HIV infection significantly elevates cellular senescence markers including SA-βGal, p16INK4a, and γH2AX in T-cells and monocytes, along with inflammatory SASP factors like IL-6, IL-10, and TNF receptors. These markers remained persistently elevated after one year of antiretroviral therapy in patients with chronic and advanced HIV infection, though not in those treated during primary infection. The 39-patient cohort demonstrated strong correlations between senescence biomarkers and immunosenescence, T-cell activation, and viral load. This research illuminates why HIV patients experience accelerated aging and increased age-related comorbidities despite viral suppression. The persistence of senescence markers suggests that HIV establishes a state of premature cellular aging that standard antiretroviral therapy cannot fully reverse once chronic inflammation is established. The finding that early treatment prevents this senescent phenotype underscores the critical importance of immediate HIV diagnosis and treatment initiation. For the broader longevity field, this work validates cellular senescence as a therapeutic target and suggests that senolytic drugs—compounds that selectively eliminate senescent cells—could meaningfully improve healthspan in HIV patients and potentially other chronic inflammatory conditions.