Research ArticleHIV

SIV Replication in the Infected Rhesus Macaque Is Limited by the Size of the Preexisting TH17 Cell Compartment

Science Translational Medicine  30 May 2012:
Vol. 4, Issue 136, pp. 136ra69
DOI: 10.1126/scitranslmed.3003941

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Contextual Cues

Every person’s immune system is unique—shaped by a combination of genetics and environmental insults such as the flu or food poisoning. An individual’s immunological ecosystem evolves over time, and the immune response to a particular organism may vary depending on the current status of the system. For example, some HIV-infected individuals display a rapid decline in immune health in the absence of treatment, whereas others resist disease progression. Discovering which factors contribute to these divergent responses may help to identify new ways to control, and perhaps eradicate, this disease. A logical place to look for such defining factors is among the many components of the primate immune system. Hartigan-O’Connor et al. find in macaques that the size of a particular T cell population before infection may influence simian immunodeficiency virus (SIV) replication.

The authors first measured in macaques the size of a population of proinflammatory T cells—T helper 17 (TH17) cells—and found that animals with larger TH17 cell populations before SIV infection had lower peak and set-point viral loads. Moreover, depleting TH17 cells—and thus changing the ratio between TH17 cells and regulatory T cells—resulted in higher viral set points 6 months after SIV infection. Therefore, the preexisting state of the host immune system has a direct effect on the relative success of SIV infection. These observations suggest that intricate dissection of individual immunological ecosystems may help to explain the variability of HIV progression in patients.