Cellular factors associated with latency and spontaneous Epstein-Barr virus reactivation in B-lymphoblastoid cell lines
- PMID: 20153012
- DOI: 10.1016/j.virol.2010.01.002
Cellular factors associated with latency and spontaneous Epstein-Barr virus reactivation in B-lymphoblastoid cell lines
Abstract
EBV-immortalized B-lymphoblastoid cell lines are used as models for cellular transformation and as antigen-presenting cells in immunological assays. LCLs vary in surface markers and other phenotypic properties, but it is not known how this heterogeneity relates to the EBV life cycle. To explore correlations, we examined 62 LCLs for cellular and viral phenotypes. LCLs generated from pediatric and adult donors could similarly be categorized as either low in EBV copy number or fluctuating within a high range. High-copy status accompanied higher lytic viral gene expression and lower latent gene expression. Inhibiting lytic EBV replication did not affect cellular phenotype or lytic switch protein expression, indicating that an LCL's lytic permissivity was a stable property. Among the cellular genes overexpressed in permissive LCLs were unfolded protein response genes and plasma cell markers. Among genes overexpressed in non-permissive LCLs were transcription factors involved in maintaining B cell lineage, in particular EBF1. This study suggests previously undetected mechanisms by which cellular pathways influence the lytic reactivation of EBV.
Copyright 2010 Elsevier Inc. All rights reserved.
Similar articles
-
Cellular differentiation regulator BLIMP1 induces Epstein-Barr virus lytic reactivation in epithelial and B cells by activating transcription from both the R and Z promoters.J Virol. 2015 Feb;89(3):1731-43. doi: 10.1128/JVI.02781-14. Epub 2014 Nov 19. J Virol. 2015. PMID: 25410866 Free PMC article.
-
Human B cells on their route to latent infection--early but transient expression of lytic genes of Epstein-Barr virus.Eur J Cell Biol. 2012 Jan;91(1):65-9. doi: 10.1016/j.ejcb.2011.01.014. Epub 2011 Mar 29. Eur J Cell Biol. 2012. PMID: 21450364 Review.
-
Regulation and dysregulation of Epstein-Barr virus latency: implications for the development of autoimmune diseases.Autoimmunity. 2008 May;41(4):298-328. doi: 10.1080/08916930802024772. Autoimmunity. 2008. PMID: 18432410 Review.
-
The Epstein-Barr virus (EBV) nuclear antigen 1 BamHI F promoter is activated on entry of EBV-transformed B cells into the lytic cycle.J Virol. 1992 Dec;66(12):7461-8. doi: 10.1128/JVI.66.12.7461-7468.1992. J Virol. 1992. PMID: 1331531 Free PMC article.
-
Variable methylation of the Epstein-Barr virus Wp EBNA gene promoter in B-lymphoblastoid cell lines.J Virol. 2004 Dec;78(24):14062-5. doi: 10.1128/JVI.78.24.14062-14065.2004. J Virol. 2004. PMID: 15564516 Free PMC article.
Cited by
-
Maintenance of Epstein-Barr Virus Latent Status by a Novel Mechanism, Latent Membrane Protein 1-Induced Interleukin-32, via the Protein Kinase Cδ Pathway.J Virol. 2015 Jun;89(11):5968-80. doi: 10.1128/JVI.00168-15. Epub 2015 Mar 25. J Virol. 2015. PMID: 25810549 Free PMC article.
-
EBV and KSHV Infection Dysregulates Autophagy to Optimize Viral Replication, Prevent Immune Recognition and Promote Tumorigenesis.Viruses. 2018 Oct 31;10(11):599. doi: 10.3390/v10110599. Viruses. 2018. PMID: 30384495 Free PMC article. Review.
-
In utero cell transfer between porcine littermates.Reprod Fertil Dev. 2011;23(2):297-302. doi: 10.1071/RD10165. Reprod Fertil Dev. 2011. PMID: 21211462 Free PMC article.
-
Transcriptomic profile reveals gender-specific molecular mechanisms driving multiple sclerosis progression.PLoS One. 2014 Feb 28;9(2):e90482. doi: 10.1371/journal.pone.0090482. eCollection 2014. PLoS One. 2014. PMID: 24587374 Free PMC article.
-
Keeping it quiet: chromatin control of gammaherpesvirus latency.Nat Rev Microbiol. 2013 Dec;11(12):863-75. doi: 10.1038/nrmicro3135. Epub 2013 Nov 6. Nat Rev Microbiol. 2013. PMID: 24192651 Free PMC article. Review.
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
