Why does COVID-19 disproportionately affect older people?
Top Cited Papers
Open Access
- 29 May 2020
- journal article
- review article
- Published by Impact Journals, LLC in Aging
- Vol. 12 (10), 9959-9981
- https://doi.org/10.18632/aging.103344
Abstract
The severity and outcome of coronavirus disease 2019 (COVID-19) largely depends on a patient's age. Adults over 65 years of age represent 80% of hospitalizations and have a 23-fold greater risk of death than those under 65. In the clinic, COVID-19 patients most commonly present with fever, cough and dyspnea, and from there the disease can progress to acute respiratory distress syndrome, lung consolidation, cytokine release syndrome, endotheliitis, coagulopathy, multiple organ failure and death. Comorbidities such as cardiovascular disease, diabetes and obesity increase the chances of fatal disease, but they alone do not explain why age is an independent risk factor. Here, we present the molecular differences between young, middle-aged and older people that may explain why COVID-19 is a mild illness in some but life-threatening in others. We also discuss several biological age clocks that could be used in conjunction with genetic tests to identify both the mechanisms of the disease and individuals most at risk. Finally, based on these mechanisms, we discuss treatments that could increase the survival of older people, not simply by inhibiting the virus, but by restoring patients' ability to clear the infection and effectively regulate immune responses.Keywords
This publication has 176 references indexed in Scilit:
- DNA methylation age of human tissues and cell typesGenome Biology, 2013
- Anti-inflammatory activity of IgG1 mediated by Fc galactosylation and association of FcγRIIB and dectin-1Nature Medicine, 2012
- Regulation of Immune Responses by mTORAnnual Review of Immunology, 2012
- Factors that may impact on immunosenescence: an appraisalImmunity & Ageing, 2010
- Age‐Associated Inflammation and Toll‐Like Receptor Dysfunction Prime the Lungs for Pneumococcal PneumoniaThe Journal of Infectious Diseases, 2009
- Mechanisms of immunosenescenceImmunity & Ageing, 2009
- SIRT6 Links Histone H3 Lysine 9 Deacetylation to NF-κB-Dependent Gene Expression and Organismal Life SpanCell, 2009
- SIRT1 Redistribution on Chromatin Promotes Genomic Stability but Alters Gene Expression during AgingCell, 2008
- Human Immunodeficiency Virus Type 1 Tat Protein Inhibits the SIRT1 Deacetylase and Induces T Cell HyperactivationCell Host & Microbe, 2008
- Sialic acid receptor detection in the human respiratory tract: evidence for widespread distribution of potential binding sites for human and avian influenza virusesRespiratory Research, 2007