Abstract
Hepatitis B virus (HBV) X-gene product activates transcription of the chloramphenicol acetyltransferase (CAT) gene under control of the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR). To identify a cis-acting regulatory sequence within the HIV-1 LTR which is responsive to the HBV X-gene trans-activating function, we examined the effects of HBV X-gene expression in cells with a series of LTR/CAT deletion mutants. A region of the HIV-1 LTR containing the previously identified kappa B-like enhancer element was found to be responsive to HBV X-gene activation, and this effect was independent of, and additive with, the effect of the HIV-1 tat-III protein on CAT expression. Since kappa B-like enhancer sequences are known to regulate transcription of a variety of viruses and cellular genes, our results suggest that the X gene could activate such a gene during HBV infection and replication.
MeSH Terms
Cell Line
Chloramphenicol O-Acetyltransferase/genetics
DNA, Viral/genetics
Enhancer Elements, Genetic
Gene Expression Regulation
HIV-1/genetics
Hepatitis B virus/genetics
Humans
Promoter Regions, Genetic
Regulatory Sequences, Nucleic Acid
Repetitive Sequences, Nucleic Acid
Transcription, Genetic
Transcriptional Activation
Chemicals
DNA, Viral
Chloramphenicol O-Acetyltransferase
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Twu J S
Department of Medicine, Stanford University School of Medicine, California 94305.
Rosen C A
Haseltine W A
Robinson W S
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