Transmitted Drug Resistance in Nonsubtype B HIV-1 Infection

Abstract

HIV-1 nonsubtype B variants account for the majority of HIV infections worldwide. Drug resistance in individuals who have never undergone antiretroviral therapy can lead to early failure and limited treatment options and, therefore, is an important concern. Evaluation of reported transmitted drug resistance (TDR) is challenging owing to varying definitions and study designs, and is further complicated by HIV-1 subtype diversity. In this article, we discuss the importance of various mutation lists for TDR definition, summarize TDR in nonsubtype B HIV-1 and highlight TDR reporting and interpreting challenges in the context of HIV-1 diversity. When examined carefully, TDR in HIV-1 non-B protease and reverse transcriptase is still relatively low in most regions. Whether it will increase with time and therapy access, as observed in subtype-B-predominant regions, remains to be determined.

The prevalence of drug resistance among treatment-naïve HIV-1-infected individuals in China during pre- and post- 2004

“…There was different prevalence of resistance among subtype B, CRF_01AE and CRF_07BC/08BC. Resistance was significantly higher in ARV-naïve patients who were infected with subtype B than in those infected with CRF01_AE viruses ( p  = 0.0030), which was similar with previously published studies [17–19, 31, 32]. Although subtypes may vary in mutational pathways, it is unclear whether subtype B was more prone to mutation [33].…”

The Geogenomic Mutational Atlas of Pathogens (GoMAP) Web System

“…We observed several patterns of regional concentration in DRMs that generally were not coincidental with the established global subtype distributions [36]. The I50L primary mutation in protease for Atazanavir and Amprenavir is predominant in South America, but not in the same countries as the B or BF subtype distributions.…”

A Phylogenetic Analysis of Human Immunodeficiency Virus Type 1 Sequences in Kiev: Findings Among Key Populations

“…Previous TDR estimates have been higher (31,32) but have used different definitions of TDR mutations from ours, in particular the inclusion of accessory NRTI mutation A62V, a reported polymorphism in non-B subtypes. (33,34).…”