Journal
JOURNAL OF VIROLOGY
Volume 85, Issue 18, Pages 9646-9650Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.05327-11
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Funding
- U.S. National Institutes of Health [AI093203, AI078799, AI089339]
- Doris Duke Clinical Scientist Development Award
- European Molecular Biology Laboratory (EMBL)
- NIH [CA135401, DK082690]
- Medical Service of the U.S. Department of Veterans Affairs
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Elite controllers spontaneously maintain undetectable levels of HIV-1 replication for reasons that remain unclear. Here, we show that in elite controllers, direct ex vivo infection of purified CD4 T cells without prior in vitro activation results in disproportionately low levels of integrated HIV-1 DNA relative to the quantity of reverse transcripts, while the levels of two-long terminal repeat (2-LTR) circles were excessively elevated relative to those of integrated HIV-1 DNA. This indicates that chromosomal HIV-1 integration is inhibited in ex vivo-infected CD4 T cells from elite controllers. This defect in HIV-1 integration was unrelated to p21, a host protein that can restrict early HIV-1 replication steps, and was not visible following infection of in vitro-activated CD4 T cells from elite controllers. These data contribute to increasing evidence that intrinsic inhibition of specific HIV-1 replication steps plays an important role in the ability of elite controllers to maintain undetectable viral loads.
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