Abstract
Hepatitis B virus (HBV) reactivation occurs as a major complication of immunosuppressive therapy among persons who have recovered from acute hepatitis and those who have controlled chronic infection. Recent literature data emphasize the presence of a high degree of S gene variability in HBV isolates from patients who developed reactivation. In reactivated HBV, the most frequently detected mutations belong to the second loop of “a” determinant in HBsAg. These mutations were identified to be immune escape and responsible for vaccine- and diagnostic-escape phenomena. Their emergence clearly provides survival in the presence of a developed humoral immune response and is often associated with impaired serological diagnosis of HBV reactivation. The knowledge of their existence and roles can elucidate the process of reactivation and strongly highlights the importance of HBV DNA detection in monitoring all patients with a history of HBV infection who are undergoing immunosuppression. This review discusses the possible influence of the most frequently found immune-escape mutations on HBV reactivation.
Highlights
Upon prolonged suppression of Hepatitis B virus (HBV) replication and a decline of antigen in patients treated with nucleos(t)ide analogues (NA), partial restoration of the T-cell function occurs, which indicates the significance of T-cell inhibition in chronic infection [11]
The HBV genome is in the form of partially double-stranded circular DNA, which is contained in an icosahedric capsid, itself enveloped by a lipid bilayer bearing three different surface proteins
HBV surface antigen (HBsAg) mutations were found in cases of reactivation caused by different immunosuppressive factors, those within the “a” determinant are thought to be essential for reactivation in patients undergoing treatment with anti-CD20 monoclonal antibodies [82]
Summary
It is estimated that more than two billion people around the world have been infected by hepatitis B virus (HBV) [1]. HBeAg-negative (“immune escape-mutant”) active chronic hepatitis follows in some patients and is characterized by a lack of serum HBeAg with detectable anti-HBe antibodies, moderate to high levels of HBV DNA (>2000 IU/mL), with fluctuating ALT levels and necroinflammation, and more rapid progression to cirrhosis. Upon prolonged suppression of HBV replication and a decline of antigen in patients treated with nucleos(t)ide analogues (NA), partial restoration of the T-cell function occurs, which indicates the significance of T-cell inhibition in chronic infection [11] It is less known how the B-cell response and specific antibodies can contribute to viral control in an established chronic infection. The risk of HBV reactivation was observed in HBV/HCV co-infected patients undergoing anti-HCV direct-acting antiviral therapy (DAA) [19]. The immunological changes occurring after HCV clearance can be related to this phenomenon rather than direct interference between HCV and HBV [22]
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