Alterations in the C-terminal region of the HIV-1 accessory gene vpr do not confer clinical advantage to subjects receiving nucleoside antiretroviral therapy.
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.
Cavert
Winston
W
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota 55455, USA. winston@lenti.med.umn.edu.
Webb
Chui-Ho
CH
Balfour
Henry H
HH
D018791:CD4 Lymphocyte Count; D016336:Gene Products, vpr / Q000235:genetics*; D015658:HIV Infections / Q000188:drug therapy / Q000503:physiopathology* / Q000821:virology; D015497:HIV-1 / Q000187:drug effects / Q000472:pathogenicity*; D006801:Humans; D009154:Mutation; D009705:Nucleosides / Q000627:therapeutic use*; D011110:Polymorphism, Genetic; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use*; D017422:Sequence Analysis, DNA; D016896:Treatment Outcome; D054325:vpr Gene Products, Human Immunodeficiency Virus
D016336:Gene Products, vpr; D009705:Nucleosides; D018894:Reverse Transcriptase Inhibitors; D054325:vpr Gene Products, Human Immunodeficiency Virus