Abstract
Reactivation of hepatitis B virus (HBV) is a major problem in patients receiving chemotherapy for malignant diseases or immunosuppression therapies. It has been thought that a reduction in the immune responses might result in the reactivation of HBV replication from covalently closed circular DNA (cccDNA) residing in hepatocytes. However, not only the host’s immune status, but also viral mutations have been reported to be associated with reactivation. Especially, several case reports about amino acid mutations in hepatitis B surface antigen (HBsAg) that escape from immune reactions have been reported, and recent reports showed that the frequencies of such mutations are higher than previously expected. In this review, we summarize the characteristics of viral mutations, including immune escape mutations in HBV-reactivated patients, and discuss their significance.
Highlights
Hepatitis B virus (HBV) infection is a worldwide health problem
hepatitis B surface antigen (HBsAg)-positive patients with high levels of serum HBV DNA and alanine aminotransferase (ALT) are targets of anti-viral therapies because they are at high risk of liver cirrhosis and hepatocellular carcinoma (HCC) [1]
It is known that anti-cancer chemotherapies or immunosuppressive therapies can induce HBV reactivation in HBsAg-positive patients, and in HBsAg-cleared patients [4]
Summary
Hepatitis B virus (HBV) infection is a worldwide health problem. HBsAg-positive patients with high levels of serum HBV DNA and alanine aminotransferase (ALT) are targets of anti-viral therapies because they are at high risk of liver cirrhosis and hepatocellular carcinoma (HCC) [1]. It is known that anti-cancer chemotherapies or immunosuppressive therapies can induce HBV reactivation in HBsAg-positive patients, and in HBsAg-cleared patients [4]. It has been revealed that covalently closed circular DNA (cccDNA) persists in the hepatocytes of patients who cleared HBsAg with such immune responses [8]. The presence of cccDNA and the weakened immune responses are thought to enable HBV reactivation in patients with resolved infection [9]. HBsAg-positive), or the appearance of HBV DNA in the absence of HBsAg. In regard to the factors associated with HBV reactivation, the types of drugs used for chemo/immunosuppression therapies, and the viral mutations have been reported. We summarize the recent findings on the viral mutations, including immune escape mutations found in HBV-reactivated patients with chemo/immunosuppression therapies, and we discuss the mechanisms of HBV reactivation
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