Reactivation of a former hepatitis B virus (HBV)
infection can be triggered by immunosuppressive therapy, diseases associated with an immunocompromised state,
organ transplantation or the withdrawal of
antiviral drugs. Despite the absence of such risk factors, a spontaneous reactivation of HBV replication occurred in two elderly patients with resolved or occult HBV
infection. A 73-year-old male underwent
coronary artery bypass grafting in October 2008, and was negative for
HBsAg but positive for anti-HBs. In July 2009, his serum became positive for
HBsAg,
HBeAg and HBV
DNA (6.4 log copies/ml; genotype C), but negative for anti-HBc
IgM, with abrupt elevation of the liver
enzymes. The entire genomic sequence of HBV recovered from this patient revealed no mutations in the core promoter and precore regions that interfere with
HBeAg production. A 76-year-old male with a history of endoscopic mucosal resection for
esophageal cancer in 2002 and an initial diagnosis of
diabetes mellitus in 2009, at which time he was negative for
HBsAg. He was found to be positive for
HBsAg in September 2012 during a laboratory examination performed prior to the resection of recurrent
esophageal cancer, despite a low HBV load (2.1 log copies/ml). Three months later, without the administration of any anticancer drugs, the HBV
DNA (genotype B) level increased to 5.1 log copies/ml. A precore G1896A variant with high quasispecies diversity was recovered from the patient. Aging, surgical stress and complication of disease(s) associated with compromised immunity, such as
cancer,
arteriosclerosis and
diabetes mellitus may trigger spontaneous HBV reactivation.