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1 May 2005

Volume 191, Number 9
The Journal of Infectious Diseases 2005;191:1410–1418
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19109-0006$15.00
DOI: 10.1086/428777
MAJOR ARTICLE

Effect of Treatment, during Primary Infection, on Establishment and Clearance of Cellular Reservoirs of HIV-1

Matthew C. Strain,1,2

Susan J. Little,3

Eric S. Daar,5

Diane V. Havlir,6

Huldrych F. Günthard,8

Ruby Y. Lam,2

Otto A. Daly,4

Juin Nguyen,4

Caroline C. Ignacio,4

Celsa A. Spina,4

Douglas D. Richman,2,4 and

Joseph K. Wong2,4,7

Departments of 1Physics and 2Medicine and Pathology, University of California at San Diego, La Jolla, 3Antiviral Research Center and 4Veterans Affairs San Diego Healthcare System, San Diego, 5Division of HIV Medicine, Harbor–University of California at Los Angeles (UCLA) Medical Center, Torrance, and UCLA School of Medicine, Los Angeles, and 6San Francisco General Hospital and 7Veterans Affairs Medical Center, San Francisco, California; 8Division of Infectious Diseases and Hospital Epidemiology, University Hospital of Zürich, Zürich, Switzerland

Patients in whom virologic suppression is achieved with highly active antiretroviral therapy (HAART) retain long‐lived cellular reservoirs of human immunodeficiency virus type 1 (HIV‐1); this retention is an obstacle to sustained control of infection. To assess the impact that initiating treatment during primary HIV‐1 infection has on this cell population, we analyzed the decay kinetics of HIV‐1 DNA and of infectivity associated with cells activated ex vivo in 27 patients who initiated therapy before or <6 months after seroconversion and in whom viremia was suppressed to <50 copies/mL. The clearance rates of cellular reservoirs could not be distinguished by these techniques (median half‐life, 20 weeks) during the first year of HAART. The clearance of HIV‐1 DNA slowed significantly during the subsequent 3 years of treatment (median half‐life, 70 weeks), consistent with heterogeneous cellular reservoirs being present. Total cell‐associated infectivity (CAI) after 1 year of treatment was undetectable (<0.07 infectious units/million cells [IUPM]) in most patients initiating treatment during primary infection either before (9/9) or <6 months after (6/8) seroconversion. In contrast, all 17 control patients who initiated HAART during chronic infection retained detectable CAI after 3–6 years of treatment (median reservoir size, 1.1 IUPM; ). These results suggest that treatment <6 months after seroconversion may facilitate long‐term control of cellular reservoirs that maintain HIV‐1 infection during treatment.

Received 27 May 2004; accepted 1 November 2004; electronically published 29 March 2005.

Reprints or correspondence: Dr. Matthew C. Strain, Depts. of Medicine and Pathology, 0679, University of California at San Diego, 9500 Gilman Dr., La Jolla, CA 92093‐0679 () or Dr. Joseph K. Wong, VAMC San Francisco, 4150 Clement St., San Francisco, CA 94121 ().

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  • Presented in part: 8th Conference on Retroviruses and Opportunistic Infections, Chicago, 8–9 February 2001 (abstract 503); 9th Conference on Retroviruses and Opportunistic Infections, Seattle, 24–28 February 2002 (abstract 97); 9th International Workshop on HIV Dynamics and Evolution, Arrowhead, CA, 17–20 March 2002.

    Potential conflicts of interest: D.R.R. has consulted for Abbott, Bristol‐Myers Squibb, Merck, Pfizer, and Roche.

    Financial support: La Jolla Interfaces in Science (fellowship to M.C.S.); National Institutes of Health (grant GM 07198 to M.C.S.; grant AI51982 to D.V.H.; grants AI27670, AI38858, AI29164, and AI36214 to D.D.R.; and grant AI43752 to J.K.W.); Swiss National Science Foundation (grant 3345‐062041 to H.F.G., M.F., and M.O.); Swiss HIV Cohort Study (support to H.F.G., M.F., and M.O.); Department of Veteran Affairs (Research Merit Award to J.K.W.); Research Center for AIDS and HIV Infection of the San Diego Veterans Affairs Healthcare System.

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