HIV VIS Detail Information

> This page shows VIS [4005235] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

DVID	4005235
VISID	TVIS30000283
Chromosome	chr17
GRCh38 Location	46333043
Disease	HIV Infections Acquired Immunodeficiency Syndrome
Sample	PBMC
Virus Reference Genome	K03455.1
Target Gene	ARL17A

Literature Information

PubMed PMID	30024859
Year	2018 Aug 31;128(9):4074-4085
Journal	The Journal of clinical investigation
Title	HIV-1 proviral landscapes distinguish posttreatment controllers from noncontrollers.
Author	Sharaf R,Lee GQ,Sun X,Etemad B,Aboukhater LM,Hu Z,Brumme ZL,Aga E,Bosch RJ,Wen Y,Namazi G,Gao C,Acosta EP,Gandhi RT,Jacobson JM,Skiest D,Margolis DM,Mitsuyasu R,Volberding P,Connick E,Kuritzkes DR,Lederman MM,Yu XG,Lichterfeld M,Li JZ
Evidence	HIV posttreatment controllers (PTCs) represent a natural model of sustained HIV remission, but they are rare and little is known about their viral reservoir. We obtained 1,450 proviral sequences after near-full-length amplification for 10 PTCs and 16 posttreatment noncontrollers (NCs). Before treatment interruption, the median intact and total reservoir size in PTCs was 7-fold lower than in NCs, but the proportion of intact, defective, and total clonally expanded proviral genomes was not significantly different between the 2 groups. Quantification of total but not intact proviral genome copies predicted sustained HIV remission as 81% of NCs, but none of the PTCs had a total proviral genome greater than 4 copies per million peripheral blood mononuclear cells (PBMCs). The results highlight the restricted intact and defective HIV reservoir in PTCs and suggest that total proviral genome burden could act as the first biomarker for identifying PTCs. Total and defective but not intact proviral copy numbers correlated with levels of cell-associated HIV RNA, activated NK cell percentages, and both HIV-specific CD4+ and CD8+ responses. These results support the concept that defective HIV genomes can lead to viral antigen production and interact with both the innate and adaptive immune systems.