Abstract
Mutant HBV genomes unable to produce preS2 protein were identified in the serum of a highly viremic chronic carrier. By direct sequencing of the amplified preS region and by sequencing of 50 cloned amplified preS DNA fragments all molecules were found to have deleted the preS2 translation initiation codon and three amino acids 54 nucleotides downstream thereof. In addition, numerous amino acid changes, predominantly located between both deletions, were revealed. HBV-DNA genomes containing the mutated preS sequences were shown to be replication competent and to secrete efficiently virions that were morphologically and by the type of DNA encapsidated not distinguishable from wild-type virus. These data demonstrate that HBV with mutated preS sequences and unable to express preS2 protein can occur as a dominant or exclusive virus population in a highly viremic chronic carrier. The data also show that expression of the preS2 protein is not essential for HBV replication, virion morphogenesis and secretion.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
