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Hepatitis B virus (HBV), a member of Hepadnaviridae family, represents a small virus of about 3200 bp and infects human and higher primates. Although the virus is hepatotrophic in nature, it has been detected in many organs and tissues including blood of infected human. HBV infection is universal in nature and about 2 billion people of the world have been infected with the HBV at some point of their life. Among them, considerable numbers of HBV-infected subjects have developed protective antibody to HBV (antibody to hepatitis B surface antigen [anti-HBs]) and are immune from future HBV challenge. On the other hand, several million HBVinfected subjects express antibody to hepatitis B core antigen (anti-HBc) without expressing replication product of HBV (hepatitis B surface antigen [HBsAg]). However, these inactive HBV carriers may enter to active HBV replication cycle due to alteration of life style or several other causes. Finally, about 240 to 370 million people allow active HBV replication and express HBsAg and HBV DNA in the sera. Among these chronic HBV carriers, several millions develop chronic hepatitis B (CHB), liver cirrhosis (LC) and hepatocellular carcinoma (HCC). If these epidemiological evidences are compiled, it is evident that primary, mid-point and ultimately fate of HBV infection is not only diverse but also poorly understood. More importantly, the kinetics of HBV infection and liver-damaging properties and potentials of HBV could not be explained by HBVrelated factors. Neither the viral load (HBV concentrations) nor the expression levels of HBV-related Hepatitis B virus-related liver diseases: Identity and evidence-based control strategy