Treatment of primary human immunodeficiency virus type 1 infection with potent antiretroviral therapy reduces frequency of rapid progression to AIDS

M. Michelle Berrey, Timothy Schacker, Ann C. Collier, Theresa Shea, Scott J. Brodie, Douglas Mayers, Robert Coombs, John Krieger, Tae Wook Chun, Anthony Fauci, Steven G. Self, Lawrence Corey

Research output: Contribution to journalArticlepeer-review

94 Scopus citations

Abstract

Immunologic data supporting immediate antiretroviral therapy in primary human immuno-deficiency virus type 1 (HIV-1) infection are emerging; however, clinical benefit has not been demonstrated. The clinical and virologic course of 47 patients who were enrolled from September 1993 through June 1996 and who were not initially treated with potent therapy was compared with the course of 20 patients who immediately began therapy with zidovudine, lamivudine, and indinavir. Demographic and baseline laboratory data were comparable. During 78 weeks of follow-up, the early-treatment cohort showed a reduced frequency of opportunistic infections (5% vs. 21.3%; relative risk, 0.11; P = .02), less frequent progression to AIDS (13% vs. 0%), and significantly less frequent nonopportunistic mucocutaneous disorders and respiratory infections (P < .01). Plasma HIV-1 RNA levels were <50 copies/mL in all patients who continued therapy; however, after 9-12 months, HIV-1 remained detectable in latently infected CD4+ T cells and in lymph node mononuclear cells. Combination antiretroviral therapy during primary HIV-1 infection demonstrated a decreased frequency of minor opportunistic infections, mucocutaneous disorders, and respiratory infections and reduced progression to AIDS.

Original languageEnglish (US)
Pages (from-to)1466-1475
Number of pages10
JournalJournal of Infectious Diseases
Volume183
Issue number10
DOIs
StatePublished - May 15 2001

Bibliographical note

Funding Information:
Financial support: Merck; Glaxo Wellcome; National Institutes of Health (AI-41535; AI-31448 to Center for AIDS Research, University of Washington; AI-07140, training grant to M.M.B.).

Funding Information:
We are indebted to the patients who volunteered for this study and their medical care providers, to the University of Washington Retrovi-rology Laboratory for their dedication, and to Richard Donovan (Henry Ford Hospital) for performing the genotyping assays. Denny Guang Yeu Lee (Fred Hutchinson Cancer Research Center [FHRC], Seattle, WA) was instrumental in preliminary data analyses, and Yijian Huang (FHRC) conducted statistical analyses. We also thank Merck Research Laboratories for financial support and both Merck and Glaxo Wellcome for their support in providing medication. A special thank you is extended to Nancy Coomer (FHRC) for her tireless work on the manuscript.

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