NEW RESEARCH: Preclinical Coronavirus Study Result
Raising NAD+ Levels With Niagen® (Nicotinamide Riboside) Inhibits Coronavirus Replication in Preclinical Cell Model
New preclinical research shared on scientific publishing website bioRxiv.org has demonstrated that increasing NAD+ levels can boost the activity of protective enzymes called PARPs and reduce coronavirus replication in a mouse cell model.
Earlier preclinical research showed Coronavirus infected cells suffer significant NAD+ depletion leading to disruption of innate antiviral immune activity, while other preclinical data suggest that modulation of inflammasome activity in immune cells by NAD+ may be important in the severe inflammation observed in patients infected with COVID-19. ChromaDex’s Niagen is proven to effectively restore and maintain NAD+ levels…
THE NEW IN VITRO RESEARCH – WHAT YOU NEED TO KNOW:
NR and Other NAD+ Boosters Blunt Viral Replication – Mouse cells infected with coronavirus murine hepatitis virus (MHV, a viral “cousin” of SARS-CoV-2) had decreased viral proliferation when supplemented with the NAMPT activator SBI-797812 (SBI), niacinamide (NA), nicotinamide (NAM), or Niagen® nicotinamide riboside (NR). Importantly, SBI, NAM, and NR had significantly greater effects on blunting replication than NA.
Antiviral Activity of PARP Enzymes Were Upregulated With Increased NAD+ – NAD-dependent poly(ADP-ribose) polymerases (PARPs) are a class of repair enzymes, several of which are known to help prevent viruses from hijacking cellular machinery for replication [5]. Coronaviruses respond with their own countermeasure with an enzyme called poly-ADP ribose glycohydrolase (PARG), that functions to disable PARPs [3, 6]. This negative cycle leaves cells severely NAD+ depleted and weak, allowing the virus greater opportunity to replicate.
There’s More to Consider When Selecting a NAD+ Boosting Interventions – Although apparently effective at reducing viral replication in this in vitro model, at pharmacological doses, NAM has the potential to function as a PARP inhibitor which is the exact opposite effect of its intended use. Also, overactive NAMPT is implicated in a condition that may reduce lung capacity and adversely affect the lungs and heart, suggesting that its use may not be an appropriate strategy to maintain lung health in some people at risk for COVID-19.
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