Journal
IMMUNITY
Volume 47, Issue 4, Pages 776-+Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2017.09.018
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Funding
- NIAID, NIH [104278, 116379, 116171, 110334]
- amfAR [109354-59-RGRL]
- ORIP/OD [P51OD011132, P30AI50409]
- National Cancer Institute (NIH) [HHSN261200800001E]
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Antiretroviral therapy (ART) suppresses viral replication in HIV-infected individuals but does not eliminate the reservoir of latently infected cells. Recent work identified PD-1(+) follicular helper T (Tfh) cells as an important cellular compartment for viral persistence. Here, using ART-treated, SIV-infected rhesus macaques, we show that CTLA-4(+)PD-1(-) memory CD4(+) T cells, which share phenotypic markers with regulatory T cells, were enriched in SIV DNA in blood, lymph nodes (LN), spleen, and gut, and contained replication-competent and infectious virus. In contrast to PD-1(+) Tfh cells, SIV-enriched CTLA4 +PD-1(-) CD4(+) T cells were found outside the B cell follicle of the LN, predicted the size of the persistent viral reservoir during ART, and significantly increased their contribution to the SIV reservoir with prolonged ART-mediated viral suppression. We have shown that CTLA-4(+)PD-1(-) memory CD4+ T cells are a previously unrecognized component of the SIV and HIV reservoir that should be therapeutically targeted for a functional HIV-1 cure.
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