Journal
IMMUNITY
Volume 43, Issue 3, Pages 591-604Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2015.08.012
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Funding
- Bill and Melinda Gates Foundation
- Witten Family Foundation
- Mark and Lisa Schwartz Foundation
- International AIDS Vaccine Initiative (IAVI) [UKZNRSA1001]
- NIAID [R37AI067073]
- NIH [P30 AI060354]
- NIAID, NIH
- NCI, NIH
- NICHD, NIH
- NHLBI, NIH
- NIDA, NIH
- NIMH, NIH
- NIA, NIH
- FIC, NIH
- OAR, NIH
- Howard Hughes Medical Institute
- South African Research Chairs Initiative
- Collaboration for AIDS Vaccine Discovery
- Lundbeck Foundation [R151-2013-14624] Funding Source: researchfish
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CD8(+) T cells contribute to the control of HIV, but it is not clear whether initial immune responses modulate the viral set point. We screened high-risk uninfected women twice a week for plasma HIV RNA and identified 12 hyperacute infections. Onset of viremia elicited a massive HIV-specific CD8(+) T cell response, with limited bystander activation of non-HIV memory CD8(+) T cells. HIV-specific CD8(+) T cells secreted little interferon-gamma, underwent rapid apoptosis, and failed to upregulate the interleukin-7 receptor, known to be important for T cell survival. The rapidity to peak CD8(+) T cell activation and the absolute magnitude of activation induced by the exponential rise in viremia were inversely correlated with set point viremia. These data indicate that rapid, high magnitude HIV-induced CD8(+) T cell responses are crucial for subsequent immune control of acute infection, which has important implications for HIV vaccine design.
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