ACE2 expression declines significantly with age (Xie et al., 2006),
Xie, X., Chen, J., Wang, X., Zhang, F., & Liu, Y. (2006). Erratum to “Age-and gender-related difference of ACE2 expression in rat lung”. Life Sciences, 26(79), 2499
If that is the case, then why are elderlies more susceptible to SARS-CoV-2, since SARS-CoV-2 enter host cells via binding of spike protein (S1) to ACE2 receptors?
It is more to do with the aging immune system in older persons.
See this paper:
Figure:
Ineffective clearance of SARS-CoV-2 infection in the aged respiratory system.
- 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. 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. T cells with the appropriate receptors activate other lymphocytes or directly kill infected cells, preventing the spread of the virus. Neutrophils migrate to the sites of infection to clear infected cell debris.
- In the aged system (top right), viral alert signals are initially slow, resulting in greater viral replication. Defective macrophages and T cells with a limited repertoire of receptors are less effective (lower right). More cells are infected, inducing high levels of inflammatory cytokine signaling. The endothelial cell lining of the capillary becomes inflamed, fibroblasts are activated, and SARS-CoV-2 viral components and cytokines enter the bloodstream. Fluid fills the alveolus, reducing lung capacity and the virus infects microvascular pericytes in other organs. A cytokine storm initiates microvasculature clotting, causing severe hypoxia, coagulopathy and organ failure.
Article Why does COVID-19 disproportionately affect older people?
No harm by using ACE-inhibitors or ARBs in Elderly COVID-19 patients
In a study of critically ill elderly patients with co-morbidities admitted to ICU, there was a beneficial association of previous ACE-I use and no difference in survival with ARBs (1). Therefore, guidelines do not recommend stopping ACE inhibitors or ARBs in elderly patients with COVID-19 without any contraindications for use of these drugs (2).
1. Article Inhibitors of the Renin-Angiotensin-Aldosterone System and C...
2.Article Recommendations of RAAS Blocker Use Amidst The Coronavirus Pandemic
It is more to do with the aging immune system in older persons.
See this paper:
Figure:
Ineffective clearance of SARS-CoV-2 infection in the aged respiratory system.
- 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. 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. T cells with the appropriate receptors activate other lymphocytes or directly kill infected cells, preventing the spread of the virus. Neutrophils migrate to the sites of infection to clear infected cell debris.
- In the aged system (top right), viral alert signals are initially slow, resulting in greater viral replication. Defective macrophages and T cells with a limited repertoire of receptors are less effective (lower right). More cells are infected, inducing high levels of inflammatory cytokine signaling. The endothelial cell lining of the capillary becomes inflamed, fibroblasts are activated, and SARS-CoV-2 viral components and cytokines enter the bloodstream. Fluid fills the alveolus, reducing lung capacity and the virus infects microvascular pericytes in other organs. A cytokine storm initiates microvasculature clotting, causing severe hypoxia, coagulopathy and organ failure.
Article Why does COVID-19 disproportionately affect older people?
That is a really nice illustration accompanied by a splendid explanation. Thanks
Thanks for sharing. Along with the pertinent responses, the question is a nice opportunity to learn about this interesting topic.
Everybody is susceptible to the SARS-COV-2 virus infection. Yet, in old people the chronic low grade inflammation impairs the immune system, leads to the uncontrolled over-reaction of immune system (the cytokine storm). Cytokine storm attacks multiple organs, leads to the failure of these organs, and the death of the patients. If old people are physically fit without any metabolic syndromes, they will be much more resilient to the COVID-19 diseases, as old people actually have a much stronger immunity than younger people.
Agreed! That is why physical training is essential in all age groups.
Article The pivotal link between ACE2 deficiency and SARS-CoV-2 infection
.please note the link.
Interesting question- may be due to comorbidities, senescence, defective immune mechanisms lead to more symptomatic and severe infections. The young adult may develop a relatively asymptomatic infection.
Old people with co-morbidity mostly suffer from severity, in old people with co-morbidity mostly cause rise of ACE and ACE2 increases as a result of compensation so this might too play a role for elderly getting more effected. Another prospective local RAS might to influence it
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