期刊
CELL REPORTS
卷 28, 期 9, 页码 2386-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2019.07.085
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资金
- National Natural Science Foundation of China [81302739, 81801980, 81773631]
- National Key Research and Development Program [2017YFC1601100]
- National Science and Technology Major Projects [2018ZX09711003-005, 2019ZX09J19105]
- Beijing Municipal Natural Science Foundation [7172159]
It is known that lethal viruses profoundly manipulate host metabolism, but how the metabolism alternation affects the immediate host antiviral immunity remains elusive. Here, we report that the O-GlcNAcylation of mitochondrial antiviral-signaling protein (MAVS), a key mediator of interferon signaling, is a critical regulation to activate the host innate immunity against RNA viruses. We show that O-GlcNAcylation depletion in myeloid cells renders the host more susceptible to virus infection both in vitro and in vivo. Mechanistically, we demonstrate that MAVS O-GlcNAcylation is required for virus-induced MAVS K63-linked ubiquitination, thereby facilitating IRF3 activation and IFN beta production. We further demonstrate that D-glucosamine, a commonly used dietary supplement, effectively protects mice against a range of lethal RNA viruses, including human influenza virus. Our study highlights a critical role of O-GlcNAcylation in regulating host antiviral immunity and validates D-glucosamine as a potential therapeutic for virus infections.
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