Since the discovery of the hepatitis B virus (HBV) by Blumberg et al. in 1965, its genome,\nsequence, epidemiology, and hepatocarcinogenesis have been elucidated. Globally, hepatitis B\nvirus (HBV) is still responsible for the majority of hepatocellular carcinoma (HCC). HCC is the\nsixth-most common cancer in the world and the second-most common cancer death. The ultimate\ngoal of treating HBV infection is the prevention of HCC. Fortunately, anti-HBV treatment with\nnucleos(t)ide analogues (NAs), which began with lamivudine in 1998, has resulted in remarkable\nimprovements in the survival of patients with chronic hepatitis B and a reduced incidence of HCC.\nThese results were documented with lamivudine, entecavir, and tenofovir. Nonetheless, as the\nduration of antiviral treatment increases, the risk for HCC still remains despite undetectable HBV\nDNA in serum, as reported by different investigators with observation up to 4ââ?¬â??5 years. In our own\nexperience, we are witnessing the development of HCC in patients who have received antiviral\ntreatment. Some have enjoyed negative serum HBV DNA for over 12 years before developing HCC.\nCurrent treatment with NAs can effectively suppress the replication of the virus but cannot eradicate\nthe covalently closed circular DNA (cccDNA) that is within the nucleus of hepatocytes. There\nstill remains a great need for a cure for HBV. Fortunately, several compounds have been identified\nthat have the potential to eradicate HBV, and there are ongoing clinical trials in progress in their\nearly stages.
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