Core promoter mutations of hepatitis B virus and hepatocellular carcinoma: story beyond A1762T/G1764A mutations.

摘要

Hepatitis B virus (HBV) infection is a global health problem that causes a wide spectrum of liver disease, including acute or fulminant hepatitis, inactive carrier state, chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC).1 Thus, understanding the pathogenesis of HBV infection and the individuaiization of chronic hepatitis B therapy to prevent disease progression to end-stage liver disease as well as HCC is of paramount importance. The interactions among host, environmental, and viral factors have been reported to determine the natural course and treatment outcomes of individuals with chronic HBV infection.1 In the past decade, several critical hepatitis B viral factors predictive of clinical outcomes have been identified.2"13 Of particular note is the REVEAL-HBV study from Taiwan, which indicated that a higher baseline serum HBV-DNA level conferred a higher risk of cirrhosis as well as HCC, even in hepatitis B e-antigen (HBeAg)-negative HBV-infected people aged over 30 years after 13 years of follow up, especially in those with a persistently high viral load (>20 000 IU/mL).