From infection to cancer: how DNA tumour viruses alter host cell central carbon and lipid metabolism

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From infection to cancer : how DNA tumour viruses alter host cell central carbon and lipid metabolism. / Magon, Kamini L; Parish, Joanna L.

In: Open Biology, Vol. 11, No. 3, 210004, 03.03.2021.

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@article{2b2576dbc54246668d940d2f9b54cef9,
title = "From infection to cancer: how DNA tumour viruses alter host cell central carbon and lipid metabolism",
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.",
keywords = "oncogenic DNA viruses, virus–host interactions, metabolism, lipid, central carbon",
author = "Magon, {Kamini L} and Parish, {Joanna L}",
year = "2021",
month = mar,
day = "3",
doi = "10.1098/rsob.210004",
language = "English",
volume = "11",
journal = "Open Biology",
issn = "2046-2441",
publisher = "The Royal Society",
number = "3",

}

RIS

TY - JOUR

T1 - From infection to cancer

T2 - how DNA tumour viruses alter host cell central carbon and lipid metabolism

AU - Magon, Kamini L

AU - Parish, Joanna L

PY - 2021/3/3

Y1 - 2021/3/3

N2 - 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.

AB - 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.

KW - oncogenic DNA viruses

KW - virus–host interactions

KW - metabolism

KW - lipid

KW - central carbon

U2 - 10.1098/rsob.210004

DO - 10.1098/rsob.210004

M3 - Article

C2 - 33653084

VL - 11

JO - Open Biology

JF - Open Biology

SN - 2046-2441

IS - 3

M1 - 210004

ER -