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Epstein-Barr virus and cellular DNA damage response

Sejic, Nenad (2014)
M.Res. thesis, University of Birmingham.

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EBV is an oncogenic human gammaherpesvirus which infects B lymphocytes and epithelial cells. New virus replication occurs in both cell types and EBV encodes proteins to replicate its own DNA. Selective activation of the DNA damage response (DDR) is thought to occur in order for the virus to efficiently conserve its DNA sequence. Components of the double strand break homologous repair pathway are known to be recruited to viral replication compartments and loaded onto viral DNA to achieve efficient and faithful replication of the viral DNA.
Using an epithelial cell line latently infected with EBV, we demonstrated interactions between the phosphorylated replication protein A (RPA) and the viral lytic proteins BALF2 (DNA binding protein) and BMRF1 (polymerase accessory factor). However, despite its presence at replication centres, we failed to identify its direct interaction with the viral proteins by co-immunoprecipitation and mass spectrometry. Analysis of viral gene expression after ATM inhibition suggests that ATM does not promote the expression EBV lytic genes and is perhaps inhibitory. However, we did identify a novel interaction between BALF2 and the mitochondrial H+-Ca2+ exchanger LETM1, suggesting a new role for BALF2 possibly in inhibition of apoptosis during the viral lytic cycle.

Type of Work:M.Res. thesis.
Supervisor(s):Shannon-Lowe, Claire
School/Faculty:Colleges (2008 onwards) > College of Medical & Dental Sciences
Department:School of Cancer Sciences
Subjects:RC Internal medicine
Institution:University of Birmingham
ID Code:5506
This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder.
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