Reactivation of latently infected hepatitis B virus in a leukemia patient with antibodies to hepatitis B core antigen

Abstract

A 66-year-old man with chronic B-cell leukemia who had antibody to hepatitis B core antigen (anti-HBc) but not hepatitis B surface antigen (HBsAg) suffered from lethal hepatitis caused by hepatitis B virus (HBV) reactivation. He initially lacked circulating viral genomes in his sera and did not have a past history of liver dysfunction. In this patient, the immunosuppressive condition introduced by disease progression of leukemia induced reactivation of dormant HBV, and the withdrawal of chemotherapy resulted in fatal liver failure. Mutation-specific assay based on competitive polymerase chain reaction (PCR) and sequencing analyses revealed the predominant reactivation of an HBV strain with missence mutation (point mutation G-to-A at nucleotide 1896) in the precore regions, as well as point mutations in the core promoter regions. Therefore, it is important to note the risk of HBV reactivation, with resulting lethal hepatic failure, in anti-HBc-positive healthy individuals, even when they lack HBsAg. who receive immunomodulating therapy.

Adefovir added to lamivudine for hepatitis B recurrent infection in refractory B-cell chronic lymphocytic leukemia on prolonged therapy with Campath-1H

“…Reactivation of hepatitis B is a well-documented complication of tumor chemotherapy and immunosuppressive treatments, being observed both in patients with overt hepatitis B (HBsAg seropositive) as well as in those with occult infection (HBsAg seronegative) (Dhedin et al, 1998;Ma et al, 2003;Marusawa et al, 2001;Seth et al, 2002). Occult HBV infection is likely to be more common than previously recognized and to bear important clinical consequences (Raimondo et al, 2005).…”

Frequency and load of hepatitis B virus DNA in first-time blood donors with antibodies to hepatitis B core antigen

“…[13][14][15] Furthermore, reactivation of apparently cured HBV infection has been described under chemotherapy or immunomodulating therapy after renal and bone marrow transplantation, and in some of these cases a reverse seroconversion from anti-HBs to HBsAg has been observed. [16][17][18][19] The residual risk of posttransfusion HBV infection has been calculated by several groups in the United States and Germany on the basis of HBV incidence data and the duration of the early window period until HBsAg becomes detectable to be 1:63 000 and less than 1:100 000 blood donations, respectively. 20,21 It has been shown that blood donations of HBsAg-and anti-HBs-negative but anti-HBc-positive HBV carriers can cause posttransfusion hepatitis B.…”

Genetic basis of hepatitis virus-associated hepatocellular carcinoma: linkage between infection, inflammation, and tumorigenesis

“…Occult HBV carriers can develop HBV reactivation and liver dysfunction under certain immunosuppressive conditions [69,70]. The formation of covalently closed circular DNA is considered due to the persistent HBV infection in hepatocytes in individuals after seroconversion from HBsAg to anti-HBs [71].…”