COVID-19 Review Volume 12, Issue 18 pp 18778—18789
SARS-CoV-2, immunosenescence and inflammaging: partners in the COVID-19 crime
- 1 Department of Experimental Neurodegeneration, Center for Biostructural Imaging of Neurodegeneration, University Medical Center Goettingen, Goettingen, Germany
- 2 Center of Excellence for Science and Technology-Integration of Mediterranean Region (STIM), Faculty of Science, University of Split, Split, Croatia
- 3 Max Planck Institute for Experimental Medicine, Goettingen, Germany
- 4 Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Framlington Place, Newcastle Upon Tyne, UK
- 5 Department of Otolaryngology-Head and Neck Surgery, University Medical Center Goettingen, Goettingen, Germany
Received: June 6, 2020 Accepted: August 11, 2020 Published: September 29, 2020https://doi.org/10.18632/aging.103989
How to Cite
Copyright: © 2020 Domingues et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Pneumonia outbreak in the city of Wuhan, China, prompted the finding of a novel strain of severe acute respiratory syndrome virus (SARS-CoV-2). Here, we discuss potential long-term consequences of SARS-CoV-2 infection, and its possibility to cause permanent damage to the immune system and the central nervous system. Advanced chronological age is one of the main risk factors for the adverse outcomes of COVID-19, presumably due to immunosenescence and chronic low-grade inflammation, both characteristic of the elderly. The combination of viral infection and chronic inflammation in advanced chronological age might cause multiple detrimental unforeseen consequences for the predisposition and severity of neurodegenerative diseases and needs to be considered so that we can be prepared to deal with future outcomes of the ongoing pandemic.