HIV VIS Detail Information

> This page shows VIS [4005236] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

DVID	4005236
VISID	TVIS30000512
Chromosome	chr9
GRCh38 Location	132299714
Disease	HIV infection/AIDS
Sample	Cell line
Virus Reference Genome	K03455.1
Target Gene	SETX

Literature Information

PubMed PMID	26912621
Published year	2016
Journal	Journal of virology
Title	HIV Integration Site Analysis of Cellular Models of HIV Latency with a Probe-Enriched Next-Generation Sequencing Assay.
Author	Sunshine S,Kirchner R,Amr SS,Mansur L,Shakhbatyan R,Kim M,Bosque A,Siliciano RF,Planelles V,Hofmann O,Ho Sui S,Li JZ
Evidence	The location of retroviral integration into the human genome is thought to play a role in the clonal expansion of infected cells and HIV persistence. HIV integration site characteristics and genes were compared between these cellular models and to previously reported patient data sets. Across these cellular models, there were significant differences in integration site characteristics, including orientation relative to that of the host gene, the proportion of clonally expanded sites, and the proportion located within genic regions and exons. Despite a greater diversity of minority integration sites than expected in ACH-2 cells, their integration site characteristics consistently differed from those of the other models and from the patient samples. These findings show that integration site differences exist among the commonly used cellular models of HIV latency and in comparison to integration sites found in patient samples. IMPORTANCE: Despite the success of ART, currently there is no successful therapy to eradicate integrated proviruses. Cellular models of HIV latency are used to test the efficacy of latency-reversing agents, but it is unclear how well these models reflect HIV integration into the human genome in vivo We have developed a novel probe-based sequence enrichment assay to sequence and analyze integrated HIV. We compared HIV integration site characteristics between four cellular models and to previously described patient data sets. Significant differences were detected in the distribution of HIV integration sites between cellular models of HIV latency and compared to data sets from patient samples. The results from this study have implications for how well these cellular models of HIV infection truly reflect HIV integration in vivo and their applicability in drug discovery for novel latency-reversing agents.