Naturally occurring missense mutation in the polymerase gene terminating hepatitis B virus replication

Hubert E. Blum, Eithan Galun, T. Jake Liang, Fritz Von Weizsäcker, Jack R. Wands

Research output: Contribution to journalArticle

Abstract

A hepatitis B virus (HBV) genome was cloned from human liver. Numerous mutations in all viral genes define this HBV DNA as a mutant, divergent from all known HBV DNA sequences. Functional analyses of this mutant demonstrated a defect blocking viral DNA synthesis. The genetic basis of this defect was identified as a single missense mutation in the 5′ region of the viral polymerase gene, resulting in the inability to package pregenomic RNA into core particles. The replication defect could be trans-complemented by a full-length wild-type, but not by a full-length mutant or 3′-truncated wild-type, polymerase gene construct. Our findings indicate a critical role of the 5′ polymerase gene region in the life cycle of the virus and suggest that introducing missense mutations in this region can be a strategy to terminate viral replication in vivo.

Original languageEnglish (US)
Pages (from-to)1836-1842
Number of pages7
JournalJournal of Virology
Volume65
Issue number4
StatePublished - 1991
Externally publishedYes

ASJC Scopus subject areas

  • Immunology

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  • Cite this

    Blum, H. E., Galun, E., Liang, T. J., Von Weizsäcker, F., & Wands, J. R. (1991). Naturally occurring missense mutation in the polymerase gene terminating hepatitis B virus replication. Journal of Virology, 65(4), 1836-1842.