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15 March 2008

Volume 197, Number 6
The Journal of Infectious Diseases 2008;197:867–870
© 2008 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2008/19706-0013$15.00
DOI: 10.1086/528802
BRIEF REPORT

Preexisting Resistance to Nonnucleoside Reverse‐Transcriptase Inhibitors Predicts Virologic Failure of an Efavirenz‐Based Regimen in Treatment‐Naive HIV‐1–Infected Subjects

Daniel R. Kuritzkes,1

Christina M. Lalama,2

Heather J. Ribaudo,2

Michelle Marcial,1

William A. Meyer III,3

Cecilia Shikuma,4

Victoria A. Johnson,5,6

Susan A. Fiscus,7

Richard T. D’Aquila,8

Bruce R. Schackman,9

Edward P. Acosta,6 and

Roy M. Gulick9

1Brigham and Women’s Hospital, Harvard Medical School, and 2Harvard School of Public Health, Boston, Massachusetts; 3Quest Diagnostics, Inc., Baltimore, Maryland; 4University of Hawaii, Honolulu; 5Birmingham Veterans Affairs Medical Center and 6University of Alabama at Birmingham School of Medicine, Birmingham; 7University of North Carolina, Chapel Hill; 8Vanderbilt University, Nashville, Tennessee; 9Weill Medical College, Cornell University, New York, New York

A case‐cohort study was used to determine the effect of baseline nonnucleoside reverse‐transcriptase inhibitor (NNRTI) resistance, as assessed by viral genotyping, on the response to efavirenz‐containing regimens in AIDS Clinical Trials Group A5095. The sample included a random cohort of efavirenz‐treated subjects plus unselected subjects who experienced virologic failure. Of 220 subjects in the random cohort, 57 (26%) had virologic failure. The prevalence of baseline NNRTI resistance was 5%. The risk of virologic failure for subjects with baseline NNRTI resistance was higher than that for subjects without such resistance (hazard ratio 2.27 [95% confidence interval], 1.15–4.49; ). These results support resistance testing before starting antiretroviral therapy.

Received 23 September 2007; accepted 15 October 2007; electronically published 12 February 2008.

Reprints or correspondence: Dr. Daniel R. Kuritzkes, Section of Retroviral Therapeutics, Brigham and Women’s Hospital, 65 Landsdowne St., Rm. 449, Cambridge, MA 02139 ().

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  • Potential conflicts of interest: D.R.K. is a consultant to and has received honoraria and research grant support from Bayer, Boehringer‐Ingleheim (BI), Bristol‐Myers Squibb (BMS), and GlaxoSmithKline (GSK). E.P.A. is a consultant to BMS. R.T.D. has received grant support from BMS and is a consultant to BI and GSK. R.M.G. is a consultant to BMS and GSK. V.A.J. is a consultant to and/or has received grant support from Bayer, BMS, and GSK. C.S. has received research grant support from BMS. All other authors report no potential conflicts.

    Presented in part: 14th Conference on Retroviruses and Opportunistic Infections, Los Angeles 25–28 February 2007 (abstract 665).

    Financial support: National Institutes of Health (NIH; grants AI38858, AI068636 [AIDS Clinical Trials Group Central Grant], AI069419, AI051966, AI069472, AI069452, and RR024996); subcontracts from NIH grants AI38858 and AI06836 with the Virology Support Laboratories at Massachusetts General Hospital, the University of Alabama, the University of Colorado Health Sciences Center, the University of North Carolina, and Vanderbilt University; Birmingham Veterans Affairs Medical Center; Harvard University and University of Alabama at Birmingham Centers for AIDS Research (grants AI060354 and AI027767). Bristol‐Myers Squibb and GlaxoSmithKline provided drug for this study as well as financial support for plasma HIV‐1 RNA determinations.

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