The NF-kappa B binding sites in the human immunodeficiency virus type 1 long terminal repeat are not required for virus infectivity.
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.
Leonard
J
J
Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
Parrott
C
C
Buckler-White
A J
AJ
Turner
W
W
Ross
E K
EK
Martin
M A
MA
Rabson
A B
AB
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
D004279:DNA, Viral; D015678:Viral Structural Proteins