COVID Short telomeres and severe COVID-19

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The length of telomeres, rather than numerical age, may influence the severity of COVID-19, as indicated by a study involving 6,775 adults where telomere length was measured prior to infection. Shorter hematopoietic cell telomeres were found to precede severe COVID-19, suggesting that telomere length impacts immune response rather than being affected by the virus. Additionally, a poor T-cell response can lead to unchecked innate immune reactions, resulting in severe inflammation and lung injury. There appears to be a telomere length threshold that, once crossed, exacerbates COVID-19 severity, particularly in older adults. This highlights the potential role of telomere length in immune function and its implications for COVID-19 outcomes.
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Short telomeres and severe COVID-19
Not the numerical age directly, but the length of the telomeres seems to decide, if one gets severe COVID-19.

paper said:
Wang's study, in contrast, consists of 6,775 adults with COVID-19. The study's importance, however, rests not in its size but in the fact that hematopoietic cell telomere length (TL) measurements had been performed years before the SARS-CoV-2 pandemic. This critical fact means that short hematopoietic cell TL, as expressed in leukocyte TL (LTL), preceded the onset of severe COVID-19– a conclusion that excludes reverse causality, namely, that SARS-CoV-2 infection shortens LTL.
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Sette and Crotty have recently suggested that a poor T-cell response in patients with COVID-19 leaves the innate immune response relatively unchecked, which might result in hyper-inflammation in the form of a cytokine storm and severe lung injury.
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The TL-COVID-19 link might thus be defined by a TL “threshold”, such that TL minimally affects the course of COVID-19 until reaching this threshold. Once this threshold is crossed, largely after the sixth decade, short T-cell TL might have an amplifying, age-dependent effect on COVID-19 severity.
Source:
https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(21)00306-6/fulltext

see also:
Paternal age is positively linked to telomere length of children
Source:
https://pubmed.ncbi.nlm.nih.gov/15771613/
 
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If there is a loss of immune system function correlated with reduced telomere length, then there should be genes affecting some kind of immune system functioning, located on the chromosomes, near the telomeres (chromosome ends).
Telomere loss is often assumed to produce its negative effects by removing (or affecting the expression of) sequences, near the ends of the chromosome.

This would seem to indicate that genes for some immune function, should be located in telomeric regions of the chromosomes. This is the human genome, you should be able to look it up somewhere.
It sounds like a kind of genetic screen for mutations, where chunks of a chromosome are systematically deleted and a particular phenotype is checked for mutant effects, except it is limited to the ends of the chromosomes. People do this in Drosophila, for example.
 
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BillTre said:
If there is a loss of immune system function correlated with reduced telomere length, then there should be genes affecting some kind of immune system functioning, located on the chromosomes, near the telomeres (chromosome ends).

The reason for loss of immune system function is described here:

paper said:
Telomerase, the reverse transcriptase that elongates telomeres, is activated during T-cell clonal expansion and differentiation, but the activity of the enzyme is insufficient to counter telomere shortening with T-cell replication. T-cell replication is thus TL-dependent. As hematopoietic cell TL shorten with age, T-cells from older adults have diminished clonal expansion capacity compared to young adults. For most healthy adults, such age-dependent T-cell TL shortening might not be a major problem in absence of an acute infection, because the long half-lives of ~ 5 years of naïve cells and ~ 5 months of memory T cells in the circulation impose minimal demand on the clonal expansion capacity of T-cells. However, a massive and rapid T-cell clonal expansion might be needed after contracting SARS-CoV-2 infection.
Source:
https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(21)00306-6/fulltext
 
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BillTre said:
It sounds like a kind of genetic screen for mutations, where chunks of a chromosome are systematically deleted and a particular phenotype is checked for mutant effects, except it is limited to the ends of the chromosomes. People do this in Drosophila, for example.
Short telomeres have also an advantage:
Telomere shortening protects against cancer
...
“The data show that if you’re born with long telomeres, you are at greater risk of getting cancer, ” says de Lange.
Source:
https://www.rockefeller.edu/news/29625-telomere-shortening-protects-cancer/
 
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