NDLI: Trans-activation of the human immunodeficiency virus long terminal repeat by the hepatitis B virus X protein.

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Trans-activation of the human immunodeficiency virus long terminal repeat by the hepatitis B virus X protein.

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Trans-activation of the human immunodeficiency virus long terminal repeat by the hepatitis B virus X protein.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yen, T. S. Seto, E. Peterlin, B. M. Ou, J. H.
Description	Author Affiliation: Seto E ( Department of Pathology, Howard Hughes Medical Institute, School of Medicine, University of California, San Francisco 94143-0506.);
Abstract	Human immunodeficiency virus 1 has been implicated as the main etiologic agent of the acquired immunodeficiency syndrome. However, other infectious agents may accelerate the progression of this disease. In particular, hepatitis B virus has been suggested as one such cofactor. Therefore, we have investigated the effects of hepatitis B virus gene products on expression of the human immunodeficiency virus I in transient transfection studies of Jurkat lymphoblastic T cells, using as reporter the chloramphenicol acetyltransferase gene coupled to the long terminal repeat of human immunodeficiency virus I. As measured by the amount of chloramphenicol acetyltransferase activity, gene expression directed by the human immunodeficiency virus I long terminal repeat increased approximately 10-fold in response to the hepatitis B virus X protein. This trans-activation by the X protein is multiplicative with the effect of phorbol esters and can be accounted for by an increase in the steady-state level of chloramphenicol acetyltransferase mRNA. Analysis of deletion and clustered point mutants in the long terminal repeat indicated that the X protein exerts its effect through multiple cis-acting sites. These results provide a possible molecular basis for the association of hepatitis B virus and the acquired immunodeficiency syndrome and confirm that the X protein is a transcriptional transactivator.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	21
Volume Number	85
Language	English
Publisher	National Academy of Sciences
Publisher Date	1988-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Acquired Immunodeficiency Syndrome Microbiology Gene Expression Regulation HIV-1 Genetics Trans-Activators Viral Proteins Pharmacology Animals Cell Line Chloramphenicol O-Acetyltransferase Molecular Sequence Data RNA, Messenger Repetitive Sequences, Nucleic Acid Transfection Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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