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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 …
Contributors All authors contributed equally to this letter.
Funding Gilead Sciences.
Competing interests PR and SL have received grant/research support from Gilead Sciences; SL is an advisor for Gilead Sciences and Bristol-Myers Squibb (BMS); AT is an advisor for and has received grant/research support from Merck, Janssen/Tibotec, Gilead Sciences and Roche and speaker's fees from Merck, Roche and BMS. PR is currently in receipt of a Royal Melbourne Hospital Keir Research Fellowship.
Patient consent Obtained.
Ethics approval Gilead Sciences.
Provenance and peer review Not commissioned; internally peer reviewed.
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