Occult hepatitis b reactivation after liver transplant: The role of a novel mutation in the surface antigen

Harjot K. Bedi, Daljeet Chahal, Christopher F. Lowe, Gordon Ritchie, Trana Hussaini, Vladimir Marquez, Eric M. Yoshida

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Occult hepatitis B infection is characterized by loss of hepatitis 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 undetectable, with an undetectable HBV viral load, until eradication of his HCV infection with direct acting antiviral agents. After 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.

Original languageEnglish
Pages (from-to)136-138
Number of pages3
JournalJournal of Clinical and Translational Hepatology
Volume9
Issue number1
DOIs
StatePublished - 2021
Externally publishedYes

Keywords

  • Hepatitis
  • Hepatitis B
  • Liver transplant
  • Reactivation
  • Seroconversion
  • Transplant

Fingerprint

Dive into the research topics of 'Occult hepatitis b reactivation after liver transplant: The role of a novel mutation in the surface antigen'. Together they form a unique fingerprint.

Cite this