Hepatitis B virus X protein is not central to the viral life cycle in vitro

Hubert E. Blum*, Zhen Sheng Zhang, Eithan Galun, Fritz Von Weizsäcker, Bill Garner, T. Jake Liang, Jack R. Wands

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

132 Scopus citations

Abstract

The hepatitis B x (HBx) gene is the smallest open reading frame of the hepatitis B virus (HBV) genome. It is conserved among all mammalian hepadnaviruses and is expressed during viral infection. While the HBx protein (pX) has been shown to trans-activate the transcription of a wide range of viral and cellular genes and to induce liver cancer in transgenic mice, the significance of pX for the life cycle of HBV itself has not been elucidated. To assess the function of pX in viral replication and virion export, we designed an X-minus mutant by introduction of a stop codon at the beginning of the HBx gene without affecting the viral polymerase gene product. Transient transfection analyses using different cell lines revealed that this X-minus mutant directs the synthesis of wild-type levels of viral proteins, replicative intermediates, and virion export. These data suggest that the expression of the highly conserved HBx gene is not central for the life cycle of HBV in vitro but may be involved in the pathogenicity of hepadnavirus infection, including liver cancer development.

Original languageAmerican English
Pages (from-to)1223-1227
Number of pages5
JournalJournal of Virology
Volume66
Issue number2
StatePublished - Feb 1992
Externally publishedYes

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