Infectious Hepatitis B Virus Variant Defective in Pre-S2 Protein Expression in a Chronic Carrier
Identifieur interne : 004652 ( Main/Exploration ); précédent : 004651; suivant : 004653Infectious Hepatitis B Virus Variant Defective in Pre-S2 Protein Expression in a Chronic Carrier
Auteurs : Doris Fernholz [Italie] ; Peter R. Galle [Italie] ; Marietta Stemler [Italie] ; Maurizia Brunetto [Italie] ; Ferruccio Bonino [Italie] ; Hans Will [Italie]Source :
- Virology [ 0042-6822 ] ; 1993.
Abstract
Abstract: All human hepatitis B viruses characterized so far express three envelope proteins, pre-S1, pre-S2, and HBs, which are believed to function as binding proteins for the cellular receptor, as targets for immune-mediated virus elimination, and in virion morphogenesis and secretion. Here we report the characterization of infectious HBV variant genomes that are unable to express a pre-S2 protein and which were derived from serum of a highly viremic chronic carrier. Direct sequencing of the amplified pre-S region and sequencing of 50 cloned amplified pre-S DNA fragments revealed that in all molecules, in addition to numerous nucleotide changes, there were deletions of the pre-S2 translation initiation codon and three codons 54 nucleotides downstream thereof. No pre-S2 protein and altered pre-S1 proteins were found in the serum of the patient. Cloned infectious HBV DNA genomes having the pre-S region substituted by the variant pre-S region were replication competent in cultured hepatoblastoma cells. Morphologically normal virions were efficiently secreted and were infectious for primary human hepatocyte cultures. These data demonstrate that HBV devoid of pre-S2 protein can occur in vivo as a dominant or exclusive virus population and that expression of the pre-S2 protein is not essential for HBV replication, virion morphogenesis, secretion, or in vitro infectivity.
Url:
DOI: 10.1006/viro.1993.1243
Affiliations:
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Here we report the characterization of infectious HBV variant genomes that are unable to express a pre-S2 protein and which were derived from serum of a highly viremic chronic carrier. Direct sequencing of the amplified pre-S region and sequencing of 50 cloned amplified pre-S DNA fragments revealed that in all molecules, in addition to numerous nucleotide changes, there were deletions of the pre-S2 translation initiation codon and three codons 54 nucleotides downstream thereof. No pre-S2 protein and altered pre-S1 proteins were found in the serum of the patient. Cloned infectious HBV DNA genomes having the pre-S region substituted by the variant pre-S region were replication competent in cultured hepatoblastoma cells. Morphologically normal virions were efficiently secreted and were infectious for primary human hepatocyte cultures. These data demonstrate that HBV devoid of pre-S2 protein can occur in vivo as a dominant or exclusive virus population and that expression of the pre-S2 protein is not essential for HBV replication, virion morphogenesis, secretion, or in vitro infectivity.</div></front></TEI><affiliations><list><country><li>Italie</li></country><region><li>Piémont</li></region><settlement><li>Turin</li></settlement></list><tree><country name="Italie"><region name="Piémont"><name sortKey="Fernholz, Doris" sort="Fernholz, Doris" uniqKey="Fernholz D" first="Doris" last="Fernholz">Doris Fernholz</name></region><name sortKey="Bonino, Ferruccio" sort="Bonino, Ferruccio" uniqKey="Bonino F" first="Ferruccio" last="Bonino">Ferruccio Bonino</name><name sortKey="Brunetto, Maurizia" sort="Brunetto, Maurizia" uniqKey="Brunetto M" first="Maurizia" last="Brunetto">Maurizia Brunetto</name><name sortKey="Galle, Peter R" sort="Galle, Peter R" uniqKey="Galle P" first="Peter R." last="Galle">Peter R. Galle</name><name sortKey="Stemler, Marietta" sort="Stemler, Marietta" uniqKey="Stemler M" first="Marietta" last="Stemler">Marietta Stemler</name><name sortKey="Will, Hans" sort="Will, Hans" uniqKey="Will H" first="Hans" last="Will">Hans Will</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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