Journal
VIROLOGY
Volume 352, Issue 2, Pages 485-492Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2006.05.013
Keywords
HIV; Tat; IL-10; cyclin T1; P-TEFb; transcription; proteolysis
Categories
Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R21AI045374, R01AI045374] Funding Source: NIH RePORTER
- NIAID NIH HHS [AI45374] Funding Source: Medline
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Regulation of HIV-1 replication in human monocytes/macrophages occurs at multiple levels including transcription of the proviral genome, which depends on vitally encoded Tat protein. Interleukin-10 (IL-10), an anti-inflammatory cytokine which is up-regulated during disease progression of AIDS, has been reported to suppress HIV-1 replication in macrophages at a post-entry stage of the virus life cycle. Our previous studies have demonstrated that Tat function is regulated during the differentiation of monocyte-derived macrophages (MDMs) in a manner that correlates with the early induction and subsequent shut-off of its cellular cofactor cyclin T1. Here, we report that IL-10 down-regulates cyclin T1 expression through the induction of proteasome-mediated proteolysis in human macrophages. Using a reporter virus that is deficient in Tat function, we also demonstrate that IL-10 inhibits HIV-1 gene expression in a Tat-dependent manner. Together, these results suggest that the down-regulation of cyclin T1, and consequently Tat function, contributes to the suppressive effect of IL-10 on HIV-1 replication in human macrophages. (c) 2006 Elsevier Inc. All rights reserved.
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