Do you know the word “senescence”? Senescence is in biology the physiological process which leads to the degradation of cell functions over time. In other words, senescence, from Latin senex "great age", is the aging of organisms. Historically, scientists have sought to curb aging trying to respect the Chinese proverb taken by Malraux
"We must add life to years and not years to life".
Several recent studies tend to show that SARS-CoV2 accelerates the biological age of cells. How? 'Or' What ? By acting on the size of telomeres, those DNA sequences that protect the ends of chromosomes and shorten with each cell division.
In April 2021, a Chinese study by Yuyang Lei and Jiao Zhang, published on Circulation Research points out that the main pathogen of the Covid-19 virus is its spike protein, called Spike. The spike protein surrounds the viral capsid and allows it to enter cells to infect them. In this study, the researchers isolated Spike by placing it on an empty nucleus, then inoculated it into guinea pigs to observe its action on the body. The animals showed damage to the lungs and arteries associated with inflammation of endothelial cells. The team replicated the in vitro experiment on healthy human endothelial cells: the spike protein thus bound to ACE2 receptors, damaging the cell's mitochondria, causing micro-thrombosis and endothelitis. The conclusions are clear: Spike protein alone causes most of the symptoms of Covid-19 (Covid in the rest of the article).
Some questions then burn the lips:
If it is proven that SARS-CoV2 induces accelerated cellular aging, and that the responsible for this senescence is none other than the Spike protein, how can we be absolutely certain that the vaccines currently on the market, all based on Spike, do not not also lead to the accelerated degradation of the cells of vaccinated people?
What are the links between the mechanisms involved in senescence linked to telomere shortening and vaccines?
Some answers in this article. We warn the reader that some paragraphs require some knowledge in biology or biochemistry. The conclusion is intended for the general public.
Acceleration of biological age
In November 2020, a team of researchers from Cliniques Universitaires Saint-Luc and UC Louvain investigated the potential role of telomeres in Covid infection. Age, obesity, diabetes, hypertension and many factors of severity are now well identified complicating factors. However, patients who do not meet these criteria sometimes suffer severely from this virus.
Telomeres and their role?
A synthetic article from the same university explains what telomeres are and their role.
Telomeres are DNA sequences that protect the ends of chromosomes and shorten with each cell division. Their size decreases with the age of the cell and the individual. When they get too short, especially in the elderly, cells go into senescence, a phenomenon close to cell death. These structures therefore play the role of a cellular biological clock.
Many scientists have shown that telomere shortening decreases life expectancy.
However, telomere length is not the same for all individuals of the same age and depends, among other things, on certain genetic variants. Telomere shortening appears to affect the body's defenses against viruses, and people with shorter telomeres are thought to deplete their stock of immune cells more quickly.
In order to better understand the immune mechanisms involved in Covid-19 (the patients hospitalized for Covid almost all having a lack of lymphocytes in the blood), professors Froidure (Department of pneumology) and Decottignies investigated the potential link between telomere size and Covid.
The researchers compared the telomere size of 70 patients hospitalized for Covid during the first wave of the pandemic (between April 7 and May 27, 2020 / patients aged 27 to 96) with the results of a control group corresponding to around 500 people without Covid.
The results showed that i) the telomeres of Covid patients were shorter than those in the reference group and ii) the presence of very short telomeres (smaller in size than the 10 percentile for age) was associated with a significantly higher risk. admission to intensive care or death.
These results open up important perspectives in understanding the mechanisms of immunity to the coronavirus.
Results confirmed and refined in 2021
In January 2021, molecular oncology researcher Maria Blasco confirmed the results of Froidure et al. published in an article that went unnoticed and which titled "Telomeres of shorter lengths in patients with severe Covid disease". In summary :
The incidence of severe manifestations of Covid increases with age, with older patients having the highest mortality, suggesting that the molecular pathways underlying aging contribute to the severity of Covid. The authors recall that “one of the mechanisms of aging is the progressive shortening of telomeres, which are protective structures at the ends of chromosomes. Extremely short telomeres impair the ability of tissue to regenerate and trigger loss of tissue homeostasis and disease. The SARS-CoV2 virus infects many different cell types, forcing cell renewal and regeneration to maintain tissue homeostasis.
The authors therefore hypothesized that the presence of short telomeres in older patients limits the tissue response to SARS-CoV2 infection. They measured telomere length in peripheral blood lymphocytes from Covid patients aged 29 to 85 and found that shorter telomeres are associated with increased severity of the disease.
Few of the articles have reported on these studies except healthLog which timidly titled "what if the covid nibbles the telomeres?" "Before concluding that a question arises: does telomere shortening imply acceleration of aging and a reduction in
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