Dr Raj Patel Cockburn – Amber L. Mueller1, , Maeve S. McNamara1, , David A. Sinclair1, , 1 Glenn Center for Research in the Biology of Aging, Blavatnik Institute, Harvard Medical School, Boston, MA 20115, USA Received: April 29, 2020 1 Received : , 2020 Published: 29 May 2020 https://doi.org/10.18632/aging.103344
Mueller AL, McNamara MS, Sinclair DA,. How dangerous is COVID-19 to the elderly? Ake (Albany NY). 2020 May 2912: 9959-9981. https://doi.org/10.18632/aging.103344
Dr Raj Patel Cockburn
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Copyright © 2020 Mueller et al. This is an open access document distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which allows unrestricted use, distribution and reproduction in any context, provided that credit is given to producer and source.
The severity and outcome of the coronavirus disease 2019 (COVID-19) is highly dependent on the age of the patient. Adults over the age of 65 account for 80% of hospital admissions and are 23 times more likely to die than those under 65. In the clinic, a fever, cough and dyspnea in COVID-19 patients, from where the disease can be fatal. progression to acute respiratory syndrome, lung consolidation, cytokine release syndrome, endotheliitis, coagulation, organ failure and death. Diseases such as heart disease, diabetes and obesity increase the risk of death, but age alone does not explain why it is a separate risk factor. Here, we show the molecular differences between young, middle-aged and elderly people that explain why COVID-19 is a mild disease in some but a serious disease in others. We also discuss several biological markers that can be used in conjunction with genetic testing to identify disease processes and individuals at high risk. Finally, based on these methods, we will discuss treatments that increase the quality of life of the elderly, not only by suppressing the virus, but also by restoring the patients’ ability to eliminate in the disease and immune responses are controlled properly.
The Severe Respiratory Syndrome 2 (SARS-CoV-2) coronavirus, which is responsible for the global outbreak of the coronavirus disease (COVID-19), originated in Wuhan, China, in late 2019 . To date, more than 350,000 people have died from COVID-19, and the majority of deaths (74%) have occurred in people over 65 years of age [2, 3]. It is not yet known what causes the disease to be so harmful to the elderly and is not fully understood at the molecular level. It is clear, however, that age is the only significant factor in mortality from COVID-19 [4, 5]. Even before SARS-CoV-2, human coronaviruses and influenza viruses are known to affect the elderly , but medical strategies to protect this fraction of the population, in addition vaccines have largely failed. Of course, the severity of COVID-19 is strongly related to diseases such as hypertension, diabetes, obesity, heart disease, and diseases of the respiratory system . Whether these diseases contribute to the pathogenesis of SARS-CoV-2 or are indicative of biological age remains a question. A simplistic explanation of the effect of age on disease-related diseases, or age-related incapacity, for example, does not explain why the immune system is often unable to death.
SARS-CoV-2 is transmitted through respiratory droplets or direct contact. After entering the nose, mouth, or eyes, the virus spreads to the back of the nose, binds, and is absorbed by angiotensin converting enzyme 2 (ACE2)  as described above. at the surface of epithelial cells . From there, it spreads to the mucous membranes of the throat and lungs, where it enters the lungs and infects type 2 alveolar epithelial cells called pneumocytes. This can lead to acute respiratory distress syndrome (ARDS), characterized by loss of effective lung surfactant and increased oxidative stress and inflammation [9, 10] (Figure 1) .
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Figure 1. Inefficient clearance of SARS-CoV-2 infection in chronic influenza. The SARS-CoV-2 virus binds to ACE2 enzymes on airway epithelial cells in the upper respiratory tract where it is endocytosed and replicated (top left), alerting the immune system . Viruses travel to the alveoli and infect known type 2 pneumocytes, in the alveolar system (bottom left), by alveolar macrophytes (AMs) or dendritic cells (not pictured) that release the cytokines and present antigens for T cells and other adaptive immune cells. . cells. T cells work with appropriate receptors on other lymphocytes or directly kill infected cells, thereby preventing the spread of the virus. Neutrophils migrate to sites of infection to eliminate infected cell debris. In the old system (right), viral warning signs are slow at first, and viral replication increases. Macrophages and T cells with a limited receptor repertoire are less effective (bottom right). More cells become infected, resulting in high levels of inflammatory cytokine signaling. The endothelial cell layer of the capillary becomes inflamed, fibroblasts are activated, and SARS-CoV-2 viral particles and cytokines enter the bloodstream. Fluid fills the alveolus, reducing lung capacity, and the virus infects microvascular pericytes in other organs. Cytokine storm initiates microvasculature coagulation, leading to hypoxia, coagulopathy and organ failure. Created with BioRender.
Especially in the elderly, severe disease is characterized by lung injury and ARDS, the latter of which is treated by positive airway pressure with oxygen and auscultation or invasive ventilation. This phase is characterized by neutrophilia, lymphocytopenia, lung consolidation, and bilateral ground-glass staining on chest X-rays. ACE2 protein is expressed on the surface of epithelial and microvascular pericytes that cross multiple organs and both cell types can be infected by the virus [ 11 , 12 ]. Infiltration of immune cells at sites of infection causes inflammation and endothelial dysfunction in the lung, heart, kidney, and liver and brain, with prominent endotheliitis of the submucosal vessels. and apoptotic bodies .
Despite the decrease in the viral load in the patient, the type of cytokine release syndrome can quickly develop, characterized by intravascular coagulation (DIC), liver damage, renal disease, heart inflammation, coagulopathy and death [13, 14]. Few studies have linked aging processes to the pathogenesis of the virus. In this overview, we provide a mechanistic explanation for why COVID-19 progresses in some people and not others, especially in elderly patients, including differences in the immune system, glycation, epigenome, inflammatory activity, and biological age. We will also discuss medications to improve immunity to the virus while improving the ability of older people to recover from severe COVID-19.
The ability to control viral load is one of the best predictors of whether a patient will have mild or severe symptoms of COVID-19 . In order for the immune system to successfully remove and eliminate SARS-CoV-2, it must perform four main functions: (1) recognize, (2) be alert, (3) destroy and (4) clear. All these processes are known to be impaired and increased in the elderly [16, 17]. But it is not yet clear what activities are most relevant for the progression of COVID-19 in the elderly .
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During aging, the immune system changes in two ways. One is a decrease in immune function called immunosuppression, which prevents pathogen recognition, warning and elimination. Not to be confused with cellular senescence, an aging-related condition in which old or impaired cells stop their cell cycle, can become epigenetically locked into a pro-inflammatory state and release cytokines and chemokines. Another classic change in the immune system during aging is the continuous increase in systemic inflammation called the inflammasome, which results from an active but ineffective immune system [19 ].
A number of recent reports describing pathological and molecular changes in COVID-19 patients indicate that impairment and inflammation are the main cause of death rates in older patients. In immunity, there are errors in the innate and adaptive immune systems. Innate immunity is characterized by impaired pathogen recognition and macrophage activation, and decreased natural killer (NK) cell cytotoxicity, whereas adaptive immunity is characterized by thymic atrophy and accumulation of memory lymphocytes. sickness In both cases, these age-related changes are thought to be caused by pathogenic, genetic and lifestyle factors affecting the epigenetic status of cells and the differentiation of immune cells.
The immune system is the body’s first line of defense against coronaviruses. Sensory cells, such as macrophages and dendritic cells, recognize viral proteins stored in monophasic membrane-spanning receptors called Toll-like receptors (TLRs) that are expressed on their their faces. Deficiencies in TLR activity in innate immune cells are known to increase the severity of pneumonia in mice, especially in the context of aging and chronic inflammation. . Alveolar macrophages (AMs) are mononuclear phagocytes that scan the alveoli for dust, allergens and pathogen residues. When their TLRs detect a predator, AMs respond by producing type I interferon, which attracts immune cells to the site of infection and presents antigens to lymphocytes [ 21 , 22 ]. Although the number of AMs increases during aging, their plasticity and the change between pro- and anti-inflammatory properties are significantly reduced , as indicated by a weak response of cytokine after TLR activation  (Figure 1).
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