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Formation of a functional hepatitis B virus replication initiation complex involves a major structural alteration in the RNA template.

J Beck·M Nassal
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Abstract

The DNA genome of a hepatitis B virus is generated by reverse transcription of the RNA pregenome. Replication initiation does not involve a nucleic acid primer; instead, the hepadnavirus P protein binds to the structured RNA encapsidation signal epsilon, from which it copies a short DNA primer that becomes covalently linked to the enzyme. Using in vitro-translated duck hepatitis B virus (DHBV) P protein, we probed the secondary structure of the protein-bound DHBV epsilon RNA (Depsilon) and observed a marked conformational change compared to free Depsilon RNA. Several initiation-competent mutant RNAs with a different free-state structure were similarly altered, whereas a binding-competent but initiation-deficient variant was not, indicating the importance of the rearrangement for replication initiation and suggesting a mechanistic coupling to encapsidation.

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Base SequenceDNA ReplicationGene Products, polHepatitis B Virus, DuckMolecular Sequence DataMutationNucleic Acid ConformationRNA, ViralRNA-Binding ProteinsRNA-Directed DNA PolymeraseRibonucleoproteinsViral ProteinsJournal ArticleResearch Support, Non-U.S. Gov't

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J Beck, M Nassal. 1998. Formation of a functional hepatitis B virus replication initiation complex involves a major structural alteration in the RNA template.. https://doi.org/10.1128/mcb.18.11.6265

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