This medical review addresses the hypothesis that CD38/NADase is at the center of a functional axis (i.e., intracellular Ca²⁺ mobilization/IFNɣ response/ROS burst) driven by SARS-CoV-2 infection, as already verified in Respiratory Syncytial Virus pathology and CD38 activity in other cellular settings. Key features of the hypothesis are that: i) the substrates of CD38 (e.g., NAD⁺ and NADP⁺) are depleted by viral-induced metabolic changes; ii) the products of the enzymatic activity of CD38 (e.g., cADPR/ADPR/NAADP) and related enzymes (e.g., PARPs, Sirtuins, ADP-ribosyl hydrolase) are involved in the anti‐viral and proinflammatory response that favors the onset of lung immunopathology (e.g., cytokine storm and organ fibrosis); and iii) the pathological changes induced by this kinetic mechanism may be reduced by distinct modulators of the CD38/NAD⁺ axis (e.g., CD38 blockers; NAD⁺ suppliers, among others). This view is supported by arrays of associative basic and applied research data which are herein discussed and integrated with conclusions reported by others in the field of inflammatory, immune, tumor and viral diseases.

中文翻译：

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Covid-19 时代的 CD38：医学观点。

这篇医学评论阐述了 CD38/NADase 位于由 SARS-CoV-2 感染驱动的功能轴（即细胞内 Ca ²⁺动员/IFNɣ 反应/ROS 爆发）中心的假设，这已在呼吸道合胞病毒病理学中得到证实和其他细胞环境中的 CD38 活性。该假设的主要特征是：i) CD38 的底物（例如，NAD ⁺和 NADP ⁺) 被病毒引起的代谢变化所消耗；ii) CD38（例如，cADPR/ADPR/NAADP）和相关酶（例如，PARPs、Sirtuins、ADP-核糖水解酶）的酶活性产物参与有利于肺发病的抗病毒和促炎反应免疫病理学（例如，细胞因子风暴和器官纤维化）；iii) 这种动力学机制引起的病理变化可以通过不同的 CD38/NAD ⁺轴调节剂（例如，CD38 阻滞剂；NAD ⁺供应商等）减少。这一观点得到了一系列相关的基础和应用研究数据的支持，这些数据在此讨论并与炎症、免疫、肿瘤和病毒疾病领域的其他人报告的结论相结合。