Alterations in the C-terminal region of the HIV-1 accessory gene vpr do not confer clinical advantage to subjects receiving nucleoside antiretroviral therapy

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Abstract

The C terminus of the human immunodeficiency virus type 1 (HIV-1) accessory protein vpr acts in viral cell cycle arrest, nuclear localization, and apoptosis. Polymorphisms in this region are described in series of long-term nonprogression cases. We determined vpr sequences of archived baseline specimens from 96 participants in a historical trial of single- versus double-nucleoside reverse-transcriptase inhibitors. These sequences were then analyzed by study-entry and -outcome characteristics such as baseline absolute CD4 + T cell count, prior treatment, CD4+ T cell response, and clinical endpoints. Frequency of C-terminal mutations did not correlate to any measures of disease intensity. Changes in that portion of vpr did not attenuate disease.

Original languageEnglish (US)
Pages (from-to)2181-2184
Number of pages4
JournalJournal of Infectious Diseases
Volume189
Issue number12
DOIs
StatePublished - Jun 15 2004

Bibliographical note

Funding Information:
Received 29 May 2003; accepted 25 November 2003; electronically published 21 May 2004. Presented in part: 40th Annual Meeting of the Infectious Diseases Society of America, Chicago, 24–27 October 2002 (abstract 493). Financial support: National Institutes of Health, National Institute of Allergy and Infectious Diseases Adult AIDS Clinical Trials Group (grant UO1 AI27661). Reprints or correspondence: Dr. Winston Cavert, University of Minnesota, MMC #196, 420 Delaware St. SE, Minneapolis, MN 55455 (winston@lenti.med.umn.edu).

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