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.

摘要

由严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 引起的 COVID-19 大流行导致全球死亡率急剧上升。在开发疫苗的同时，医学界也在探索遏制这种流行病的新策略。更好地了解 SARS-CoV-2 细胞感染的分子后果可能会导致更有效和更安全的治疗。^{这篇综述讨论了 SARS-CoV-2 在调节干扰素 (IFN) 分泌和引起线粒体 NAD +}耗竭方面的潜在潜在影响，这可能与 COVID-19 的致命表现直接相关。关于 SARS-CoV-2 感染后先天免疫反应失衡和线粒体功能障碍的已知或推测，以及适时的 IFN 治疗和 NAD + 的潜在^益处讨论了 COVID-19 大流行背景下的加强疗法。