Outcomes of chronic and vertically acquired occult hepatitis B

Abstract

Background: Chronic hepatitis B virus (HBV) infection is one of the major chronic infections and still in 2017 the most common cause for liver cirrhosis and hepatocellular carcinoma (HCC, liver cancer) in the world. Occult HBV infection is a hidden variant of chronic HBV infection where some of the common serological markers for HBV infection are negative, but replicative competent HBV DNA can be found in the liver and sometimes also low levels of HBV in the blood. Aims: The general aims of this thesis were to investigate the prevalence and long-term outcomes in children with occult HBV infection, acquired from their mothers at birth. We also investigated long-term outcomes and predictive factors that influence long-term outcomes of chronic HBV infection in a Swedish cohort. Methods: In paper I, we prospectively investigated the prevalence of occult HBV infection in 44 children born to mothers with chronic HBV infection. In paper II, we retrospectively investigated a group of 66 children born between 1998-2018 to mothers with highly contagious chronic HBV infection regarding prevalence and long-term effect of occult HBV infection. In paper III, we investigated baseline factors in 100 persons with chronic HBV infections and their association with long-term outcomes up to 30 years. In paper IV, we investigated the relative contribution from replicative competent HBV DNA (cccDNA) and chromosomally integrated HBV DNA to the hepatitis B surface antigen (HBsAg) production in various clinical settings. Conclusions: We found that occult HBV infections were common in children born to highly contagious mothers and that they later can convert into overt chronic HBV infections, but that long-term effect of occult HBV infections seemed to be favorable. We also found that long-term outcomes of chronic HBV infection were dependent on HBV genotype and that a liver biopsy together with genotype information contributed to better risk prediction in patients with chronic HBV infection. At last, we found that chromosomally integrated HBV DNA was the main contributor to the HBsAg levels, except in situations with very high levels of HBV in the blood.