N 6 -methyladenosine RNA modification–mediated cellular metabolism rewiring inhibits viral replication

Author:

Liu Yang12ORCID,You Yuling1,Lu Zhike3,Yang Jiang1,Li Panpan1,Liu Lun1,Xu Henan1,Niu Yamei4ORCID,Cao Xuetao125ORCID

Affiliation:

1. National Key Laboratory of Medical Molecular Biology, Department of Immunology, Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China.

2. National Key Laboratory of Medicinal Chemical Biology, College of Life Science, Nankai University, Tianjin 300071, China.

3. School of Life Sciences, Westlake University, Hangzhou 310024, China.

4. Department of Pathology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing 100005, China.

5. National Key Laboratory of Medical Immunology, Institute of Immunology, Second Military Medical University, Shanghai 200433, China.

Abstract

RNA modification meets immune metabolism N 6 -methyladenosine (m 6 A) RNA modification regulates various cellular functions. Liu et al. found that host cells impair RNA m 6 A demethylase activity after viral infection, leading to increased m 6 A and reduced stability of α-ketoglutarate dehydrogenase (OGDH) mRNA. As a result, reduced OGDH decreases the generation of itaconate, thereby inhibiting viral replication. The authors explore the function of OGDH and itaconate in viral infection, provide insights into m 6 A RNA modification and metabolic reprogramming in modulating virus-host interaction, and suggest potential therapeutic targets for the control of viral infection. Science , this issue p. 1171

Funder

National Natural Science Foundation of China

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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