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More viral mutants, less HBsAg clearance? One size may not fit all
  1. Tai-Chung Tseng1,2,
  2. Hung-Chih Yang3,4,
  3. Jia-Horng Kao2,3,5,6
  1. 1 Department of Internal Medicine, National Taiwan University Hospital Jinshan Branch, New Taipei City, Taiwan
  2. 2 Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan
  3. 3 Division of Gastroenterology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
  4. 4 Department of Microbiology, National Taiwan University College of Medicine, Taipei, Taiwan
  5. 5 Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
  6. 6 Department of Medical Research, National Taiwan University Hospital, Taipei, Taiwan
  1. Correspondence to Professor Jia-Horng Kao, Hepatitis Research Center, National Taiwan University Hospital, 1 Chang-Te Street, Taipei 10002, Taiwan; kaojh{at}ntu.edu.tw

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Dear Sir,

We read with great interest the article by Bayliss et al 1 e-published in August 2016.

HBV is a DNA virus and viral mutants develop during the course of persistent infection because of the spontaneous error of viral reverse transcription. Some of the viral mutants will be selected and become the predominant strains under the pressure of host immunity if they bear better replication fitness. Two common HBV mutants, mutations in precore stop codon (PC) (G1896A) and basal core promoter (BCP) (A1762T/G1764A), have been shown to abolish or reduce the production of HBeAg, respectively, which contribute to disease progression.2 In previous reports, these viral variants were determined using population sequencing, which is a qualitative assay thus limits …

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