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. 2022 Jan;4(1):2-3.
doi: 10.1038/s42255-021-00507-3.

Viral infection as an NAD+ battlefield

Affiliations

Viral infection as an NAD+ battlefield

Charles Brenner. Nat Metab. 2022 Jan.

Abstract

Coronavirus replication results in expenditure of nicotinamide adenine dinucleotide (NAD+), the central catalyst of cellular metabolism, in the innate response to infection. Repleting NAD+ levels has the potential to enhance antiviral responses.

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Figures

Figure 1.
Figure 1.
Upon viral entry, pattern recognition receptors (PRRs) launch expression of inflammatory cytokines including IL6, IL10 and β-IFN. These molecules exit cells and act on the same or neighboring cells. Engagement of β-IFN with interferon receptors (IFNAR) leads to activation of the JAK-STAT pathway and interferon-stimulated gene (ISG) transcription. Among the ISGs, 5 members of the PARP superfamily are transcriptionally induced concomitant with an 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. Nicotinamide is undergoing clinical testing as an antiviral as well.

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