HIV‐1 vpr + viruses or to recombinant Vpr protein produced significantly less β chemokines compared with cells infected with HIV‐1 vpr − viruses or irrelevant control protein (Gag)‐exposed cells. These results suggest that a Vpr‐mediated increase in virus replication could be in part through down‐regulation of chemokine production.