BMB Rep. 2016; 49(4): 226-231  
Targeted disruption of EBNA1 in EBV-infected cells attenuated cell growth
Ka-Won Noh1,#, Jihyun Park1,# & Myung-Soo Kang1,2,3,*
1Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology (SAIHST), Sungkyunkwan University, 2Samsung Biomedical Research Institute (SBRI), Samsung Medical Center, Seoul 06351, 3BioMembrane Plasticity Research Center (MPRC), Seoul National University College of Medicine, Seoul 03080, Korea
Correspondence to: Tel: +82-2-740-8919; Fax: +82-2-740-8918; E-mail: emeskang@gmail.com
Received: December 18, 2015; Revised: January 11, 2016; Accepted: February 15, 2016; Published online: April 30, 2016.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

Abstract
Epstein Barr virus (EBV)-encoded nuclear antigen-1 (EBNA1) plays a pivotal in an EBV episome replication and persistence. Despite considerable attempts, there are no EBV drugs or vaccines. We attempted to eradicate EBV episomes by targeting EBNA1 using the transcription activator-like effector nucleases (TALEN) (E1TN). E1TN-mediated transient knockout (KO) of EBNA1 reduced EBNA1 expression, and caused significant loss of EBV genomes and progressive death of EBV-infected cells. Furthermore, when a mixture of EBV-infected Burkitt’s lymphoma (BL) cells and EBV-negative BL cells was targeted by E1TN, EBV-negative cells were counter-selected while most EBV-infected cells died, further substantiating that EBNA1 KO caused selective death of EBV-infected cells. TALEN-mediated transient targeting of EBNA1 attenuated the growth of EBV-infected cells, implicating a possible therapeutic application of E1TN for EBV-associated disorders.
Keywords: Cell death, EBNA1, Epstein-Barr Virus, Knockout, TALEN


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