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Recent shifts in nomenclature and the introduction of MetALD emphasize metabolic dysfunction and graded alcohol exposure as central drivers of disease and are particularly relevant to PLWH, a population in whom overlapping metabolic and behavioral risk factors are common. Epidemiologic studies demonstrate that MASLD affects approximately one-third to one-half of PLWH worldwide, often occurring at younger ages and lower body mass index thresholds than in HIV-negative individuals. Emerging data further highlight the synergistic contribution of metabolic dysfunction and alcohol use to accelerated fibrosis progression in PLWH. Pathophysiologic mechanisms linking HIV infection to MASLD and MetALD include chronic immune activation and systemic inflammation, antiretroviral therapy-associated metabolic effects, altered adipose tissue distribution, gut-liver axis dysregulation, and alcohol-metabolic synergy. 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