Contribution of the KSHV and EBV lytic cycles to tumourigenesis
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Kaposi’s Sarcoma-associated herpesvirus (KSHV) and Epstein Barr virus (EBV) are the causative agents of several malignancies. Like all herpesviruses, KSHV and EBV undergo distinct latent and lytic replication programmes. The transition between these states allows the establishment of a lifelong persistent infection, dissemination to sites of disease and the spread to new hosts. Latency-associated viral proteins have been well characterised in transformation and tumourigenesis pathways; however, a number of studies have shown that abrogation of KSHV and EBV lytic gene expression impairs the oncogenesis of several cancers. Furthermore, several lytically expressed proteins have been functionally tethered to the angioproliferative and anti-apoptotic phenotypes of virus-infected cells. As a result, the investigation and therapeutic targeting of KSHV and EBV lytic cycles may be essential for the treatment of their associated malignancies.
Manners , O , Murphy , J , Coleman , A , Hughes , D J & Whitehouse , A 2018 , ' Contribution of the KSHV and EBV lytic cycles to tumourigenesis ' , Current Opinion in Virology , vol. 32 , pp. 60-70 . https://doi.org/10.1016/j.coviro.2018.08.014
Current Opinion in Virology
Copyright © 2018 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
DescriptionResearch in the Whitehouse laboratory is supported in parts by funding from Biotechnology and Biological Sciences Research Council (BB/M006557/1, BB/N014405/1), Medical Research Council (MR/R010145/1, 95505168), Worldwide Cancer Research (16-1025), Wellcome Trust (203826/Z/16/Z) and Rosetrees Trust (M662).
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