The kappaB sites in the human immunodeficiency virus type 1 long terminal repeat enhance virus replication yet are not absolutely required for viral growth - PubMed (original) (raw)
The kappaB sites in the human immunodeficiency virus type 1 long terminal repeat enhance virus replication yet are not absolutely required for viral growth
B K Chen et al. J Virol. 1997 Jul.
Abstract
The dependence of human immunodeficiency virus type 1 (HIV-1) on its NF-kappaB binding sites (kappaB sites) for replication in transformed and primary T-cell targets was examined by infecting cells with HIV-1 reporter viruses containing kappaB site enhancer mutations. Viral transcription was measured either with luciferase-expressing HIV-1 that infects for a single round or by flow cytometric analyses with HIV-1 expressing placental alkaline phosphatase (PLAP) or green-fluorescent protein (GFP). Both PLAP- and GFP-expressing viruses spread from cell to cell and allowed analysis of viral gene expression patterns in single cells. Infection of a panel of T-cell lines with different basal levels of NF-kappaB demonstrated a direct correlation between the amount of constitutive nuclear NF-kappaB and the degree to which a wild-type virus outperformed kappaB site mutants. One T-cell line with a constitutively high level of nuclear NF-kappaB, PM1, showed a 20-fold decrease in transcription when its kappaB sites were mutated. In contrast, in a T-cell line with a low basal level of NF-kappaB, SupT1, mutation of the kappaB site in the enhancer had no effect on viral transcription or growth rate. Phytohemagglutinin-activated peripheral blood mononuclear cells showed a large dependence on the kappaB sites for optimal virus growth. Viruses without marker genes corroborated the finding that mutations to the kappaB sites impair virus production in cells with a high basal level of NF-kappaB. These data show that in T cells, HIV-1 can use NF-kappaB to enhance its growth but the virus is clearly able to grow in its absence.
Similar articles
- Analysis of the HIV-1 LTR NF-kappaB-proximal Sp site III: evidence for cell type-specific gene regulation and viral replication.
McAllister JJ, Phillips D, Millhouse S, Conner J, Hogan T, Ross HL, Wigdahl B. McAllister JJ, et al. Virology. 2000 Sep 1;274(2):262-77. doi: 10.1006/viro.2000.0476. Virology. 2000. PMID: 10964770 - Evolution of the human immunodeficiency virus type 1 long terminal repeat promoter by conversion of an NF-kappaB enhancer element into a GABP binding site.
Verhoef K, Sanders RW, Fontaine V, Kitajima S, Berkhout B. Verhoef K, et al. J Virol. 1999 Feb;73(2):1331-40. doi: 10.1128/JVI.73.2.1331-1340.1999. J Virol. 1999. PMID: 9882338 Free PMC article. - Permanent occupancy of the human immunodeficiency virus type 1 enhancer by NF-kappa B is needed for persistent viral replication in monocytes.
Jacqué JM, Fernández B, Arenzana-Seisdedos F, Thomas D, Baleux F, Virelizier JL, Bachelerie F. Jacqué JM, et al. J Virol. 1996 May;70(5):2930-8. doi: 10.1128/JVI.70.5.2930-2938.1996. J Virol. 1996. PMID: 8627768 Free PMC article. - The hepatitis B virus X protein induces HIV-1 replication and transcription in synergy with T-cell activation signals: functional roles of NF-kappaB/NF-AT and SP1-binding sites in the HIV-1 long terminal repeat promoter.
Gómez-Gonzalo M, Carretero M, Rullas J, Lara-Pezzi E, Aramburu J, Berkhout B, Alcamí J, López-Cabrera M. Gómez-Gonzalo M, et al. J Biol Chem. 2001 Sep 21;276(38):35435-43. doi: 10.1074/jbc.M103020200. Epub 2001 Jul 16. J Biol Chem. 2001. PMID: 11457829 - [Recent progress in the study of HIV-1 transcription factor NF-kappaB and its inhibitors].
Yu MY, Liu XY. Yu MY, et al. Yao Xue Xue Bao. 2007 Oct;42(10):1007-12. Yao Xue Xue Bao. 2007. PMID: 18229603 Review. Chinese.
Cited by
- Help or Hinder: Protein Host Factors That Impact HIV-1 Replication.
Moezpoor MR, Stevenson M. Moezpoor MR, et al. Viruses. 2024 Aug 10;16(8):1281. doi: 10.3390/v16081281. Viruses. 2024. PMID: 39205255 Free PMC article. Review. - The HIV-2 OGH double reporter virus shows that HIV-2 is less cytotoxic and less sensitive to reactivation from latency than HIV-1 in cell culture.
Bruggemans A, Vansant G, Van de Velde P, Debyser Z. Bruggemans A, et al. J Virus Erad. 2023 Aug 29;9(3):100343. doi: 10.1016/j.jve.2023.100343. eCollection 2023 Sep. J Virus Erad. 2023. PMID: 37701289 Free PMC article. - Human Herpesvirus 6A Tegument Protein U14 Induces NF-κB Signaling by Interacting with p65.
Aktar S, Arii J, Tjan LH, Nishimura M, Mori Y. Aktar S, et al. J Virol. 2021 Nov 9;95(23):e0126921. doi: 10.1128/JVI.01269-21. Epub 2021 Sep 22. J Virol. 2021. PMID: 34549982 Free PMC article. - HIV-1 Proviral Transcription and Latency in the New Era.
Shukla A, Ramirez NP, D'Orso I. Shukla A, et al. Viruses. 2020 May 18;12(5):555. doi: 10.3390/v12050555. Viruses. 2020. PMID: 32443452 Free PMC article. Review. - Alternate NF-κB-Independent Signaling Reactivation of Latent HIV-1 Provirus.
Acchioni C, Remoli AL, Marsili G, Acchioni M, Nardolillo I, Orsatti R, Farcomeni S, Palermo E, Perrotti E, Barreca ML, Sabatini S, Sandini S, Parolin C, Lin R, Borsetti A, Hiscott J, Sgarbanti M. Acchioni C, et al. J Virol. 2019 Aug 28;93(18):e00495-19. doi: 10.1128/JVI.00495-19. Print 2019 Sep 15. J Virol. 2019. PMID: 31243131 Free PMC article.
References
- Oncogene. 1994 Jul;9(7):1931-7 - PubMed
- J Virol. 1994 Feb;68(2):654-60 - PubMed
- EMBO J. 1994 Dec 1;13(23):5559-69 - PubMed
- EMBO J. 1995 Apr 3;14(7):1552-60 - PubMed
- J Virol. 1995 Jun;69(6):3712-20 - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources