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. 2005 May 1;191(9):1410-8.
doi: 10.1086/428777. Epub 2005 Mar 29.

Effect of treatment, during primary infection, on establishment and clearance of cellular reservoirs of HIV-1

Matthew C Strain  1 , Susan J Little, Eric S Daar, Diane V Havlir, Huldrych F Gunthard, Ruby Y Lam, Otto A Daly, Juin Nguyen, Caroline C Ignacio, Celsa A Spina, Douglas D Richman, Joseph K Wong
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Free article

Effect of treatment, during primary infection, on establishment and clearance of cellular reservoirs of HIV-1

Matthew C Strain et al. J Infect Dis. .
Free article

Abstract

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; P<.0005). These results suggest that treatment <6 months after seroconversion may facilitate long-term control of cellular reservoirs that maintain HIV-1 infection during treatment.

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