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Curr HIV Res. 2009 Jan;7(1):2-11.

The rhesus macaque pediatric SIV infection model - a valuable tool in understanding infant HIV-1 pathogenesis and for designing pediatric HIV-1 prevention strategies.

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California National Primate Research Center, and Department of Internal Medicine, Division of Infectious Diseases, School of Medicine, University of California Davis, CA, USA.


Worldwide, the AIDS pandemic continues almost relentlessly. Women are now representing the fastest growing group of newly infected HIV-1 infected patients. The risk of mother-to-child-transmission (MTCT) of HIV-1 increases proportionally as many of these women are of childbearing age. The screening of pregnant women, the early diagnosis of HIV-1 infection, and the administration of antiretroviral therapy (ART) have helped to reduce MTCT significantly. However, this holds true only for developed countries. In many resource-poor countries, access to ART is limited, and breastfeeding, a major route of HIV-1 transmission, is essential to protect the infant from other infectious diseases preponderant in those geographic regions. HIV-1 infected children, in contrast to adult patients, have higher levels of virus replication that decline only slowly, and a subset progresses to AIDS within the first two years. Thus, it is imperative to understand pediatric HIV-1 pathogenesis to design effective prevention strategies and/or a successful pediatric HIV-1 vaccine. The review summarizes how MTCT of HIV-1 in humans can be modeled in the infant macaque model of SIV infection. Importantly, the infant macaque model of SIV infection provides the opportunity to study early virus-host interactions in multiple anatomic compartments. Furthermore, the review underlines the importance of evaluating SIV/HIV immune responses in the context of the normal developmental changes the immune system undergoes in the newborn. Thus, the pediatric SIV infection model provides a unique resource for preclinical studies of novel intervention therapies and vaccine strategies to stop MTCT of HIV-1.

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