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Key features of the hypothesis are that 1) the substrates of CD38 (e.g., NAD<jats:sup>+<\/jats:sup>and NADP<jats:sup>+<\/jats:sup>) are depleted by viral-induced metabolic changes; 2) the products of the enzymatic activity of CD38 [e.g., cyclic adenosine diphosphate-ribose (ADPR)\/ADPR\/nicotinic acid adenine dinucleotide phosphate] and related enzymes [e.g., poly(ADP-ribose)polymerase, Sirtuins, and ADP-ribosyl hydrolase] are involved in the anti\u2010viral and proinflammatory response that favors the onset of lung immunopathology (e.g., cytokine storm and organ fibrosis); and 3) the pathological changes induced by this kinetic mechanism may be reduced by distinct modulators of the CD38\/NAD<jats:sup>+<\/jats:sup>axis (e.g., CD38 blockers, NAD<jats:sup>+<\/jats:sup>suppliers, among others). 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