Viral dynamics in chronic hepatitis B patients

A chronic hepatitis B infection (HBV) is a potentially progressive liver disease which affects around 350 million people world-wide with an annual mortality rate of around 1 million people. (1). Together with malaria and tuberculosis it is among the top three of most prevalent infectious diseases. The evolution of this viral infection is dependent on the activity of the inflammation which is induced by both host and viral factors. HBV may be responsible for death due to liver cirrhosis or hepatocellular carcinoma (HCC) with a lifetime risk of 40- 50% in men and 15% in women (2). Universal vaccination which is common practice in over 80 countries world-wide (3) has the potential to eradicate this viral disease completely and prevent HCC. Although vaccination in highly prevalent areas is much cheaper compared to the western world, universal vaccination still generates substantial costs per prevented infection. Screening for the presence of HBV in pregnant women is a more low-scale intervention which is capable of protecting selected neonates by post-natal immunization. This program is capable of protecting infants who otherwise run a great risk to become chronically infected (4). However, since at present there is a reservoir of millions of people who are chronically infected, we are in need of effective antiviral therapies. The main initial goal of antiviral therapy should be induction of HBeAg seroconversion and normalization of serum transaminases. This results in a low infective individual with a quiescent disease in whom the chance of further liver damage has been minimized (5,6). Since patients who express active viral replication (as shown by HBeAg positivity and high levels of HBV DNA) and/or elevated serum transaminases are at the higbest risk to develop complications of the liver disease, therapy should primarily be aimed at this subgroup of chronically infected patients.

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