Chronic Hepatitis B Inactive Carrier

By Thomas Sim, 10 June, 2008


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There is long been confusion among patients regarding who is actually a Chronic Hepatitis B Carrier. It can be understood by layman that sero-converted surface antigen HBsAg to presence of HBsAb in the blood is taken as the ultimate ‘cure’ from the infection. However, is that so? Let us look at some recent publications.

Before I go on, let me briefly explain the meaning of Chronic Inactive Hepatitis B. 'Chronic' here signifies that the person is still under infection, whether persistently with viral replication or minimal residual viral activity. If the viral replication is active, i.e. with viral DNA measurable in the blood and significantly high, this patient is having Chronic ACTIVE disease. However, if there is undetectable or low DNA in the blood stream, this patient is having Chronic INACTIVE disease and therefore with minimal risk of liver damage or infection to others. With this fundamental information in mind, we take a step forward to see what is clinically encountered in practice.

I once attended a meeting by haematologists during which treatment of lymphoma in HBV and HCV patients was one of the topics for discussion. One of the participants said that he had patients who were supposed to have gained immunity to HBV (presence of antibody), unfortunately after having received chemotherapy, their HBV came back. So, the question of ‘cure’ in this spontaneous seroclearance of HBsAg patients may not confer total eradication of the Hepatitis B Virus in the real sense.

My previous article also touched on the Italian Study that the spontaneous sero-conversion is around 1% per year. This is again supported by a recent Taiwanese Study by Chu et al entitled: HBsAg seroclearance in asymptomatic carriers of high endemic areas: appreciably high rates during a long-term follow-up. Hepatology 2007; 45: 1187-1192.

The expert commentary mentioned that if such question by patient is asked: ‘Will I ever be cured of my hepatitis B infection?’ Chu et al allows us to answer, with some confidence, that is possible, but is an uncommon event, occurring at a rate of approximately 1% per year.

Another confirmation to the scenario above, it may still be possible for hepatocellular carcinoma to develop particularly in those with cirrhosis, and second, even though serologic evidence of HBV infection is gone, HBV DNA still persists and can be reactivated during periods of severe immunosuppression. An earlier Japanese study did find the presence of HBV DNA in such patients after 9 years of follow-up.

So, who is actually ‘cured’ of HBV infection? At this moment, I guess nobody really knows. However, if there is no liver cirrhosis and the status is asymptomatic inactive, such patient, even though still considered chronic carrier, would have good chance of ‘reasonably long life’ and a potential to experience seroclearance of HBsAg. The highest rate of conversion happens after age 50 at annual rate of 1.83%.

From Chu et al, the annual conversion rate ranges from 0.77% to 1.83% from age groups of <30>50 years with the average at 1.15% per year.