Hepatitis B Virus Genetic Diversity: Disease Pathogenesis

Hepatitis B Virus (HBV) infection is a global health problem: an estimated two billion people (one-third of the global population) have been infected with HBV at some point in their life; of these, more than 350 million suffer from chronic HBV infection, resulting in over 600,000 deaths each year, mainly from cirrhosis or liver cancer [1]. More than 10% of the global chronic HBV population resides in India [2]; infection may lead to liver damage that results in acute or chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC) (Figure 1). HBV infection was first identified in 1965 when Blumberg and co-workers [3] found the hepatitis B surface antigen (HBsAg), originally termed as Australia antigen. Enhanced viral replication leading to a vigorous and extensive immune response may lead to massive liver injury resulting spontaneously into fulminant hepatic failure. The seriousness of disease incidence is mainly related to various host factors (age, gender, duration of infection, immune response) and viral factors (viral load, genotype, quasispecies) (Figure 2). Recent evidence shows that considerable molecular variation occurs throughout the HBV genome, which is correlated with geographical distribution of genotypes and severity of disease.