Abstract
Variability of the HIV reverse transcriptase (RT) and protease (PR) genes has been used as indicators of drug resistance and as a mean to evaluate phylogenetic relationships among circulating virus. However, these studies have been carried in HIV mono-infected populations. The goal of this study was to evaluate, for the first time, the HIV PR and RT sequences from HIV/HBV and HIV/HCV co-infected patients. HIV PR and RT genes were amplificated and sequenced to resistance analysis. The bioinformatics analysis was performed to infer about sequences clustering and molecular evolution. The results showed that the most frequent amino acid substitutions in RT were L214F (67.6%), I135T (55.9%), and in PR was V15I (41.2%). The molecular clock analysis showed that the HIV circulating in co-infected patients were separated in two clusters in the years 1999–2000. Some patients included as HIV mono-infected according patients’ medical records and inside the co-infected cluster were, in fact, co-infected by PCR analysis. Analysis of the decision trees showed susceptibility to lamivudine and emtricitabine were important attribute to characterize co-infected patients. In conclusion, the results obtained in this study suggest, for the first time, that HIV RT and PR genes variability could be a genetic biomarker to coinfection.
Highlights
Distinct HIV subtypes, circulating recombinant forms (CRF) and quasispecies have been isolated from infected patients[4,5,6,7] due to the high degree of HIV genetic variability[8], a consequence of the selective pressure of the host immune system and/or antiretroviral therapy[9]
G2 had a higher number of mutations to nucleoside analog reverse-transcriptase inhibitors (NRTI), and this group presented more wild type variation than G1 to non-nucleoside analog reverse-transcriptase inhibitors (NNRTI) (P < 0.05)
The results showed there more NRTI resistance mutations than those for other drug classes (NNRTI and protease inhibitors (PI)) in both groups (Table 2)
Summary
Distinct HIV subtypes, circulating recombinant forms (CRF) and quasispecies have been isolated from infected patients[4,5,6,7] due to the high degree of HIV genetic variability[8], a consequence of the selective pressure of the host immune system and/or antiretroviral therapy[9]. Several studies have been reported in the literature about HIV genetic variability in PR and RT genes as indicators of drug resistance[13,14,15], viral fitness[16], and transmitted resistance[17,18] and as a mean to evaluate phylogenetic relationships among circulating virus[19]. These studies have been carried in HIV mono-infected (mi) populations. Studies have demonstrated that HIV infected patients using HAART had mortality when presenting with HCV or HBV22
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