3rd International AIDS Society Conference on HIV Pathogenesis and Treatment


Rio de Janeiro - July 24 - 27, 2005

PATTERNS OF HIV-1 GENOTYPIC ANTIRETROVIRAL RESISTANCE IN CLINICAL PRACTICE: A SURVEY OF THE BRAZILIAN NETWORK FOR GENOTYPIC RESISTANCE

IAS Conf HIV Pathog Treat 2005 Jul 24-27;3rd: Abstract No. TuPp0301

Munerato P.1, Andreo S.M.1, Sucupira M.C.1, Mamede S.2, Mota G.1, Sá Filho D.1, Cavalieri E.1, Arakaki D.2, Marins J.R.P.2, Diaz R.S.1
1UNIFESP, São Paulo, Brazil, 2Coordenação Nacional DST/AIDS, Brasília, Brazil

INTRODUCTION: This survey describes antiretroviral resistance profile among patients failing therapy, according to clade, and antiretroviral used.

METHODS: We analyzed 1,170 samples collected from January 2002 to August 2004, from patients from the city of São Paulo, Brazil.

RESULTS: 17% of patients were in the 1st virologic failure, 33% in the 2nd, and 50% in the 3rd or more. Prevalence of resistance to NRTI was 88%, to NNRTI was 54.4%, and to PI was 58.1%. 8.4% of individuals were resistant to 1 class, 42.9% to 2 classes, and 47.5% to 3 classes. 86% were HIV-1 clade B, 5% F, 1.9% C, and 7.1% B/F recombinants. 70% of patients had Thymidine Analog Mutations (TAM), 68.5% of them with 3 or more TAM. There was a negative correlation between 210W and 215F. 67.7% of patients failing Efavirenz presented K103N whereas 41.8% of patients failing Nevirapine did (p<.001). 168 patients were failing Nelfinavir as first PI, and the pathway for resistance showed for clade B (n=120) 52.5% of 30N, 38.3% of 90M, and 9.1% of both. Non-B strains (n=48) showed 18.7% of 30N, 27% of 90M, 4.1% of both, and 50% without 30N or 90M. End point PCR showed that 30N and 90M did no coexist in the same strain. Protease mutations at codons 10, 20, 36, 54, 82, 89 were more prevalent in clade F, whereas mutations at 30, 63, 71, 77, and 88 were more prevalent in Bs (p<.001).

CONCLUSIONS: We found high prevalence of TAM. Almost half of patients failing Nelfinavir had limited chances of salvage by other PI. Resistance to Nelfinavir in non-B strains most frequently related to other mutations than 30N or 90M. The genotypic patterns of resistance between clades B and F are distinct in protease, revealing a poor understanding of resistance correlates in F strains.

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Clinical | TuPp0301 | R.S. Diaz
4.1 643 4.1 Resistance surveillance

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