Fig. 1: Deployment of NAD+ in antiviral innate immunity. | Nature Metabolism

Fig. 1: Deployment of NAD+ in antiviral innate immunity.

From: Viral infection as an NAD+ battlefield

Fig. 1

Upon viral entry, pattern recognition receptors (PRRs) launch expression of inflammatory cytokines including IL6, IL10 and IFNβ. These molecules exit cells and act on the same or neighboring cells. Engagement of IFNβ with interferon receptors (IFNAR) leads to activation of the JAK–STAT pathway and interferon-stimulated gene (ISG) transcription. Among the ISGs, five members of the PARP superfamily are transcriptionally induced concomitant with expenditure of cellular NAD+ and transcriptional upregulation of genes for nicotinamide (NAM) and nicotinamide riboside (NR) salvage. Repletion of cellular NAD+ with NR is being tested as a means to boost the antiviral activities of the PARP superfamily members and has been found to be associated with calming the cytokine storm. NAM is undergoing clinical testing as an antiviral as well. ADPR, ADPribose; NAMPT, NAM phosphoribosyltransferase; NMN, NAM mononucleotide; NMRK, NR kinase.

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