This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Twu, J S Articles by Schloemer, R H Search for Related Content PubMed PubMed Citation Articles by Twu, J S Articles by Schloemer, R H

 Previous Article  |  Next Article 

J Virol. 1987 November; 61(11): 3448-3453

Transcriptional trans-activating function of hepatitis B virus.

Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis 46223.

ABSTRACT

The ability of hepatitis B virus (HBV) to stimulate the expression of a cellular gene was investigated by using a transient-expression system. A plasmid in which the expression of the bacterial chloramphenicol acetyltransferase (cat) gene had been placed under the control of the DNA sequences that regulate the expression of the human beta-interferon gene was constructed. In Vero cells, cotransfection of the 2.7-kilobase BglII DNA fragment of HBV together with the test plasmid containing the cat gene resulted in stimulation of the expression of the cat gene. This HBV DNA fragment was specific in its trans-activation; no significant stimulation of CAT activity was observed in constructs when the promoter and enhancer elements were derived from the murine sarcoma viral long terminal repeat, Rous sarcoma virus, BK virus, or simian virus 40. Results of subcloning of the HBV DNA fragment indicate that the trans-activating function resides in a 944-base-pair EcoRV-BglII DNA fragment of the HBV genome that contains the X structural gene and its promoter element. Removal of the promoter from the X structural gene resulted in loss of the trans-activating function. A frameshift mutation within the X gene region also eliminated the trans-activating activity. These results suggest that the X antigen could play a role in HBV infections by activating the expression of cellular genes.

This article has been cited by other articles:

• Kim, J.-H., Kang, S., Kim, J., Ahn, B.-Y. (2003). Hepatitis B Virus Core Protein Stimulates the Proteasome-Mediated Degradation of Viral X Protein. J. Virol. 77: 7166-7173 [Abstract] [Full Text]  
• Henkler, F., Hoare, J., Waseem, N., Goldin, R. D., McGarvey, M. J., Koshy, R., King, I. A. (2001). Intracellular localization of the hepatitis B virus HBx protein. J. Gen. Virol. 82: 871-882 [Abstract] [Full Text]  
• Benvegnu, L, Noventa, F, Bernardinello, E, Pontisso, P, Gatta, A, Alberti, A (2001). Evidence for an association between the aetiology of cirrhosis and pattern of hepatocellular carcinoma development. Gut 48: 110-115 [Abstract] [Full Text]  
• Seeger, C., Mason, W. S. (2000). Hepatitis B Virus Biology. Microbiol. Mol. Biol. Rev. 64: 51-68 [Abstract] [Full Text]  
• Perini, G., Oetjen, E., Green, M. R. (1999). The Hepatitis B pX Protein Promotes Dimerization and DNA Binding of Cellular Basic Region/Leucine Zipper Proteins by Targeting the Conserved Basic Region. J. Biol. Chem. 274: 13970-13977 [Abstract] [Full Text]  
• Qadri, I., Ferrari, M. E., Siddiqui, A. (1996). The Hepatitis B Virus Transactivator Protein, HBx, Interacts with Single-stranded DNA (ssDNA). BIOCHEMICAL CHARACTERIZATIONS OF THE HBx-ssDNA INTERACTIONS. J. Biol. Chem. 271: 15443-15450 [Abstract] [Full Text]  
• Maguire, H., Hoeffler, J., Siddiqui, A (1991). HBV X protein alters the DNA binding specificity of CREB and ATF-2 by protein-protein interactions. Science 252: 842-844 [Abstract]  
• Jaitovich-Groisman, I., Benlimame, N., Slagle, B. L., Perez, M. H., Alpert, L., Song, D. J., Fotouhi-Ardakani, N., Galipeau, J., Alaoui-Jamali, M. A. (2001). Transcriptional Regulation of the TFIIH Transcription Repair Components XPB and XPD by the Hepatitis B Virus x Protein in Liver Cells and Transgenic Liver Tissue. J. Biol. Chem. 276: 14124-14132 [Abstract] [Full Text]