HIV-1 primary and secondary antiretroviral drug resistance and genetic diversity among pregnant women from central Brazil

✍ Scribed by Ludimila Paula Vaz Cardoso; Gisner Alves Souza Pereira; Ângela Alves Viegas; Luiza Emylce Pelá Rosado Schmaltz; Mariane Martins de Araújo Stefani

• Publisher: John Wiley and Sons
• Year: 2010
• Tongue: English
• Weight: 148 KB
• Volume: 82
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.21722

✦ Synopsis

Abstract

Antiretroviral (ARV) resistance mutations in HIV‐1 may reduce the efficacy of prophylactic therapy to mother‐to‐child transmission and impact future treatment options. ARV resistance mutations and HIV‐1 phylogenetic diversity in protease (PR) and reverse transcriptase (RT) genes were assessed among 77 pregnant women (35 naïve, 42 treated with ARV) from Goiânia/Goiás, central west Brazil. ARV mutations in PR/RT genes were analyzed against the Stanford Database, PR/RT HIV‐1 subtypes were assigned by phylogenetic analysis and env/gag subtypes were identified by heteroduplex mobility analysis (HMA). Naïve patients had accessory mutations in the PR gene [A71T (1/6), L10V (2/6), L10I (3/6)] and in the RT gene [V118I (2/6), V179D (1/6), V106I (1/6), K101Q (1/6), H221Y (1/6)]. Seven patients (16.7%) under ARV presented drug resistance mutations, one of them to three ARV classes. Most isolates (67.5%) were subtype B, 11.7% subtype F1 and 3.9% subtype C. Recombinant B^PR^/F1^RT^ viruses represented 10.4% while F1^PR^/B^RT^ viruses made up 6.5%. HIV‐1 envgag/PRRT genes were identified as 66.2% subtype B, 3.9% subtype C, 6.5% subtype F1 and approximately 25% B and F1 viruses. HIV‐1 genetic diversity in envgag/PRRT genes indicates the spread and dissemination of BF1 recombinant viruses among a significant proportion of patients from central west Brazil. Moreover, discovery of HIV‐1 secondary resistance among a considerable number of pregnant women under ARV therapy indicates the importance of genotypic testing during pregnancy for optimal prophylactic intervention. J. Med. Virol. 82:351–357, 2010. © 2010 Wiley‐Liss, Inc.