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Contribution of NF-kappa B and Sp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1: distinct patterns of viral growth are determined by T-cell types
- Source :
- Journal of virology. 65(8)
- Publication Year :
- 1991
-
Abstract
- Starting with a replication-incompetent molecular clone of human immunodeficiency virus type 1, lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat (LTR), proviruses containing reconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation. Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human T-cell types depending on which element(s) was present in the LTR. For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites), a hierarchy of cellular permissivity to virus replication (peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat) was observed. Of note was the associated emergence of second-site LTR revertants which involved an alteration of the TATA box. These results suggest that the human immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different T-cell types and is capable of changing depending on the particular combination of transcriptional factors present.
- Subjects :
- Permissiveness
DNA Replication
Sp1 Transcription Factor
TATA box
viruses
T-Lymphocytes
Immunology
Molecular Sequence Data
Biology
Transfection
Virus Replication
Microbiology
Jurkat cells
Polymerase Chain Reaction
Virus
Cell Line
Proviruses
Virology
Humans
Binding site
Repetitive Sequences, Nucleic Acid
Base Sequence
DNA replication
NF-kappa B
Molecular biology
Long terminal repeat
Enhancer Elements, Genetic
Viral replication
Insect Science
DNA, Viral
HIV-1
Mutagenesis, Site-Directed
RNA, Viral
Research Article
Subjects
Details
- ISSN :
- 0022538X
- Volume :
- 65
- Issue :
- 8
- Database :
- OpenAIRE
- Journal :
- Journal of virology
- Accession number :
- edsair.doi.dedup.....d4124e80c2e649c9fa4a98cc1cc49109