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Are Associated With Phenotypic Differences in Replication Capacity and Disease Progression

By David Serwadda Susan H. Eshleman and Thomas C

Abstract

Background. Determinants of intersubtype differences in human immunodeficiency virus type 1 (HIV-1) clini-cal disease progression remain unknown. Methods. HIV-1 subtype was independently determined for 5 separate genomic regions in 396 HIV-1 sero-converters from Rakai, Uganda, using a multiregion hybridization assay. Replication capacities (RC) in samples from a subset of 145 of these subjects were determined. HIV-1 genomic regions and pol RC were examined for asso-ciation with disease progression. Amino acid polymorphisms were examined for association with pol RC. Results. In multivariate analyses, the hazard for progression to the composite end point (defined as a CD4+ T-cell count <250 cells/mm3, antiretroviral therapy initiation, or death) among patients with subtype D pol infection was 2.4 times the hazard for those infected with subtype A pol infection (P =.001). Compared with subtype A pol (the reference group), the hazard for progression to the composite end point for subtype D pol infection with a pol RC>67 % (ie, the median pol RC) was significantly greater (HR, 4.6; 95 % confidence interval [CI], 1.9–11.0; P =.001), whereas the hazard for progression to the composite end point for subtype D pol infection with a pol RC ≤67 % was not significantly different (HR, 2.2; 95 % CI, 1.0–4.9; P =.051). Amino acid substitutions at protease posi

Year: 2016
OAI identifier: oai:CiteSeerX.psu:10.1.1.917.3635
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