| First Author | Song N | Year | 2019 |
| Journal | Cell Rep | Volume | 28 |
| Issue | 9 | Pages | 2386-2396.e5 |
| PubMed ID | 31461653 | Mgi Jnum | J:284075 |
| Mgi Id | MGI:6378044 | Doi | 10.1016/j.celrep.2019.07.085 |
| Citation | Song N, et al. (2019) MAVS O-GlcNAcylation Is Essential for Host Antiviral Immunity against Lethal RNA Viruses. Cell Rep 28(9):2386-2396.e5 |
| abstractText | 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 IFNbeta 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. |
