PMI-controlled mannose metabolism and glycosylation determines tissue tolerance and virus fitness

Ronghui Liang, Zi-Wei Ye, Zhenzhi Qin, Yubin Xie, Xiaomeng Yang, Haoran Sun, Qiaohui Du, Peng Luo, Kaiming Tang, Bodan Hu, Jianli Cao, Xavier Hoi-Leong Wong, Guang-Sheng Ling, Hin Chu, Jiangang Shen, Feifei Yin, Dong-Yan Jin, Jasper Fuk-Woo Chan, Kwok-Yung Yuen and Shuofeng Yuan ()
Additional contact information
Ronghui Liang: Hainan Medical University-The University of Hong Kong Joint Laboratory of Tropical Infectious Diseases, Key Laboratory of Tropical Translational Medicine of Ministry of Education
Zi-Wei Ye: Pokfulam
Zhenzhi Qin: Pokfulam
Yubin Xie: Pokfulam
Xiaomeng Yang: Pokfulam
Haoran Sun: Pokfulam
Qiaohui Du: Pokfulam
Peng Luo: Pokfulam
Kaiming Tang: Pokfulam
Bodan Hu: Pokfulam
Jianli Cao: Pokfulam
Xavier Hoi-Leong Wong: Hong Kong Baptist University
Guang-Sheng Ling: Pokfulam
Hin Chu: Pokfulam
Jiangang Shen: Pokfulam
Feifei Yin: Hainan Medical University-The University of Hong Kong Joint Laboratory of Tropical Infectious Diseases, Key Laboratory of Tropical Translational Medicine of Ministry of Education
Dong-Yan Jin: Pokfulam
Jasper Fuk-Woo Chan: Hainan Medical University-The University of Hong Kong Joint Laboratory of Tropical Infectious Diseases, Key Laboratory of Tropical Translational Medicine of Ministry of Education
Kwok-Yung Yuen: Hainan Medical University-The University of Hong Kong Joint Laboratory of Tropical Infectious Diseases, Key Laboratory of Tropical Translational Medicine of Ministry of Education
Shuofeng Yuan: Pokfulam

Nature Communications, 2024, vol. 15, issue 1, 1-15

Abstract: Abstract Host survival depends on the elimination of virus and mitigation of tissue damage. Herein, we report the modulation of D-mannose flux rewires the virus-triggered immunometabolic response cascade and reduces tissue damage. Safe and inexpensive D-mannose can compete with glucose for the same transporter and hexokinase. Such competitions suppress glycolysis, reduce mitochondrial reactive-oxygen-species and succinate-mediated hypoxia-inducible factor-1α, and thus reduce virus-induced proinflammatory cytokine production. The combinatorial treatment by D-mannose and antiviral monotherapy exhibits in vivo synergy despite delayed antiviral treatment in mouse model of virus infections. Phosphomannose isomerase (PMI) knockout cells are viable, whereas addition of D-mannose to the PMI knockout cells blocks cell proliferation, indicating that PMI activity determines the beneficial effect of D-mannose. PMI inhibition suppress a panel of virus replication via affecting host and viral surface protein glycosylation. However, D-mannose does not suppress PMI activity or virus fitness. Taken together, PMI-centered therapeutic strategy clears virus infection while D-mannose treatment reprograms glycolysis for control of collateral damage.

Date: 2024
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DOI: 10.1038/s41467-024-46415-4

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