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Drug resistance mutations in protease gene of HIV-1 subtype C infected patient population
Author(s) -
Mohammad Misbah,
Poonam Gupta,
Gaurav Roy,
Suresh Kumar,
Mohammad Husain
Publication year - 2021
Publication title -
virusdisease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.375
H-Index - 22
eISSN - 2347-3517
pISSN - 2347-3584
DOI - 10.1007/s13337-021-00725-z
Subject(s) - drug resistance , regimen , protease inhibitor (pharmacology) , drug , protease , hiv 1 protease , reverse transcriptase , medicine , population , virology , gene mutation , mutation , resistance mutation , pharmacology , gene , biology , human immunodeficiency virus (hiv) , antiretroviral therapy , viral load , genetics , polymerase chain reaction , enzyme , biochemistry , environmental health
Failure of antiretroviral therapy (ART) in HIV-1 infection is a critical issue for the physicians treating HIV patients. The major cause of drug failure is the development of resistance mutations in reverse transcriptase (RT) and/or protease (PR) genes. Mutations associated with drug resistance decrease drug effectiveness. This study was conducted to assess drug resistance profile of the entire PR gene in 90 HIV-1 patients consisting of 23 ART non-responsive, 32 ART responsive and 35 drug naive patients. It was observed that the majority of the sequences (94.4%) belonged to subtype C and (5.5%) to subtype A1. The ART non-responsive and responsive patients were treated with either first line of ART regimen (two NRTI and one NNRTI) or second line of ART regimen that included additional one protease inhibitor (PI). All the patients in each group except one responsive patient had various minor resistance mutations. Thus, drug failures in ART non-responsive patients may not always be due to drug resistance mutations instead other factors may also be responsible for drug failures such as non-compliance, suboptimal dose or drug interaction. The presence of minor drug resistance mutations in drug naive patients is suggestive of transmitted resistance mutations.

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