title: The NF-kappa B binding sites in the human immunodeficiency virus type 1 long terminal repeat are not required for virus infectivity.
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.
authors: Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
authors: J
authors: J
authors: Leonard
authors: C
authors: C
authors: Parrott
authors: A J
authors: AJ
authors: Buckler-White
authors: W
authors: W
authors: Turner
authors: E K
authors: EK
authors: Ross
authors: M A
authors: MA
authors: Martin
authors: A B
authors: AB
authors: Rabson
mesh_terms: D001483:Base Sequence; D002460:Cell Line; D002478:Cells, Cultured; D004279:DNA, Viral / Q000235:genetics; D005809:Genes, Regulator; D005814:Genes, Viral; D015497:HIV-1 / Q000235:genetics* / Q000502:physiology; D006801:Humans; D008969:Molecular Sequence Data; D009154:Mutation; D012091:Repetitive Sequences, Nucleic Acid; D015183:Restriction Mapping; D013601:T-Lymphocytes / Q000166:cytology; D014162:Transfection; D015678:Viral Structural Proteins / Q000235:genetics*; D014779:Virus Replication
chemical_list: D004279:DNA, Viral; D015678:Viral Structural Proteins