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Supporting information
“In addition, the age-associated dysfunction of enzymes in NAD+ production, such as QPRT (quinolinate phosphoribosyl transferase) [58] in the de novo pathway, may be a reason why elderly persons are more susceptible to severe COVID-19. Minhas et al. reported that aged human macrophages had lower QPRT expression that was associated with an induction of upstream KP (kynurenine pathway) metabolites culminating in the accumulation of QA (quinolinic acid), but decreased production of the downstream metabolites NAMN (nicotinic acid mononucleotide), NAAD (nicotinic acid dinucleotide), and NAD+ [58] (Fig. 2). Reduced expression of QPRT was found in several lung cell lines infected with SARS-CoV-2 [59], suggesting that the dysfunction of QPRT expression and reduction of NAD+ may be exacerbated in COVID-19. Other mechanisms for the age-related reduction of NAD+ could result from increases in NAD+-consuming enzymes (NADases). NADases include SIRTs (sirtuins) and CD38, and in particular, CD38 is activated in the elderly population [60]. NAD+ deficiency is shared amongst the comorbidities of COVID-19 (Table 1) and thus potentially represents a critical component of the disease.”
“Therefore, NAD+ boosters would be effective for the prevention of COVID-19 or immediately after the infection with SARS-CoV-2.”
https://www.nature.com/articles/s41418-021-00892-y -
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