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1 October 2006

Volume 194, Number 7
The Journal of Infectious Diseases 2006;194:926–930
© 2006 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2006/19407-0009$15.00
DOI: 10.1086/507312
BRIEF REPORT

Prevalence of CXCR4 Tropism among Antiretroviral‐Treated HIV‐1–Infected Patients with Detectable Viremia

Peter W. Hunt,1

P. Richard Harrigan,10,11

Wei Huang,9

Michael Bates,9

David W. Williamson,3,8

Joseph M. McCune,4

Richard W. Price,2

Serena S. Spudich,2

Harry Lampiris,5

Rebecca Hoh,1

Teri Leigler,1

Jeffrey N. Martin,1,6,7 and

Steven G. Deeks1

1Positive Health Program and 2Department of Neurology, San Francisco General Hospital, 3Graduate Program in Biological and Medical Informatics, 4Division of Experimental Medicine, Department of Internal Medicine, 5San Francisco Veterans Affairs Medical Center, 6Center for AIDS Prevention Studies, and 7Department of Epidemiology and Biostatistics, University of California, San Francisco, 8Gladstone Institute of Virology and Immunology, San Francisco, and 9Monogram Biosciences, Inc., South San Francisco, California; 10British Columbia Centre for Excellence in HIV/AIDS, Providence Health Care, and 11Faculty of Medicine, University of British Columbia, Vancouver, Canada

Although CXCR4‐tropic viruses are relatively uncommon among untreated human immunodeficiency virus (HIV)–infected individuals except during advanced immunodeficiency, the prevalence of CXCR4‐tropic viruses among treated patients with detectable viremia is unknown. To address this issue, viral coreceptor usage was measured with a single‐cycle recombinant‐virus phenotypic entry assay in treatment‐naive and treated HIV‐infected participants with detectable viremia sampled from 2 clinic‐based cohorts. Of 182 treated participants, 75 (41%) harbored dual/mixed or X4‐tropic viruses, compared with 178 (18%) of the 976 treatment‐naive participants ( ). This difference remained significant after adjustment for CD4+ T cell count and CCR5 Δ32 genotype. Enrichment for dual/mixed/X4‐tropic viruses among treated participants was largely but incompletely explained by lower pretreatment nadir CD4 + T cell counts. CCR5 inhibitors may thus be best strategically used before salvage therapy and before significant CD4 + T cell depletion.

Received 15 March 2006; accepted 17 May 2006; electronically published 29 August 2006.

Reprints or correspondence: Dr. Peter W. Hunt, Positive Health Program, San Francisco General Hospital, Bldg. 80, Ward 84, 995 Potrero Ave., San Francisco, CA 94110 ().

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  • Presented in part: 13th Conference on Retroviruses and Opportunistic Infections, Denver, 5–8 February 2006 (abstract 43).

    Potential conflicts of interest: M.B. and W.H. are employees of Monogram, Inc. S.G.D. has received honoraria from Monogram Biosciences. For all other authors, no conflicts are reported.

    Financial support: University‐Wide AIDS Research Program (grant CC99‐SF‐001); University of California, San Francisco/Gladstone Institute of Virology and Immunology Center for AIDS Research (grants P30 AI27763 and P30 MH59037); National Institutes of Health (NIH; grants R01 AI52745, R37 AI40312, NS 37660, and K23 AI65244); General Clinical Research Center at San Francisco General Hospital (grant 5‐MO1‐RR00083‐37); Center for AIDS Prevention Studies (grant P30 MH62246); Burroughs Wellcome Fund (Clinical Scientist Award in Translational Research to J.M.M.); NIH Director’s Pioneer Award Program, NIH Roadmap for Medical Research (grant DPI OD00329 to J.M.M.).

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