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* Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania;
The Wistar Institute, Philadelphia, Pennsylvania; and
University of Pittsburgh, Department of Infectious Diseases and Microbiology/GSPH, Pittsburgh, Pennsylvania
Correspondence: Velpandi Ayyavoo, Ph.D., University of Pittsburgh, Department of Infectious Diseases and Microbiology/GSPH, 130 DeSoto Street, Pittsburgh, PA 15261. E-mail: Velpandi+{at}pitt.edu
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-
B-mediated transcription. NF-B, 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 ß chemokines (MIP-1
, MIP-1ß, 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 ß
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.
Key Words: HIV-1 • Vpr • ß chemokine • macrophages • PBLs
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