Mitochondria: In the Cross Fire of SARS-CoV-2 and Immunity
Johannes Burtscher, Giuseppe Cappellano, Akiko Omori, Takumi Koshiba, Grégoire P. Millet
Abstract
The pathophysiology, immune reaction, and differential vulnerability of different population groups and viral host immune system evasion strategies of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are not yet well understood. Here, we reviewed the multitude of known strategies of coronaviruses and other viruses to usurp mitochondria-associated mechanisms involved in the host innate immune response and put them in context with the current knowledge on SARS-CoV-2. We argue that maintenance of mitochondrial integrity is essential for adequate innate immune system responses and to blunt mitochondrial modulation by SARS-CoV-2. Mitochondrial health thus may determine differential vulnerabilities to SARS-CoV-2 infection rendering markers of mitochondrial functions promising potential biomarkers for SARS-CoV-2 infection risk and severity of outcome. Current knowledge gaps on our understanding of mitochondrial involvement in SARS-CoV-2 infection, lifestyle, and pharmacological strategies to improve mitochondrial integrity and potential reciprocal interactions with chronic and age-related diseases, e.g., Parkinson disease, are pointed out.