Preclinical research shows that COVID-19 infection may dysregulate NAD+ synthesis

May 1, 2020

A new preclinical study found that SARS-CoV-2 (the virus that causes COVID-19) infection of cell lines, infected ferrets, and a deceased patient’s lung dysregulates nicotinamide adenine dinucleotide (NAD+) synthesis and utilization. 

A new preclinical study found that SARS-CoV-2 (the virus that causes COVID-19) infection of cell lines, infected ferrets, and a deceased patient’s lung dysregulates nicotinamide adenine dinucleotide (NAD+) synthesis and utilization. Explaining the findings that led to this current preclinical study, Charles Brenner, PhD, chief scientific advisor to ChromaDex (Los Angeles, CA), and co-author of the study states: “We started by looking at the effect of a related coronavirus that infects mice. It disturbs the gene set that controls cellular NAD. Moreover, we showed that within 12 hours of initial infection, the virus greatly depresses levels of NAD, the central catalyst of metabolism.”

In the current preclinical study, Brenner explains, researchers found that the COVID-19- causing virus turns off two gene pathways for NAD production and increases gene activity in two other pathways when it infects a cell. “The nicotinamide riboside pathway is frequently up-regulated in conditions of metabolic stress. Viral infection is such a condition,” says Benner.

The study provides important evidence about the nature of immune defense to the virus, but further research is necessary to determine potential treatments. “Our data says that the innate immune defense against viral infection depends on NAD and that it may be more effective at higher NAD,” says Brenner. “We’re looking at whether nicotinamide riboside, a vitamin that is available as Niagen, will protect against viral infection in cells and animals. We need a bit more proof of concept, and then we’ll be able to do human clinical studies.”

While the preclinical research described here is promising, it was published as a preprint and has yet to be peer reviewed.