Cross-sectional study reveals high HIV-1 genetic diversity and inflammatory responses affecting antiretroviral drug resistance in patients with virological failure.
Abstract The high genetic diversity of HIV-1, persistent immune activation, and rising antiretroviral drug resistance continue to hinder HIV treatment, especially in Sub-Saharan Africa. This study examined inflammatory responses in relation to HIV-1 genetic subtypes and antiretroviral drug (ARVD) resistance among patients experiencing virological failure in Minna, Niger State, Nigeria. A cross-sectional design involved people living with HIV-1 (PLWH-1) on ART with virological failure (defined as repeated viral load ≥ 1000 copies/mL). Plasma levels of IL-6, IL-10, hs-CRP, and TNF-α were assessed as markers of inflammation; CD4 + counts and viral load served as immune and virological indicators. Genotypic analysis of HIV-1 targeted the protease and reverse transcriptase regions to identify subtypes and resistance mutations. HIV-1 subtypes G and CRF02_AG predominated. Subtype G was linked to elevated TNF-α and IL-6 levels and a higher frequency of drug resistance mutations, suggesting subtype-specific polymorphisms and elevated pro-inflammatory markers which correlated with poor treatment outcomes. Co-infections with HBV, HCV, and Mtb were also common, especially among individuals with heightened inflammatory markers and virological failure, complicating disease progression. IL-6, IL-10, hs-CRP, and TNF-α emerged as potential surrogate biomarkers for predicting virological failure and immune reconstitution inflammatory syndrome (IRIS). The findings underscore the importance of integrating inflammatory profiling and genotypic resistance testing to inform clinical decisions and improve ART outcomes. A personalized approach to HIV care—accounting for viral subtype, immune-inflammatory status, and resistance patterns—is recommended to enhance treatment efficacy and reduce HIV-related morbidity and mortality in resource-limited settings.
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