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One of the conundrums of chronic infection with the hepatitis B virus (HBV) is identifying those individual patients who are at risk for the development of the serious sequelae of cirrhosis and hepatocellular carcinoma (HCC). It has been estimated that 25–40% of patients with chronic hepatitis B (CHB) who acquire the virus early in life (perinatal or early horizontal transmission from an HBeAg-positive source) will eventually develop these serious and disastrous consequences.1 Viral factors associated with the outcome of CHB include hepatitis B e antigen (HBeAg) status, HBV DNA and HBsAg levels (>2000 IU/mL) in serum, HBV genotype and HBV variants, all of which have been shown to positively enhance the risk for disease progression.2–4 The viral variants considered significant risk factors include the basal core promoter (BCP) mutants A1762T/G1764A which have been strongly associated with the development of HCC.5 However, these viral factor associations are not absolute and the need for a viral biomarker that achieves such a goal in patients with CHB is very strong.
Dr Tai-Chung Tseng and colleagues6 from Taiwan provide compelling evidence that the presence of BCP mutants A1762T/G1764A in patients 1 year after HBeAg seroconversion significantly increases risk of cirrhosis in Asian subjects. Moreover, using a quantitative molecular analysis based on pyrosequencing, they also found that patients harbouring a higher percentage (≥45%) of A1762T BCP mutant, had a higher risk for liver cirrhosis than those with a lower A1762T BCP mutant percentage (<10%). By contrast, the A1762T …