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Contribution of the KSHV and EBV lytic cycles to tumourigenesis

Research output: Contribution to journalReview articlepeer-review

Author(s)

Oliver Manners, James Murphy, Alex Coleman, David J. Hughes, Adrian Whitehouse

School/Research organisations

Abstract

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.
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Details

Original languageEnglish
Pages (from-to)60-70
JournalCurrent Opinion in Virology
Volume32
Early online date28 Sep 2018
DOIs
Publication statusPublished - Oct 2018

    Research areas

  • Virus, Oncogenic viruses, Lytic, Gammaherpesvirus, Kaposis-sarcoma

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