Immunosenescence and COVID-19
It is very clear from the data, as is the case for influenza, the mortality of the COVID-19 pandemic is suffered near entirely by the old. This is because the aged immune system is less capable of fighting off pathogens, but also because the state of chronic inflammation and other dysfunctions resulting from immune system aging makes the cytokine storm of a severe SARS-Cov-2 viral infection that much more likely and that much more severe. Patients with inflammatory age-related conditions, or conditions associated with obesity, a prominent cause of chronic inflammation, are much more likely to die from SARS-Cov-2 infection.
Since the first reported cases with severe acute respiratory syndrome caused by a novel coronavirus (SARS-CoV2), this disease called coronavirus disease (COVID-19) has expanded worldwide being considered by World Health Organization as a pandemic. Although this virus may infect people regardless of age, race or sex, older subjects have been identified as a high-risk group regarding the clinical outcome of the disease, both for developing severe pneumonia with respiratory distress and death. Although global mortality rate directly related to SARS-CoV2 infection is unknown (a real infectious rate is not well known), mortality rate among severely elderly patients (between 60-90 years old) is around 50%, even in countries with significant lower deaths. Hence, apart from other risk factors linked to a poor clinical outcome, such as hypertension, diabetes, cardiovascular disease, cancer, or chronic lung disease, old age itself can be also considered as an independent risk factor associated with SARS-CoV2-related severe pneumonia and death.
From an immunopathogenic viewpoint, COVID-19 disease has probably a multifactorial nature and the final severe lung damage observed in COVID-19 could be caused by an uncontrolled proinflammatory cytokine cascade (called "cytokine storm"), driven mainly by interleukin-6 (IL-6) and other proinflammatory cytokines such as IL1β, IL8, CXCL10, and CCL2. Based on this hypothesis, apart from non-specific antiviral agents, anti-inflamatory drugs have been proposed to be used in patients with advanced COVID-19 disease. However, which immunopathogenic status precedes this "cytokine storm" and why the elderly population is more severely affected, are currently unanswered questions. Thus, we propose that immunosenescence and age-related thymic dysfunction could play a relevant role in current COVID-19 disease scenario.
According to our dual physiopathological hypothesis, in addition to impaired thymic function, we believe that elderly subjects at baseline show a systemic low-level chronic inflammation. Their population of monocytes generate a great amount and variety of cytokines (multiple circulating cytokines). These cells of elderly subjects, when stimulated by pathogen-associated molecular patterns receptors like TLR by a novel agonist (SARS-CoV2 antigen), could generate the massive and polyfunctional proinflammatory cytokine release that characterized COVID-19, and that would trigger the respiratory distress and multiorgan failure as clinical outcome.
I just read from Pfizer about their vaccine: "Efficacy was consistent across age, gender, race and ethnicity demographics; observed efficacy in adults over 65 years of age was over 94%"
If immune systems in the elderly are compromised and not as effective, how is this possible?
My only guess is that the efficacy of the vaccine at its WORST is this effective for the elderly, and far more effective for healthier immune systems (who might actually need much less of a dose?)
Would love to hear some thoughts on this.
@ gregory
they are simply lying.
While diminished the immune system of 65 y. Olds is still working. otherwise we would have them dying in drives from any minor cold. On the other hand 90 year is a much grimmer story...
The efficacy of the immune system decreases with agee, specially for T lymphocytes (there are hardly any new T lymphocytes produced in adults) but not for B lymphocytes (whose production continues throughout life ).
Vaccines stimulate the production of antibodies by B lymphocytes and still work in the elderly.
Sorry, no big pharma lies, we can rather thank them for working so efficiently!
It is still unknown how long double vaccination lasts in the elderly, before it wears off and they have to be re-vaccinated ....... as compared to youngsters. I expect that elderly will have to be re-vaccinated more frequently as compared to younger population.
There are in fact two major Pandemics in the world now: 1- COVID, 2- AGEing.
BUT World Health Organization or any government does not acknowledge the AGEing Pandemic or even as a decease that requires treatment. AGEing is not infectious, but hereditary and always deadly. It is the major contributing cause of death over the AGE of 80 in addition to infectious and chronic illnesses, accident and trauma. - AND it is not acknowledged by mainstream and official media.
Are they (doctors) really saving lives when curing patients of COVID or any other illness.?
No, they are only delaying death, because the same patients who recover and celebrate their recovery will soon - in a few years or decades will get sick again and die. Doctors at best are only rescheduling appointments for patients with the Grim Reaper.
To save human lives means to cure of any illness and disorder and AGEing and extend it infinitely or indefinitely. But no one is able to do it. So the Prognosis for the future of humanity is very GRIM. ......... no one who knows this can be happy.
@gregory
Given the extremely high politicization of the SARS-CoV2 virus, and its abuse for achieving nefarious political agendas worldwide, and the brazen manipulation and outright fabrication of a lot of medical + statistical data related to the virus, the only sane approach is to not waste time with it, or if you have to deal with it then at least treat any data produced after 2019 as very unreliable.