Drastic decrease of transcription activity due to hypermutated long terminal repeat (LTR) region in different HIV-1 subtypes and recombinants.
In: Antiviral research, Jg. 88 (2010-11-01), Heft 2, S. 152-9
academicJournal
Zugriff:
Transcriptional activation of HIV-1 gene expression is partially controlled by the interaction between viral and cellular transcription factors acting at HIV-1 long terminal repeat (LTR) sequences. HIV-1 subtyping at LTR region and nucleotide LTR variability from clinical samples in 48 subjects carrying different HIV-1 subtypes (9A, 5C, 3D, 3F, 21G, 2H, 3J and 2 undefined) at the protease (PR) gene, were performed. LTR sequences from each HIV-1 clade were cloned in luciferase-expression vectors to determine basal and Tat-induced transcriptional activities in the presence and absence of PMA stimulation. A high number (37.8%) of recombinants at LTR/PR regions were identified. All HIV-1 promoters presented low basal transcriptional activity that was nevertheless induced by Tat and PMA. LTR activity was similar across the majority of HIV-1 variants in response to Tat and cell activation. Only subtype C and CRF01_AE LTRs presented higher basal and induced-PMA transcription activities than HXB2 clade B promoter. No basal or Tat/PMA induced activity was found in those promoters presenting G to A hypermutation compared to the wild type promoter activities. G to A hypermutation at some important transcription binding-factor sites within LTR compromised the activity of the viral promoter, decreasing the in vitro viral transcription of the luciferase gene.
(Copyright © 2010 Elsevier B.V. All rights reserved.)
Titel: |
Drastic decrease of transcription activity due to hypermutated long terminal repeat (LTR) region in different HIV-1 subtypes and recombinants.
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Autor/in / Beteiligte Person: | de Arellano ER ; Alcamí, J ; López, M ; Soriano, V ; Holguín, A |
Zeitschrift: | Antiviral research, Jg. 88 (2010-11-01), Heft 2, S. 152-9 |
Veröffentlichung: | Amsterdam : Elsevier ; <i>Original Publication</i>: [Amsterdam ; New York : Elsevier/North-Holland Biomedical Press, c1981-, 2010 |
Medientyp: | academicJournal |
ISSN: | 1872-9096 (electronic) |
DOI: | 10.1016/j.antiviral.2010.08.007 |
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