Hepatitis B surface antigen genetic elements critical for immune escape correlate with hepatitis B virus reactivation upon immunosuppression

Romina Salpini, Luna Colagrossi, Maria Concetta Bellocchi, Matteo Surdo, Christina Becker, Claudia Alteri, Marianna Aragri, Alessandra Ricciardi, Daniele Armenia, Michela Pollicita, Fabiola Di Santo, Luca Carioti, Yoram Louzoun, Claudio Maria Mastroianni, Miriam Lichtner, Maurizio Paoloni, Mariarosaria Esposito, Chiara D'Amore, Aldo Marrone, Massimo MarignaniCesare Sarrecchia, Loredana Sarmati, Massimo Andreoni, Mario Angelico, Jens Verheyen, Carlo Federico Perno, Valentina Svicher

Research output: Contribution to journalArticlepeer-review

Abstract

Hepatitis B virus (HBV) reactivation during immunosuppression can lead to severe acute hepatitis, fulminant liver failure, and death. Here, we investigated hepatitis B surface antigen (HBsAg) genetic features underlying this phenomenon by analyzing 93 patients: 29 developing HBV reactivation and 64 consecutive patients with chronic HBV infection (as control). HBsAg genetic diversity was analyzed by population-based and ultradeep sequencing (UDS). Before HBV reactivation, 51.7% of patients were isolated hepatitis B core antibody (anti-HBc) positive, 31.0% inactive carriers, 6.9% anti-HBc/anti-HBs (hepatitis B surface antibody) positive, 6.9% isolated anti-HBs positive, and 3.4% had an overt HBV infection. Of HBV-reactivated patients, 51.7% were treated with rituximab, 34.5% with different chemotherapeutics, and 13.8% with corticosteroids only for inflammatory diseases. In total, 75.9% of HBV-reactivated patients (vs. 3.1% of control patients; P

Original languageEnglish
Pages (from-to)823-833
Number of pages11
JournalHepatology
Volume61
Issue number3
DOIs
Publication statusPublished - Mar 1 2015

ASJC Scopus subject areas

  • Hepatology
  • Medicine(all)

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