Antiretroviral Drug Resistance in Brazilian Children Infected by Human Immunodeficiency Virus Type 1
- *Corresponding Author:
- Dr. Sandra Cecília Botelho Costa
Faculty of Medical Sciences, CP 6111
State University of Campinas (UNICAMP)
Cep: 13083-970, Campinas, Sao Paulo, Brazil
E-mail: [email protected]
Received Date: August 13, 2012; Accepted Date: September 01, 2012; Published Date: September 07, 2012
Citation: Bismara BA, Anjos EB, Andrade PD, Albuquerque DM, Silva MT, et al. (2012) Antiretroviral Drug Resistance in Brazilian Children Infected by Human Immunodeficiency Virus Type 1. J Antivir Antiretrovir 4: 066-074. doi: 10.4172/jaa.1000048
Copyright: © 2012 Bismara BA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The purpose is to determine the prevalence of drug-resistance mutations in HIV-1 infected children under antiretroviral treatment from Brazil. Blood samples from sixty one human immunodeficiency virus type 1 (HIV-1) vertically-infected Brazilian children are studied. DNA was extracted from the samples, and a 1.0 kb fragment containing HIV-1 PR and RT-coding sequence were amplified by Nested Polymerase Chain Reaction sequencing. The HIV-1 sequencing, based on the polymerase gene sequences (protease and reverse transcriptase regions), was as follows; subtype B (83.6%), subtype F (9.8%) and B/F viral recombinant forms (6.6%). Two major protease inhibitor-resistance associated mutations, M36I and L90M, were most prevalent in our samples (32.8%), as well as the polymorphism L63P (42.6%). Many mutations associated with reduced susceptibility to nucleoside or nonnucleoside reverse-transcriptase inhibitors were detected: M184V (42.6%), M41L (37.7%), D67N (26.2 %), T215Y (24.6%), L210W (21%). This study showed that 85.2% of the studied population showed evidence of therapy failure, with the presence of viral genomic mutations associated with drug resistance.