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Potential Impact of Antiretroviral Therapy on HIV-1 Transmission and AIDS Mortality in Resource-Limited Settings

Abbas, Ume L. MD*; Anderson, Roy M. PhD; Mellors, John W. MD*

JAIDS Journal of Acquired Immune Deficiency Syndromes: April 15th, 2006 - Volume 41 - Issue 5 - p 632-641
doi: 10.1097/01.qai.0000194234.31078.bf
Epidemiology and Social Science

Objective: To estimate the potential impact of antiretroviral therapy on the heterosexual spread of HIV-1 infection and AIDS mortality in resource-limited settings.

Methods: A mathematic model of HIV-1 disease progression and transmission was used to assess epidemiologic outcomes under different scenarios of antiretroviral therapy, including implementation of World Health Organization guidelines.

Results: Implementing antiretroviral therapy at 5% HIV-1 prevalence and administering it to 100% of AIDS cases are predicted to decrease new HIV-1 infections and cumulative deaths from AIDS after 10 years by 11.2% (inter-quartile range [IQR]: 1.8%-21.4%) and 33.4% (IQR: 26%-42.8%), respectively. Later implementation of therapy at endemic equilibrium (40% prevalence) is predicted to be less effective, decreasing new HIV-1 infections and cumulative deaths from AIDS by 10.5% (IQR: 2.6%-19.3%) and 27.6% (IQR: 20.8%-36.8%), respectively. Therapy is predicted to benefit the infected individual and the uninfected community by decreasing transmission and AIDS deaths. The community benefit is greater than the individual benefit after 25 years of treatment and increases with the proportion of AIDS cases treated.

Conclusions: Antiretroviral therapy is predicted to have individual and public health benefits that increase with time and the proportion of infected persons treated. The impact of therapy is greater when introduced earlier in an epidemic, but the benefit can be lost by residual infectivity or disease progression on treatment and by sexual disinhibition of the general population.

From the *Division of Infectious Diseases, School of Medicine, University of Pittsburgh, Pittsburgh, PA; and †Department of Infectious Disease Epidemiology, Imperial College, Faculty of Medicine, University of London, London, United Kingdom.

Received for publication May 10, 2005; accepted October 21, 2005.

R.M. Anderson acknowledges grant support from the Wellcome Trust. J.W. Mellors acknowledges support from the Bristol Myers Squibb Research Foundation and grants from the National Institute of Allergy and Infectious Diseases (U01AI38858) and from the National Cancer Institute (Science Applications International Corporation (SAIC) contract 20XS190A).

Reprints: Ume L. Abbas, Division of Infectious Diseases, University of Pittsburgh School of Medicine, Falk Medical Building, Suite 3-A, 3601 Fifth Avenue, Pittsburgh, PA 15213 (e-mail: abbasu@dom.pitt.edu).

© 2006 Lippincott Williams & Wilkins, Inc.