Abstract
blood samples revealed that the percentage of viruses with at least one of these stop codons ranged from 3% to 79%. In two cases even additional stop codons in the HBsAg reading frame were detected in clonal experiments. Different stop codons were located either in the same HBV genome or in distinguished virus populations. Of note, the polymerase mutation A181T did not always lead to a stop codon in the HBsAg, which for one case was disclosed by clonal experiments. Furthermore, clonal experiments showed that in the vast majority of HBV clones the polymerase mutations M204V and A181T were not located in the same genome. Conclusions: The overlapping reading frames of viral HBsAg and polymerase lead to the occurrence of mutations with complex mutational patterns. The exact and sensitive detection of truncated HBsAgs in HBV resistant isolates is limited by using population sequencing methods in routine HBV drug resistance assays.
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