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Clinical and virological features of occult hepatitis B in patients with HBsAg seroclearance post‐treatment or spontaneously
Author(s) -
Cheng HueiRu,
Kao JiaHorng,
Wu HuiLin,
Chen TingChih,
Tseng TaiChung,
Liu ChenHua,
Su TungHung,
Chen PeiJer,
Chen DingShinn,
Liu ChunJen
Publication year - 2014
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/liv.12324
Subject(s) - hbsag , medicine , hepatitis b virus , ribavirin , gastroenterology , context (archaeology) , virology , hepatitis b , hbeag , virus , immunology , hepatitis c virus , biology , paleontology
Background Occult hepatitis B virus ( HBV ) infection ( OHB ) may exist in patients experiencing hepatitis B surface antigen ( HB sAg) seroclearance. Aims We examined the clinical and virological features of OHB in patients who lost HB sAg post‐treatment or spontaneously. Methods We collected 44 patients with HB sAg seroclearance: 15 patients with dual HBV /hepatitis C virus ( HCV ) infection who lost HB sAg after peginterferon alfa‐2a ( PEG ‐ IFN ) plus ribavirin therapy; 13 HBV mono‐infected patients who lost HB sAg after various oral antiviral therapies; and 16 patients who lost HB sAg spontaneously. OHB was defined as detectable serum HBV DNA in the absence of HB sAg. Viral mutations associated with OHB were identified by comparison with matched controls that remained positive for HB sAg, and further characterized in vitro . Results The prevalence of OHB was 34.1% (15/44) in all patients, which was not significantly different among three groups. One mutation in surface promoter/polymerase region, C3050T (preS1T68I), was identified to be associated with the seroclearance of HB sAg in six cases. This mutation does not change the amino acid sequence of the polymerase protein. The S promoter activity was significantly lower in the construct containing C3050T mutation as compared with the wild‐type ( P = 0.0008). However, this mutation did not affect HBV replication, transcription and translation in the context of the full‐length HBV genome. OHB was not rare in patients with HB sAg seroclearance. Conclusions One mutation, C3050T (preS1T68I), decreased S promoter activity; nevertheless, other factors may play more important role in the clearance of HB sAg in these OHB patients.