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Regulation of Telomere Homeostasis during Epstein-Barr virus Infection and Immortalization

1
Department of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, 751 23 Uppsala, Sweden
2
Department of Cell and Molecular Biology, Karolinska Institutet, 171 77 Stockholm, Sweden
*
Author to whom correspondence should be addressed.
Academic Editors: Benedikt B. Kaufer and Paul Lieberman
Viruses 2017, 9(8), 217; https://doi.org/10.3390/v9080217
Received: 3 July 2017 / Revised: 25 July 2017 / Accepted: 26 July 2017 / Published: 9 August 2017
(This article belongs to the Special Issue Viruses and Telomeres)
The acquisition of unlimited proliferative potential is dependent on the activation of mechanisms for telomere maintenance, which counteracts telomere shortening and the consequent triggering of the DNA damage response, cell cycle arrest, and apoptosis. The capacity of Epstein Barr virus (EBV) to infect B-lymphocytes in vitro and transform the infected cells into autonomously proliferating immortal cell lines underlies the association of this human gamma-herpesvirus with a broad variety of lymphoid and epithelial cell malignancies. Current evidence suggests that both telomerase-dependent and -independent pathways of telomere elongation are activated in the infected cells during the early and late phases of virus-induced immortalization. Here we review the interaction of EBV with different components of the telomere maintenance machinery and the mechanisms by which the virus regulates telomere homeostasis in proliferating cells. We also discuss how these viral strategies may contribute to malignant transformation. View Full-Text
Keywords: telomere; EBV; telomerase; ALT telomere; EBV; telomerase; ALT
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Kamranvar, S.A.; Masucci, M.G. Regulation of Telomere Homeostasis during Epstein-Barr virus Infection and Immortalization. Viruses 2017, 9, 217.

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