脂肪变性
医学
病毒性肝炎
肝细胞癌
免疫学
肝病
病毒学
肝炎
病毒
病毒载量
丙型肝炎病毒
乙型肝炎
乙型肝炎病毒
疾病
血糖性
脂质代谢
胰岛素抵抗
丁型肝炎
丙型肝炎
胰岛素
生物信息学
慢性肝炎
脂肪肝
慢性感染
病毒性疾病
丁型肝炎病毒
纤维化
炎症
作者
Shang‐Chin Huang,Yi-Fen Shih,C C Liu
标识
DOI:10.3350/cmh.2026.0387
摘要
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.
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