Insights into the modulation of the interferon response and NAD+ in the context of COVID-19
| dc.contributor.author | Habeichi, Nada J. | |
| dc.contributor.author | Tannous, Cynthia | |
| dc.contributor.author | Yabluchanskiy, Andriy | |
| dc.contributor.author | Altara, Raffaele | |
| dc.contributor.author | Mericskay, Mathias | |
| dc.contributor.author | Booz, George Warren | |
| dc.contributor.author | Zouein, Fouad A. | |
| dc.contributor.department | Pharmacology and Toxicology | |
| dc.contributor.faculty | Faculty of Medicine (FM) | |
| dc.contributor.institution | American University of Beirut | |
| dc.date.accessioned | 2025-01-24T11:39:56Z | |
| dc.date.available | 2025-01-24T11:39:56Z | |
| dc.date.issued | 2022 | |
| dc.description.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. © 2021 Taylor & Francis Group, LLC. | |
| dc.identifier.doi | https://doi.org/10.1080/08830185.2021.1961768 | |
| dc.identifier.eid | 2-s2.0-85112211412 | |
| dc.identifier.pmid | 34378474 | |
| dc.identifier.uri | http://hdl.handle.net/10938/29394 | |
| dc.language.iso | en | |
| dc.publisher | Taylor and Francis Ltd. | |
| dc.relation.ispartof | International Reviews of Immunology | |
| dc.source | Scopus | |
| dc.subject | Innate immune system | |
| dc.subject | Mitochondrial dysfunction | |
| dc.subject | Nicotinamide adenine dinucleotide | |
| dc.subject | Sars-cov-2 | |
| dc.subject | Antiviral agents | |
| dc.subject | Covid-19 | |
| dc.subject | Humans | |
| dc.subject | Interferons | |
| dc.subject | Nad | |
| dc.subject | Pandemics | |
| dc.subject | Interferon | |
| dc.subject | Antivirus agent | |
| dc.subject | Article | |
| dc.subject | Coronavirus disease 2019 | |
| dc.subject | Cytokine release | |
| dc.subject | Human | |
| dc.subject | Innate immunity | |
| dc.subject | Mitochondrion | |
| dc.subject | Mortality | |
| dc.subject | Nonhuman | |
| dc.subject | Pandemic | |
| dc.subject | Severe acute respiratory syndrome coronavirus 2 | |
| dc.title | Insights into the modulation of the interferon response and NAD+ in the context of COVID-19 | |
| dc.type | Article |
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