Glucose Metabolism Regulation of the Antiviral Innate Immunity against SARS-CoV-2

Hua Li, Chaofeng Han and Tengfei Zhang

Shanghai No.2 Homeless Aid Station, Shanghai, China
Department of Histology and Embryology, Shanghai Key Laboratory of Cell Engineering, Naval Medical University, China
Department of Gynecology and Obstetrics, The People’s Hospital of Zhuji, The Affiliated Zhuji Hospital of Wenzhou Medical University, China

^*Correspondance to: Tengfei Zhang 

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Abstract:

Host induces antiviral innate immunity responses by inducing type I interferon's through Pattern-Recognition Receptors (PRRs), which requires energy supply quickly. On the same time, virus also hijacks glucose, lipid metabolism of host cell to escape anti-viral immune and replicate itself. Severe Acute Respiratory Syndrome-related Coronavirus 2 (SARS-CoV-2) has been found inhibits antiviral innate immunity through its Non-Structure (NS) and Open Reading Frame (ORF) proteins. Recent research found that the high glucose or enhanced glycolysis in host cell aggravated SARS-CoV-2 infection, which needs to be discussed. Here we summarized the recent progress of glucose metabolism during SARS-CoV-2 infection.

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Cite the Article:

Li H, Han C, Zhang T. Glucose Metabolism Regulation of the Antiviral Innate Immunity against SARS-CoV-2. Clin Oncol. 2022;7:1952..