Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
THE HEPATITIS B VIRUS TRANS-ACTIVATOR PROTEIN X
Diss Abstr Int [B]; 51(8):3697 1991. Unique Identifier : AIDSLINE ICDB/91672722 Seto E; Univ. of California, San Francisco
Abstract:
The hepatitis B virus (HBV) is a small, human DNA virus that causes acute and chronic hepatitis and is strongly associated with the development of primary hepatocellular carcinoma. In addition to the genes that code for the major structural proteins, and a gene coding for the viral polymerase, the HBV genome contains an open reading frame which could code for a protein of 154 amino acids, termed X. Several laboratories have recently reported that the X protein can stimulate transcription from a number of viral and cellular genes. Since HBV infection has been proposed as a co-factor in the development of the acquired immunodeficiency syndrome (AIDS), we investigated the effects of HBV gene products on the expression of the human immunodeficiency virus (HIV). With transient transfection assays in Jurkat T-lymphoblastic cells, we found that gene expression directed by the HIV-1 long terminal repeat (LTR) increased approx 10-fold in response to the HBV X protein. Our results, therefore, established HBV as a potential co-factor in AIDS, and confirmed that the X protein is a trans-activator. During our studies, we found that levels of X protein trans-activation vary with the host cell used. This raised the possibility that a cellular factor(s) might be involved. We pursued this idea by studying trans-activation by the X protein in a large panel of cultured cell lines. We showed that this trans-activation is cell type but not species specific, and that only a subset of promoters is trans-activated in any particular cell type. Since we were unable to localize precisely the cis DNA sequences on the HIV-1 LTR that respond to trans-activation by the X protein in Jurkat cells, we used the simian virus 40 (SV40) enhancer, which is similarly trans-activated by X. We found that trans-activation of the SV40 enhancer by the X protein depends on different transcription factor binding sites in different cell lines. We conclude that X can act through multiple distinct cellular DNA-binding transcription factors, and present a model for its action. Finally, we initiated experiments to study the interaction of the X protein with the SV40 large tumor antigen. (Full text available from University Microfilms International, Ann Arbor, MI, as Order No. AAD91-00598).
Keywords: Gene Expression Hepatitis B Virus/*GENETICS Human HIV Long Terminal Repeat Polyomavirus macacae/GENETICS Trans-Activators/*PHARMACOLOGY Viral Proteins/*PHARMACOLOGY THESIS 910930
M9190732
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Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
