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The Effect of HAART on HIV RNA Trajectory Among Treatment-naïve Men and Women: A Segmental Bernoulli/Lognormal Random Effects Model With Left Censoring

Chu, Haitaoa; Gange, Stephen J.b; Li, Xiuhongb; Hoover, Donald R.c; Liu, Chenglongd; Chmiel, Joan S.e; Jacobson, Lisa P.b

Epidemiology:
doi: 10.1097/EDE.0b013e3181ce9950
Methodologic Issues in Environmental Exposures: Mixtures and Limits of Detection: Original Article
Abstract

Background: Highly active antiretroviral therapy (HAART) rapidly suppresses human immunodeficiency virus (HIV) viral replication and reduces circulating viral load, but the long-term effects of HAART on viral load remain unclear.

Methods: We evaluated HIV viral load trajectories over 8 years following HAART initiation in the Multicenter AIDS Cohort Study and the Women's Interagency HIV Study. The study included 157 HIV-infected men and 199 HIV-infected women who were antiretroviral naive and contributed 1311 and 1837 semiannual person-visits post-HAART, respectively. To account for within-subject correlation and the high proportion of left-censored viral loads, we used a segmental Bernoulli/lognormal random effects model.

Results: Approximately 3 months (0.30 years for men and 0.22 years for women) after HAART initiation, HIV viral loads were optimally suppressed (ie, with very low HIV RNA) for 44% (95% confidence interval = 39%–49%) of men and 43% (38%–47%) of women, whereas the other 56% of men and 57% of women had on average 2.1 (1.5–2.6) and 3.0 (2.7–3.2) log10 copies/mL, respectively.

Conclusion: After 8 years on HAART, 75% of men and 80% of women had optimal suppression, whereas the rest of the men and women had suboptimal suppression with a median HIV RNA of 3.1 and 3.7 log10 copies/mL, respectively.

Author Information

From the aDepartment of Biostatistics and the Lineberger Comprehensive Cancer Center, the University of North Carolina, Chapel Hill, NC; bDepartment of Epidemiology, The Johns Hopkins University, Baltimore, MD; cInstitute for Health, Health Care Policy, and Aging Research, Rutgers University, New Brunswick, NJ; dDepartment of Medicine, School of Medicine, Georgetown University, Washington DC; and eDepartment of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL.

Submitted 8 September 2008; accepted 23 November 2009; posted 8 April 2010.

Supported in part by the Lineberger Cancer Center Core Grant CA16086 from the U.S. National Cancer Institute, the Center for AIDS Research Grant P30-AI-50410 from the U.S. National Institutes of Health (to H.C.), and a grant from the American Chemistry Council to Enrique Schisterman that enabled the formation of a working group with H.C. as a paid participant. The MACS is funded by the National Institute of Allergy and Infectious Diseases, with additional supplemental funding from the National Cancer Institute; and the National Heart, Lung, and Blood Institute: UO1-AI-35042, 5-M01-RR-00052 (GCRC), UO1-AI-35043, UO1-AI-37984, UO1-AI-35039, UO1-AI-35040, UO1-AI-37613, and UO1-AI-35041. The WIHS is funded by the National Institute of Allergy and Infectious Diseases, with additional supplemental funding from the National Cancer Institute; the National Institute of Child Health & Human Development; The National Institute on Drug Abuse; the National Institute of Craniofacial and Dental Research; and the National Heart, Lung, and Blood Institute: U01-AI-35004, U01-AI-31834, U01-AI-34994, U01-AI-34989, U01-HD-32632, U01-AI-34993, U01-AI-42590, M01-RR00079 and M01-RR00083.

This work was initiated while Dr. Chu was in the Department of Epidemiology, The Johns Hopkins University, Baltimore, MD.

Correspondence: Haitao Chu, Department of Biostatistics and the Lineberger Comprehensive Cancer Center, The University of North Carolina, Chapel Hill, NC 27599. E-mail: hchu@bios.unc.edu.

© 2010 Lippincott Williams & Wilkins, Inc.