Insights into the modulation of the interferon response and NAD+ in the context of COVID-19.

Department of Pharmacology and Toxicology, American University of Beirut Faculty of Medicine, Beirut, Lebanon. Department of Signaling and Cardiovascular Pathophysiology, Université Paris-Saclay, Inserm, UMR-S 1180, Châtenay-Malabry, France. Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway. KG Jebsen Center for Cardiac Research, Oslo, Norway. Department of Pathology, School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA. Department of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA.

International reviews of immunology. 2022;(4):464-474
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Abstract

The COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in dramatic worldwide mortality. Along with developing vaccines, the medical profession is exploring new strategies to curb this pandemic. A better understanding of the molecular consequences of SARS-CoV-2 cellular infection could lead to more effective and safer treatments. This review discusses the potential underlying impact of SARS-CoV-2 in modulating interferon (IFN) secretion and in causing mitochondrial NAD+ depletion that could be directly linked to COVID-19's deadly manifestations. What is known or surmised about an imbalanced innate immune response and mitochondrial dysfunction post-SARS-CoV-2 infection, and the potential benefits of well-timed IFN treatments and NAD+ boosting therapies in the context of the COVID-19 pandemic are discussed.

Methodological quality

Publication Type : Review

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