Inflammatory responses in HIV-1 genetic subtypes in relationship with anti-retroviral drug resistance in Minna, Niger State, North Central Nigeria

BACKGROUND: 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. METHODOLOGY: 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 targeting the HIV-1 protease and reverse transcriptase regions was performed to identify subtypes and resistance mutations. RESULTS: 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). CONCLUSION: 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 are recommended to enhance treatment efficacy and reduce HIV-related morbidity and mortality in resource-limited settings.