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PMID: 2795721 Published · ppublish English Journal Article

The NF-kappa B binding sites in the human immunodeficiency virus type 1 long terminal repeat are not required for virus infectivity.

Journal of virology ·Vol. 63 ·No. 11 ·1989-11-00 ·Pages 4919-24

Leonard J, Parrott C, Buckler-White AJ, Turner W, Ross EK, Martin MA, Rabson AB

Abstract

Mutations were introduced into the regulatory sequences in the long terminal repeat of an infectious molecular clone of the human immunodeficiency virus. Viruses in which the NF-kappa B binding sites were deleted or ones in which one or two Sp1 binding sites were mutated still replicated efficiently in human T lymphocytes. A deletion of the two NF-kappa B sites plus the three Sp1 sites or a mutation of the tat-responsive region rendered the virus replication incompetent. Thus, the NF-kappa B sequences are not required for human immunodeficiency virus infectivity; however, a tat-responsive region is essential.

MeSH Terms
Base Sequence Cell Line Cells, Cultured DNA, Viral/genetics Genes, Regulator Genes, Viral HIV-1/genetics,physiology Humans Molecular Sequence Data Mutation Repetitive Sequences, Nucleic Acid Restriction Mapping T-Lymphocytes/cytology Transfection Viral Structural Proteins/genetics Virus Replication
Chemicals
DNA, Viral Viral Structural Proteins
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Leonard J
Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
Parrott C
Buckler-White A J
Turner W
Ross E K
Martin M A
Rabson A B
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
DOI
10.1128/JVI.63.11.4919-4924.1989
Published
1989-11-00
Pages
4919-24
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC251138
Subset
IM
External Links
PubMed source DOI: 10.1128/JVI.63.11.4919-4924.1989 PMC Full Text View journal details
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