Abstract
Long noncoding RNA (LncRNA), a noncoding RNA over 200nt in length, can regulate glycolysis through metabolic pathways, glucose metabolizing enzymes, and epigenetic reprogramming. Upon viral infection, increased aerobic glycolysis providzes material and energy for viral replication. Mitochondrial antiviral signaling protein (MAVS) is the only protein-specified downstream of retinoic acid-inducible gene I (RIG-I) that bridges the gap between antiviral immunity and glycolysis. MAVS binding to RIG-I inhibits MAVS binding to Hexokinase (HK2), thereby impairing glycolysis, while excess lactate production inhibits MAVS and the downstream antiviral immune response, facilitating viral replication. LncRNAs can also regulate antiviral innate immunity by interacting with RIG-I and downstream signaling pathways and by regulating the expression of interferons and interferon-stimulated genes (ISGs). Altogether, we summarize the relationship between glycolysis, antiviral immunity, and lncRNAs and propose that lncRNAs interact with glycolysis and antiviral pathways, providing a new perspective for the future treatment against virus infection, including SARS-CoV-2.
Highlights
Aerobic glycolysis refers to the glycolytic reaction in cells even under aerobic conditions, generating large amounts of lactate
By reviewing the pairwise relationship among glycolysis, antiviral innate immunity, and Long noncoding RNAs (lncRNAs), we propose that lncRNA may affect viral replication by regulating glycolytic flux
Mammalian target of rapamycin is an influential node in the transition from aerobic phosphorylation to glycolysis and is a key metabolic regulator that promotes glycolysis in multiple immune cells, including T cells, B cells, dendritic cells, macrophages, neutrophils, mast cells, and natural killer cells (Xu et al, 2012). mammalian target of rapamycin (mTOR) appears as two distinct protein complexes and is divided into mTOR Complex1 and 2
Summary
Aerobic glycolysis refers to the glycolytic reaction in cells even under aerobic conditions, generating large amounts of lactate. It has been shown that SARS-CoV-2 infection of human monocytes upregulates glycolytic genes, promoting virus replication and the expression of proinflammatory factors (Codo et al, 2020). By reviewing the pairwise relationship among glycolysis, antiviral innate immunity, and lncRNA, we propose that lncRNA may affect viral replication by regulating glycolytic flux. The above insight supplies a hypothesis that lncRNAs participate in Abbreviations: PKM2, Pyruvate kinase M2; HK, hexokinase; LDHA, lactate dehydrogenase A; PFK, phosphofructokinase; RAF, tumor necrosis factor receptorassociated factors; NEMO, NF-κB essential modulator; TBK1, TANK-binding kinase 1; ISGs, IFN-stimulated genes; IRFs, interferon regulatory factors; JAK, Janus Kinase; STAT, signal transducer and activator of transcription. The interaction of SARS-CoV-2 associated antiviral innate immunity and glycolysis regulation. Glycolytic metabolic enzymes and glucose transporters (GLUTs) regulate glycolysis. Metabolic enzymes in glycolysis [HK, LDHA, and pyruvate kinase (PKM)] and lactate have regulatory effects on glycolysis
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