The overlapping epidemics of chronic viral hepatitis and metabolic dysfunction-associated steatotic liver disease (MASLD) present a complex challenge in modern hepatology. In chronic hepatitis B, a unique "steatosis paradox" emerges: while isolated hepatic steatosis provides a suppressive microenvironment that promotes hepatitis B viral clearance, the concomitant systemic cardiometabolic burden acts dose-dependently to drive fibrogenesis and hepatocellular carcinoma (HCC). Conversely, chronic hepatitis C and host metabolic dysfunctions exhibit synergistic destruction. Hepatitis C virus actively hijacks lipid metabolism and induces insulin resistance. Even after viral eradication via direct-acting antivirals, residual steatosis and glycemic abnormalities remain formidable drivers of HCC. Consequently, the traditional virocentric paradigm is no longer sufficient. Clinical management should pivot toward precision risk stratification and a multidisciplinary dual-target approach, equally prioritizing sustained viral suppression and aggressive metabolic remission. This review summarizes the divergent virus-MASLD interactions, optimal clinical strategies, current challenges and future opportunities.
