Posted: April 30, 2020 - This version is a preprint and has not been certified by peer review.
This article shows that SARS-CoV-2 infection of cell lines, infected ferrets, and a deceased patient’s lung consistently and strikingly dysregulates NAD+ (nicotinamide adenine dinucleotide) gene set with respect to NAD+ synthesis and utilization. Further, it shows that MHV infection induces an attack on host cell NAD+ and NADP+ (nicotinamide adenine dinucleotide phosphate)
- “…viral replication and host cell homeostasis both depend on the four nicotinamide adenine dinucleotide (NAD) coenzymes, NAD+, NADH, NADP+ and NADPH, which are the central catalysts of metabolism (Belenky, Bogan, & Brenner, 2007). These coenzymes accept and donate electrons in essential, ubiquitous processes of fuel oxidation, biosynthesis, and the generation and detoxification of reactive oxygen species” (emphasis added)
- “…SARS-CoV-2 infection of ferrets and the human also appears to down-regulate synthesis of NAD from tryptophan and nicotinic acid (NA) while upregulating synthesis capacity from nicotinamide (NAM) and nicotinamide riboside (NR)…” (emphasis added)
- “…The data justify further analysis of how nutritional and therapeutic modulation of NAD status may potentially restrict viral infection by boosting innate immunity...." (emphasis added)
- “… NAD boosting approaches have the potential to support the innate immune system and address the age-, smoking- and comorbid conditions associated with worse SARS-CoV-2 outcomes (Yang et al., 2020). Coupled with good hygiene, the potential societal benefit of a safe and readily available molecule to support prevention and public health is hard to overstate, especially as people emerge from sheltering in place and re-enter public spaces with potentially substantive viral contamination…" (emphasis added)