A cytokine storm initiates microvasculature clotting, causing severe hypoxia, coagulopathy and organ failure. Fluid fills the alveolus, reducing lung capacity and the virus infects microvascular pericytes in other organs. The endothelial cell lining of the capillary becomes inflamed, fibroblasts are activated, and SARS-CoV-2 viral components and cytokines enter the bloodstream. More cells are infected, inducing high levels of inflammatory cytokine signaling. Defective macrophages and T cells with a limited repertoire of receptors are less effective (lower right).

In the aged system (top right), viral alert signals are initially slow, resulting in greater viral replication. Neutrophils migrate to the sites of infection to clear infected cell debris. T cells with the appropriate receptors activate other lymphocytes or directly kill infected cells, preventing the spread of the virus. Viruses then travel to the alveoli and infect type 2 pneumocytes which, in the youthful system (lower left), are recognized by alveolar macrophages (AMs) or dendritic cells (not pictured) that release cytokines and present antigens to T cells and other adaptive immune cells. The SARS-CoV-2 virus binds to ACE2 enzymes on airway epithelial cells in the upper respiratory tract where they are endocytosed and replicated (top left), alerting the immune system. Ineffective clearance of SARS-CoV-2 infection in the aged respiratory system. This can lead to acute respiratory distress syndrome (ARDS), characterized by a loss of beneficial lung surfactant and an increase in oxidative stress and inflammation ( Figure 1). From there, it spreads to the mucous membranes of the throat and bronchial tubes, eventually entering the lungs where it infects type 2 alveolar epithelial cells called pneumocytes. Entering the nose, mouth or eyes, the virus spreads to the back of the nasal passages, where it binds to and enters via the dimerized angiotensin-converting enzyme 2 (ACE2) on the surface of airway epithelial cells. SARS-CoV-2 is transmitted through respiratory droplets or by direct contact. For example, simple explanations for the impact of age that are based solely on co-morbidities or on a general lack of resilience in aging, for example, fail to explain why the immune system often reacts uncontrollably. Whether these comorbidities contribute specifically to SARS-CoV-2 pathogenesis or whether they are primarily indicators of biological age remains an open question. The severity of COVID-19 is, of course, strongly associated with comorbidities such as hypertension, diabetes, obesity, cardiovascular disease, and respiratory system diseases. Even prior to SARS-CoV-2, human coronaviruses and influenza viruses have been known to impact older people disproportionately, yet therapeutic strategies to protect this fraction of the population, with the exception of vaccines, have largely failed. It is clear, however, that age alone is by far the most significant risk factor for death due to COVID-19.

Why the disease is particularly dangerous in older people is not yet known and poorly understood at the molecular level. COVID-19 has so far killed more than 350,000 people, with the majority of deaths (74%) occurring in people over the age of 65. Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2), which is responsible for the worldwide pandemic of coronavirus disease (COVID-19) originated in Wuhan, China, in late 2019. 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 patientsвЂ™ ability to clear the infection and effectively regulate immune responses. 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. 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. 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. 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. Adults over 65 years of age represent 80% of hospitalizations and have a 23-fold greater risk of death than those under 65. The severity and outcome of coronavirus disease 2019 (COVID-19) largely depends on a patientвЂ™s age.

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