907 Relationship Between HIV-1 Viral Subtype, Disease Progression, and Response to Antiretroviral Therapy P. J. Easterbrook*1, M. Smith1, J. Mullen3, S. OShea3, A. M. Geretti1, S. Murad1, I. Chrystie3, A. M. de Ruiter3, M. Mvere1, B. Kulasegaram3, M. Zuckerman1, The Guys, Kings, and St. Thomas HIV Collaborative Group1 1King's Coll, London, UK and 3St Thomas' Hosp, London, UK
Background: To compare the rate of disease progression prior to antiretroviral therapy (ART) and the initial response to ART in patients (pts) infected with B compared to A, C, and D non-B HIV-1 subtypes in an ethnically diverse population of HIV infected pts in South London.
Methods: A total 867 HIV-1 infected pts from Kings and St. Thomas hospital HIV clinics have been subtyped using an in-house EIA assay based on the CDC peptide antigens to discriminate between B (47.8%) and non-B (30.8%) subtypes. Of these, 82 (9.5%) were of mixed reactivity and 104 (12.0%) were either non-reactive or below detectable limits. Env gene sequencing was used to confirm the precise distribution of non-B subtypes and various mosaic strains. Rate of disease progression was determined using rate of CD4 cell decline (initial 2 years after diagnosis) stratified according to initial CD4 count (= 100, 101-200, 201-400 > 400 cells), and pre-treatment viral load profile; response to ART was assessed on time to a viral load = 400 copies/ml.
Results: 87.5% of non-B subtypes identified on EIA were confirmed on env sequencing. Analyses were based on 594 pts with complete data; 408 were B, and 186 were non-B subtype, of which 40 (21.5%) were A, 81 (43.5%) were C, 14 (7.5%) were D, and 51 (27.4%) were infected with recombinant strains: the most common was CRF02A/G (n = 15). The majority (85.2%) of non-B and recombinant strains were found in black Africans from sub-Saharan Africa (most commonly Uganda, Zimbabwe, Nigeria, Ivory Coast, and Ghana). B subtype pts were mainly Caucasian. There was a trend (p = 0.05) towards a slightly faster initial rate of CD4 decline among pts with subtype non-B, particularly, subtype C compare to B after adjustment for baseline CD4 count and after initiation of ART, the % with a VL = 400 copies/ml was lower among B (30.4%) vs non-B (33.9%) subtype pts, p = 0.097.
Conclusions: We found some evidence to suggest for subtype specific differences in disease progression, but no initial virological response to antiretroviral therapy between B and the non-B subtypes.
