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HIV-1 Promoter Single Nucleotide Polymorphisms Are Associated with Clinical Disease Severity
Journal article   Open access

HIV-1 Promoter Single Nucleotide Polymorphisms Are Associated with Clinical Disease Severity

Michael R Nonnemacher, Vanessa Pirrone, Rui Feng, Brian Moldover, Shendra Passic, Benjamas Aiamkitsumrit, Will Dampier, Adam Wojno, Evelyn Kilareski, Brandon Blakey, …
PloS one, v 11(4), pp e0150835-e0150835
2016
PMID: 27100290
url
https://doi.org/10.1371/journal.pone.0150835View
Published, Version of Record (VoR) Open

Abstract

Severity of Illness Index Cross-Sectional Studies HIV Infections - virology Humans Middle Aged CD4-Positive T-Lymphocytes - metabolism Genetic Association Studies - methods HIV Long Terminal Repeat - genetics Male Binding Sites - genetics Transcription Factors - genetics HIV-1 - genetics Viral Load - genetics Promoter Regions, Genetic - genetics HIV Infections - pathology Polymorphism, Single Nucleotide - genetics Female CD4-Positive T-Lymphocytes - virology Longitudinal Studies HIV Infections - metabolism
The large majority of human immunodeficiency virus type 1 (HIV-1) markers of disease progression/severity previously identified have been associated with alterations in host genetic and immune responses, with few studies focused on viral genetic markers correlate with changes in disease severity. This study presents a cross-sectional/longitudinal study of HIV-1 single nucleotide polymorphisms (SNPs) contained within the viral promoter or long terminal repeat (LTR) in patients within the Drexel Medicine CNS AIDS Research and Eradication Study (CARES) Cohort. HIV-1 LTR SNPs were found to associate with the classical clinical disease parameters CD4+ T-cell count and log viral load. They were found in both defined and undefined transcription factor binding sites of the LTR. A novel SNP identified at position 108 in a known COUP (chicken ovalbumin upstream promoter)/AP1 transcription factor binding site was significantly correlated with binding phenotypes that are potentially the underlying cause of the associated clinical outcome (increase in viral load and decrease in CD4+ T-cell count).

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Collaboration types
Domestic collaboration
Web of Science research areas
Virology
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