Document Detail


Host genetic influences on highly active antiretroviral therapy efficacy and AIDS-free survival.
MedLine Citation:
PMID:  18391751     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We studied the influence of AIDS restriction genes (ARGs) CCR5-Delta32, CCR2-64I, SDF1-3'A, IL10-5'A, CX3CR1-V249I, CX3CR1-T280M, and MDR1-C3435T and haplotypes of the CCR5 P1 promoter and RANTES variants -403A, In1.1C, 3'222C, and -28G among HIV-1 infected patients on highly active antiretroviral therapy (HAART) in the Multicenter AIDS Cohort Study (MACS) and the Multicenter Hemophilia Cohort Study (MHCS). Our results indicate that several ARGs also influence therapy efficacy (ie, the success in viral suppression) and subsequent progression to AIDS while on HAART. CCR5-Delta32 decreased time to viral suppression (<200 HIV RNA copies/mL, relative hazard [RH]=1.40; P=0.008) and was protective against AIDS (RH=0.11; P=or<0.0001), whereas the CCR5 P1 haplotype was associated with delayed viral suppression (RNA<50 copies/mL, odds ratio [OR]=0.65; P=0.03) and accelerated time to AIDS (RH=2.68; P=0.02). SDF1-3'A reduced viral suppression (OR=0.61; P=0.02) and accelerated AIDS (RH=3.18; P=0.009). Accelerated AIDS progression was also observed with the RANTES haplotype carrying RANTES-IN1.1C and RANTES-3'222C (P=0.005 to 0.007). In contrast, the RANTES haplotype H1, which lacks suspected deleterious single-nucleotide polymorphisms, was protective against AIDS. CX3CR1-V249I seemed to accelerate viral suppression (RNA<50 copies/mL, OR=1.27; P=0.01). ARG influence after HAART suggests residual HIV-1 replication, and spread continues even in patients successfully suppressing detectable viral RNA.
Authors:
Sher L Hendrickson; Lisa P Jacobson; George W Nelson; John P Phair; James Lautenberger; Randall C Johnson; Lawrence Kingsley; Joseph B Margolick; Roger Detels; James J Goedert; Stephen J O'Brien
Publication Detail:
Type:  Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural    
Journal Detail:
Title:  Journal of acquired immune deficiency syndromes (1999)     Volume:  48     ISSN:  1525-4135     ISO Abbreviation:  J. Acquir. Immune Defic. Syndr.     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-06-26     Completed Date:  2008-07-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100892005     Medline TA:  J Acquir Immune Defic Syndr     Country:  United States    
Other Details:
Languages:  eng     Pagination:  263-71     Citation Subset:  IM; X    
Affiliation:
Laboratory of Genomic Diversity, National Cancer Institute, Frederick, MD 21702-1201, USA.
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MeSH Terms
Descriptor/Qualifier:
Acquired Immunodeficiency Syndrome / genetics*
Antiretroviral Therapy, Highly Active*
CD4 Lymphocyte Count*
Chemokine CCL5 / genetics
Cohort Studies
Disease Progression
European Continental Ancestry Group
Genotype
HIV-1 / drug effects*
Humans
Male
P-Glycoprotein / genetics*
Polymorphism, Single Nucleotide
Grant Support
ID/Acronym/Agency:
5-M01-RR-00722/RR/NCRR NIH HHS; N01-CO-12400/CO/NCI NIH HHS; U01-AI-35039/AI/NIAID NIH HHS; U01-AI-35040/AI/NIAID NIH HHS; U01-AI-35041/AI/NIAID NIH HHS; U01-AI-35042/AI/NIAID NIH HHS; U01-AI-35043/AI/NIAID NIH HHS; U01-AI-37613/AI/NIAID NIH HHS; U01-AI-37984/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Chemokine CCL5; 0/P-Glycoprotein

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