The Action of the Epstein-Barr Virus Oncogene LMP1 in Chronic Inflammation and Tumourigenesis (original) (raw)

Yan, Shuangye and Wilson, Joanna ORCID: https://orcid.org/0000-0003-4715-2530(2022) The Action of the Epstein-Barr Virus Oncogene LMP1 in Chronic Inflammation and Tumourigenesis. Microbiology Society JGV Roadshow, Glasgow, UK, 17 October 2022.

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Abstract

Epstein-Barr virus (EBV) is one of the most common human viruses, with over 95% of the adult population having been infected and the virus persists (usually asymptomatically) for the lifetime of the individual. EBV is the etiologic agent of infectious mononucleosis, is a risk factor for multiple sclerosis, but also is associated with the development of several cancers, including Burkitt lymphoma, Hodgkin's lymphoma, and nasopharyngeal carcinoma (NPC). NPC is a malignant tumour of epithelial origin and shows a high degree of immune cell infiltration. Studies from our lab have shown that one of the viral genes expressed in the tumour, encoding the latent membrane protein 1 (LMP1), can lead to chronic inflammation and likely contributes to the immune cell infiltrate seen in tumours. Chronic inflammation has long been implicated in the development of cancer, but the mechanism remains unclear. In the investigation of our LMP1-induced model of chronic inflammation, we have found that a family of cellular proteins, called the chitinase-like proteins (CLPs), are hugely over-expressed in the inflamed tissues. We have gone on to explore the role of these proteins in inflammation and carcinogenesis. To understand the relationship between the CLPs, LMP1 and chronic inflammation and the impact of these upon carcinogenesis, we have used a genetic knock-out model, combined with LMP1 transgenics. Our studies suggest that one of the CLPs, namely Chil1, may be protective at the early stages of tumour development, despite its proposed role as a mediator of inflammation.

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