JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lin, X.
Right arrow Articles by Peterlin, B. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lin, X.
Right arrow Articles by Peterlin, B. M.
Journal of Virology, August 2003, p. 8227-8236, Vol. 77, No. 15
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.15.8227-8236.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Transcriptional Profiles of Latent Human Immunodeficiency Virus in Infected Individuals: Effects of Tat on the Host and Reservoir

Xin Lin,1 Dan Irwin,1 Satoshi Kanazawa,1 Laurence Huang,2 Joseph Romeo,3 T. S. Benedict Yen,4 and B. Matija Peterlin1*

Departments of Medicine, Microbiology, and Immunology,1 Positive Health Program, San Francisco General Hospital, Center for AIDS Research,2 Department of Pathology, University of California, San Francisco,4 Center for Biomedical Laboratory Sciences, San Francisco State University, San Francisco, California3

Received 9 January 2003/ Accepted 24 April 2003

The persistence of human immunodeficiency virus (HIV) in optimally treated infected individuals poses a major therapeutic problem. In latently infected cells, one of the observed phenotypes is absent elongation of viral transcription. Thus, the positive elongation factor b (P-TEFb), which is usually recruited by NF-{kappa}B or Tat, is not present on the HIV long terminal repeat (LTR). Although most attempts to activate these proviruses centered on NF-{kappa}B, we investigated effects of Tat. To this end, we generated transgenic mice, which secreted a chimera between Tat and the green fluorescent protein from ß cells of the pancreas. This extracellular Tat distributed widely, entered nuclei of resting cells, and specifically transactivated the HIV LTR. No deleterious side effects of Tat were found. Next, we determined that Tat can activate latent proviruses in optimally treated infected individuals. In their cells, T-cell activation or exogenous Tat could induce viral replication equivalently. Thus, P-TEFb could activate the majority of the latent HIV, in this case by Tat.


* Corresponding author. Mailing address: Rm. N215, UCSF-Mt. Zion Cancer Center, 2340 Sutter St., San Francisco, CA 94115. Phone: (415) 502-1905. Fax: (415) 502-1901. E-mail: matija{at}itsa.ucsf.edu.


Journal of Virology, August 2003, p. 8227-8236, Vol. 77, No. 15
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.15.8227-8236.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2003 by the American Society for Microbiology. All rights reserved.