Abstract
Infections cause 13% of all cancers globally, and DNA tumour viruses account for almost 60% of these cancers. All viruses are obligate intracellular parasites and hijack host cell functions to replicate and complete their life cycles to produce progeny virions. While many aspects of viral manipulation of host cells have been studied, how DNA tumour viruses manipulate host cell metabolism and whether metabolic alterations in the virus life cycle contribute to carcinogenesis are not well understood. In this review, we compare the differences in central carbon and fatty acid metabolism in host cells following infection, oncogenic transformation, and virus-driven cancer of DNA tumour viruses including: Epstein-Barr virus, hepatitis B virus, human papillomavirus, Kaposi's sarcoma-associated herpesvirus and Merkel cell polyomavirus.
Highlights
All viruses, including DNA tumour viruses, depend on host cell function for life cycle completion, including the hijacking of host metabolic processes and the use of host macromolecules
Than control cells, suggesting a decrease in oxidative phosphorylation. This was demonstrated in combination with an increase in the stability of HIF1α and in the expression of GLUT1, an enzyme involved in glucose uptake, suggesting an increase in aerobic glycolysis; the expression of viral micro RNA (miRNA) contributed to enhanced growth under hypoxic conditions and this is important for maintaining viral latency [71]
This review has highlighted the various ways in which oncogenic DNA tumour viruses manipulate central carbon and lipid metabolism in early infection, oncogenic transformation and in virus-driven cancers
Summary
All viruses, including DNA tumour viruses, depend on host cell function for life cycle completion, including the hijacking of host metabolic processes and the use of host macromolecules. Of the 13% of cancers which are caused by infections globally, oncogenic DNA tumour viruses account for almost 60% of these cancers [1], and represent a significant health burden. It was determined in the 1950s by Otto Warburg that tumours have a different metabolic profile to normal tissues [2] and since there has been an increase in research focused on tumour metabolism, with altered cellular metabolism defined as a hallmark of cancer [3]. This review summarizes the changes in host metabolism during viral infection and oncogenic DNA tumour virus-driven cancers
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