HIV-1/HTLV-1 coinfection drives coordinated adaptive and innate immune dysregulation associated with increased risk of disease progression: a pilot exploratory study

Human Immunodeficiency Virus type 1 (HIV-1) and Human T-cell Lymphotropic Virus type 1 (HTLV-1) coinfection is associated with persistent immune activation and disease progression. We performed a cross-sectional immunophenotypic analysis of peripheral blood samples from HIV-1 monoinfected (n=15), HTLV-1 monoinfected (n=14), HIV-1/HTLV-1 coinfected (n=15), and healthy individuals (n=20) using multiparameter flow cytometry. HIV-infected and coinfected individuals exhibited marked CD4+ T-cell depletion, increased activation and exhaustion of CD4+ and CD8+ lymphocytes, expansion of circulating plasmablasts, and a shift toward inflammatory non-classical monocytes. HIV viral load correlated positively with T-cell exhaustion, plasmablast expansion, and inflammatory monocyte frequencies, whereas longer duration since HTLV-1 diagnosis was associated with progressive immune remodeling. Despite these alterations, HIV viral load did not differ significantly between mono-infected and coinfected individuals. These findings identify immune exhaustion and inflammatory biomarkers as potential indicators of disease progression and provide pilot evidence of coordinated adaptive and innate immune dysregulation during HIV-1/HTLV-1 coinfection.