As always, we continue to search, research and generate information to keep you up to date with the latest scientific advances in anti-aging, well-being and quality of life.
This time we have focused, once again, on COVID-19.
The SARS-CoV-2 virus never ceases to surprise the scientific community and we are all learning a little more about it.
Today we will take a brief look at how it affects telomeres and most importantly, what we can do to improve it.

A little refresher

Telomeres are one of the key pillars of aging.
These are a kind of caps that protect the ends of chromosomes.
They contain sequences rich in repeated thymine and guanine that, when the cells divide, must be constantly replaced to avoid chromosomal erosion and, therefore, genomic instability.

Telomeres are one of the key pillars of aging.

Telomeres are involved in regulating cell proliferation and could play a role in stabilizing genomic regions in response to stress. Telomeres shorten with each cell division and are therefore the limiting factor in the life of human cells, to a finite number and therefore induce replicative senescence, differentiation or apoptosis.

Post-COVID-19 persistent syndrome

SARS-CoV-2 infection determines COVID-19 syndrome characterized, in the worst cases, by severe respiratory distress, cardiac and pulmonary fibrosis, release of inflammatory cytokines, and immunosuppression.

Among survivors of the disease, there is the so-called post-COVID-19 persistent syndrome (PPCS) and that, apparently, is a fairly common finding.

Patients who have overcome severe COVID-19 disease have one or more symptoms, which are very similar to the symptoms we often associate with aging.
These symptoms include:

• Chronic fatigue
  • Dyspnea
• Memory loss
• Sleep disorders
• Difficulty concentrating

This was what prompted a group of scientists to hypothesize that age-like symptoms were linked to severe COVID-19 post-infection and telomere shortening.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7835063/

Scientific reviews of COVID-19 and its relationship with telomeres

Patients who have had severe COVID-19 disease appear to have significantly shorter telomeres, according to a study published by the journal Aging and carried out by researchers at Spain’s National Cancer Research Centre (CNIO) in collaboration with the COVID-IFEMA Field Hospital. https://doi.org/10.18632/aging.202463

In another study, called Wang and published by the famous journal The Lancet, it consisted of 6,775 adults with COVID-19.
For this study, measurements of the telomere length of hematopoietic cells were made several years before the SARS-CoV-2 pandemic and compared with post-disease measurements.
The result was an observation of a significant shortening of the telomere length of leukocytes. https://doi.org/10.1016/j.ebiom.2021.103485

There is evidence of telomere shortening due to COVID-19

On the other hand, telomerase, which has the function of lengthening/repairing telomeres, is activated during the clonal expansion and differentiation of T cells. But the enzyme’s activity is insufficient to counteract telomere shortening with the replication of these cells.
Therefore, T cell replication depends on telomere length, and as the telomere length of hematopoietic cells shortens with age, T cells from older adults have a decreased clonal expansion capacity compared to young adults.

Consequences of telomere shortening and COVID-19

The incidence of severe manifestations of COVID-19 increases with age and older patients show the highest mortality, suggesting that molecular pathways underlying aging contribute to the severity of COVID-19.
One mechanism of aging is the progressive shortening of telomeres. Critically short telomeres impair the regenerative capacity of tissues and trigger loss of homeostasis and tissue disease. https://doi.org/10.1016/j.ebiom.2021.103513

The medical, public health, and scientific communities are grappling with monumental challenges in containing COVID-19, developing effective vaccines, identifying effective treatments for infection and its complications, and working to find biomarkers that detect patients at risk of severe disease.
The focus of these studies is to emphasize a potential biomarker, the short length of telomeres.

Short telomeres are associated with a deterioration in health

Telomere length of leukocytes is a highly heritable human trait that shows wide inter-individual variation and is reflected in all cells, including hematopoietic cells.
Within each person, hematopoietic stem cells top the hierarchy he

matopoietic and show age-dependent telomere shortening.
Although telomerase is active in subsets of hematopoietic cells, in most of these cells, the activity is insufficient to prevent telomere shortening that ultimately leads to cellular senescence, culminating in the cessation of replication.
DOI: 10.1101/cshperspect.a003558

Currently, the etiology of lymphopenia in patients with COVID-19 is not well understood, but prompt recovery of the immune response requires massive lymphopoiesis, which is telomere length dependent.
Shorter telomeres in hematopoietic cells in the elderly, people with cardiometabolic disease, and being male can prevent cell proliferation, particularly CD4/CD8 lymphopoisis, against COVID-19, increasing the risk of severe disease. https://doi.org/10.1096/fj.202001025

Advantages of having a longer leukocyte telomere length

The average telomere length of leukocytes at birth in the U.S. is 9.5 kb.
Thereafter, this length is shortened by 2 kb in the third decade and by 3.5 kb in the ninth decade of life.
We know little about how much telomeres are shortened by replication of hematopoietic cells in vivo.
Estimates (approximately 0.05-0.1 kb) are based on cultured cells.
However, if we consider a child whose telomere length of leukocytes is only 1 kb longer than that of an adult and based on the loss of 0.1 kb per replication, all other things being equal, the telomere length-dependent replication capacity of the first responders is 1024 times greater (2¹⁰) for the child than for the adult.
This means that the child has a huge restorative advantage compared to the adult in the ability to respond to an acute and massive loss of circulating cells.

Critically short telomeres impair the regenerative capacity of tissues

Similarly, the average difference in telomere length of leukocytes between adults without cardiovascular disease versus those with cardiovascular disease is approximately 0.3 kb.
The telomere length-dependent replication capacity of the first responding cells in adults without cardiovascular disease would therefore be greater than in those with this type of pathology.

Possible solution

For COVID-19 survivors, there is a possible solution that involves the maintenance and/or lengthening of telomeres.
This option could be beneficial in preventing potential health problems in the future.

TA-65® is a dietary supplement that has been shown through clinical studies to improve the immune system.
TA-65® would reduce the number of immunosenescent cells – which are those that can be considered non-functional, harmful or zombie cells – while rejuvenating the remaining cells of the immune system.

In one study, they wanted to verify whether the preparation of fermented papaya had a clear and scientifically observed anti-aging effect in vivo.
In addition, the induction of a systemic antioxidant reaction was measured.
For this purpose, mice treated with water supplemented with fermented papaya were studied and compared with other mice that received only tap water.
After ten months in treatment, telomerase activity, plasma levels of reactive oxygen species, and telomere length in the bone marrow and ovaries were assessed in both groups of mice.

The results showed that mice that drank water supplemented with fermented papaya increased telomere length in the bone marrow and ovary, along with an increase in plasma levels of telomerase activity, and antioxidant levels, with a decrease in reactive oxygen species.
Early treatment was found to be more effective, suggesting a key potential of this ferment in preventing age-related molecular damage. https://doi.org/10.3390/antiox9020144

At Salengei we pursue scientific rigor.
We hope you found this article interesting.