HIV VIS Detail Information

> This page shows VIS [4002774] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

DVID	4002774
VISID	TVIS30001241
Chromosome	chr2
GRCh38 Location	197303887, 197304775
Disease	HIV Infections Acquired Immunodeficiency Syndrome
Sample	PBMC
Virus Reference Genome	Not given
Target Gene	ANKRD44

Literature Information

PubMed PMID	25011556
Year	2014 Aug 1;345(6196):570-3
Journal	Science (New York, N.Y.)
Title	HIV latency. Proliferation of cells with HIV integrated into cancer genes contributes to persistent infection.
Author	Wagner TA,McLaughlin S,Garg K,Cheung CY,Larsen BB,Styrchak S,Huang HC,Edlefsen PT,Mullins JI,Frenkel LM
Evidence	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.