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Science. 2014 Aug 1;345(6196):570-3. doi: 10.1126/science.1256304. Epub 2014 Jul 10.

HIV latency. Proliferation of cells with HIV integrated into cancer genes contributes to persistent infection.

Author information

1
Seattle Children's Research Institute, 1900 9th Avenue, Seattle, WA 98101, USA. University of Washington, Seattle, WA, USA.
2
Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
3
University of Washington, Seattle, WA, USA.
4
Seattle Children's Research Institute, 1900 9th Avenue, Seattle, WA 98101, USA.
5
University of Washington, Seattle, WA, USA. Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
6
Seattle Children's Research Institute, 1900 9th Avenue, Seattle, WA 98101, USA. University of Washington, Seattle, WA, USA. lfrenkel@uw.edu.

Abstract

Antiretroviral treatment (ART) of HIV infection suppresses viral replication. Yet if ART is stopped, virus reemerges because of the persistence of infected cells. We evaluated the contribution of infected-cell proliferation and sites of proviral integration to HIV persistence. A total of 534 HIV integration sites (IS) and 63 adjacent HIV env sequences were derived from three study participants over 11.3 to 12.7 years of ART. Each participant had identical viral sequences integrated at the same position in multiple cells, demonstrating infected-cell proliferation. Integrations were overrepresented in genes associated with cancer and favored in 12 genes across multiple participants. Over time on ART, a greater proportion of persisting proviruses were in proliferating cells. HIV integration into specific genes may promote proliferation of HIV-infected cells, slowing viral decay during ART.

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PMID:
25011556
PMCID:
PMC4230336
DOI:
10.1126/science.1256304
[Indexed for MEDLINE]
Free PMC Article

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