Next Article in Journal
Variations in the Peritrophic Matrix Composition of Heparan Sulphate from the Tsetse Fly, Glossina morsitans morsitans
Next Article in Special Issue
The Microenvironment in Epstein–Barr Virus-Associated Malignancies
Previous Article in Journal
Navigating the Host Cell Response during Entry into Sites of Latent Cytomegalovirus Infection
Previous Article in Special Issue
EBV-Positive Lymphoproliferations of B- T- and NK-Cell Derivation in Non-Immunocompromised Hosts
Article Menu

Export Article

Open AccessFeature PaperReview
Pathogens 2018, 7(1), 31; https://doi.org/10.3390/pathogens7010031

The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency

Molecular Virology, Department of Medicine, Imperial College London, London W2 1PG, UK
*
Author to whom correspondence should be addressed.
Received: 30 January 2018 / Revised: 26 February 2018 / Accepted: 7 March 2018 / Published: 17 March 2018
(This article belongs to the Special Issue Emerging Topics in Epstein-Barr virus-Associated Diseases)
View Full-Text   |   Download PDF [2333 KB, uploaded 3 May 2018]   |  

Abstract

The Epstein–Barr nuclear antigen 3 (EBNA3) family of proteins, comprising EBNA3A, EBNA3B, and EBNA3C, play pivotal roles in the asymptomatic persistence and life-long latency of Epstein–Barr virus (EBV) in the worldwide human population. EBNA3-mediated transcriptional reprogramming of numerous host cell genes promotes in vitro B cell transformation and EBV persistence in vivo. Despite structural and sequence similarities, and evidence of substantial cooperative activity between the EBNA3 proteins, they perform quite different, often opposing functions. Both EBNA3A and EBNA3C are involved in the repression of important tumour suppressive pathways and are considered oncogenic. In contrast, EBNA3B exhibits tumour suppressive functions. This review focuses on how the EBNA3 proteins achieve the delicate balance required to support EBV persistence and latency, with emphasis on the contribution of the Allday laboratory to the field of EBNA3 biology. View Full-Text
Keywords: Epstein–Barr virus; EBNA3 proteins; epigenetic regulation; viral oncogenes; viral tumour suppressor; CDKI regulation Epstein–Barr virus; EBNA3 proteins; epigenetic regulation; viral oncogenes; viral tumour suppressor; CDKI regulation
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Styles, C.T.; Paschos, K.; White, R.E.; Farrell, P.J. The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency. Pathogens 2018, 7, 31.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Pathogens EISSN 2076-0817 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top