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Reply: ‘More viral mutants, less HBsAg clearance? One size may not fit all'
  1. Alex Thompson1,
  2. Stephen Locarnini2,
  3. Peter Revill2
  1. 1Department of Gastroenterology, St. Vincent's Hospital, Melbourne, Victoria, Australia
  2. 2Victorian Infectious Diseases Reference Laboratory, Royal Melbourne Hospital at the Peter Doherty Institute of Infection and Immunity, Melbourne, Victoria, Australia
  1. Correspondence to Dr Peter Revill, Victorian Infectious Diseases Reference Laboratory, Royal Melbourne Hospital at the Peter Doherty Institute of Infection and Immunity, 792 Elizabeth St, Melbourne, 3000 VIC, Australia; Peter.revill{at}mh.org.au

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We thank Dr Tseng and colleagues for their interest1 in our recent study that identified a negative association between the presence of hepatitis B virus (HBV) basal core promoter (BCP)/precore (PC) and precore (PC) variants mutants at baseline and lower likelihood of hepatitis B surface antigen (HBsAg) loss among 157 subjects with hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) treated for 4 years with tenofovir therapy. 2–4 The likelihood of HBsAg loss was 41% in subjects with wild-type (WT) sequence at the BCP/PC loci versus 3% in subjects with detectable BCP/PC variants (next generation sequencing (NGS), Illumina MiSeq—threshold for detection >1%). The cohort included subjects with a broad range of HBV genotypes (genotype A, n=36 (23%); genotype B, n=24 (15%); genotype C, n=51 (32%) and …

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