Predictors of Residual Viremia in HIV‐Infected Patients Successfully Treated with Efavirenz and Lamivudine plus either Tenofovir or Stavudine
1Department of Medicine, San Francisco General Hospital, University of California at San Francisco, and 2Veterans Affairs Medical Center, San Francisco, 3Department of Medicine, University of California at San Diego and 4San Diego Veterans Affairs Healthcare System, La Jolla, and 5Gilead Sciences, Inc., Foster City, California
In human immunodeficiency virus (HIV)–infected patients successfully treated with highly active antiretroviral therapy (HAART), a low level of HIV RNA persists in plasma at steady state for years and varies among patients. To understand predictors of residual viremia, we measured HIV RNA levels <50 copies/mL in patients after 1 year of treatment with efavirenz and lamivudine plus either tenofovir disoproxil fumarate (
) or stavudine (
), by use of an HIV RNA assay with a limit of detection of 2.5 copies/mL. The mean posttreatment HIV RNA levels were 0.58 log10 copies/mL (3.8 copies/mL) in the tenofovir arm and 0.61 log10copies/mL (4.1 copies/mL) in the stavudine arm (
). Forty‐seven percent of patients receiving tenofovir, compared with 29% of patients receiving stavudine, had undetectable residual viremia (
). In multivariate analyses, we found that lower baseline HIV RNA levels in plasma, lower HIV DNA levels in peripheral blood mononuclear cells, and inclusion in the tenofovir arm each independently predicted undetectable residual viremia (
). However, a level of residual viremia <50 copies/mL was not associated with CD4 cell count changes or risk of virologic rebound through 72 weeks of follow‐up.
Received 1 July 2004; accepted 1 November 2004; electronically published 28 February 2005.
Cited by
Online publication date: 1-Jul-2009.
CrossRef
Online publication date: 1-Feb-2009.
CrossRef
Online publication date: 11-Apr-2008.
CrossRef
Online publication date: 1-Feb-2008.
Online publication date: 15-Dec-2007.
Online publication date: 1-Jun-2006.
CrossRef
-
Presented in part: 12th International Workshop on HIV Drug Resistance and Treatment Strategies, Los Cabos, Mexico, 10–14 June 2003 (abstract S66).
Potential conflicts of interest: N.M., B.L., and M.D.M. are employees of Gilead Sciences, Inc.; J.K.W. received testing kits from Roche Diagnostics.
Financial support: National Institutes of Health/National Institute of Allergy and Infectious Diseases (NIH/NIAID) (Mid‐Career Investigator Award in Patient‐Oriented Research K24 AI51982 and Center for AIDS Research grant P30 A127763 to D.V.H.); NIH/RO1 (grants AI 43752 and AI 47745 to J.K.W.); University‐wide AIDS Research Program (to J.K.W.); Gilead Services, Inc. (to M.D.M).