Occult hepatitis B infection is characterized by loss of hepa-titis B surface antigen(HBsAg)and persistence of low levels of hepatitis B virus(HBV)replication that may or may not be detectable in plasma/serum.We prese...Occult hepatitis B infection is characterized by loss of hepa-titis B surface antigen(HBsAg)and persistence of low levels of hepatitis B virus(HBV)replication that may or may not be detectable in plasma/serum.We present a case of HBV reactivation in a male patient who underwent orthotopic liver transplant for hepatocellular carcinoma secondary to active hepatitis C(HCV)infection.Pre-transplant,he was HBsAg-negative and hepatitis B core antibody-positive,with an undetectable HBV viral load that was incidentally found to be positive at a very low HBV viral load on the day of transplant.Post-transplant,his HBsAg remained undetect-able,with an undetectable HBV viral load,until eradication of his HCV infection with direct acting antiviral agents.Af-ter eradication of HCV,there was reactivation of HBV,with a high viral load and emergence of serum HBsAg.A deep sequencing genetic analysis of his HBV both pre-and post-transplant revealed the presence of a mutation in the"a"determinant of the HBV surface antigen.The role of HBV genotype'a'determinant mutation in HBV reactivation post-transplant is unknown and needs further examination.Our experience suggests a possible role for antiviral prophylaxis in these patients or monitoring of HBV viral loads post-transplant.展开更多
文摘Occult hepatitis B infection is characterized by loss of hepa-titis B surface antigen(HBsAg)and persistence of low levels of hepatitis B virus(HBV)replication that may or may not be detectable in plasma/serum.We present a case of HBV reactivation in a male patient who underwent orthotopic liver transplant for hepatocellular carcinoma secondary to active hepatitis C(HCV)infection.Pre-transplant,he was HBsAg-negative and hepatitis B core antibody-positive,with an undetectable HBV viral load that was incidentally found to be positive at a very low HBV viral load on the day of transplant.Post-transplant,his HBsAg remained undetect-able,with an undetectable HBV viral load,until eradication of his HCV infection with direct acting antiviral agents.Af-ter eradication of HCV,there was reactivation of HBV,with a high viral load and emergence of serum HBsAg.A deep sequencing genetic analysis of his HBV both pre-and post-transplant revealed the presence of a mutation in the"a"determinant of the HBV surface antigen.The role of HBV genotype'a'determinant mutation in HBV reactivation post-transplant is unknown and needs further examination.Our experience suggests a possible role for antiviral prophylaxis in these patients or monitoring of HBV viral loads post-transplant.