With the widespread implementation of combination antiretroviral therapy (cART), HIV infection has evolved into a manageable chronic condition, with life expectancy significantly extended-approaching that of the general population in some cases (1).However, the central nervous system, as an "immune-privileged site" and potential viral reservoir, may harbor residual virus and persistent inflammation even under effective plasma viral suppression (2,3) Studies show that neuronal injury can still occur in people living with HIV in the cART era, driven by factors including viral protein neurotoxicity, microglial activation, glutamate excitotoxicity, immune dysregulation, comorbidities, and antiretroviral neurotoxicity (4,5).HIV-associated neurocognitive disorders (HAND) have thus emerged as a major challenge in chronic disease management, with a prevalence ranging from 30% to 50% (6,7). The milder forms of HAND-namely, asymptomatic neurocognitive impairment (ANI) and mild neurocognitive disorder-are the most common. Despite subtle or absent clinical symptoms, they may reflect early neurodegenerative processes (7,8).
Wang et al. (Fri,) studied this question.