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Researchers at the University of Washington (UW) in the US noted that the immune system’s ability to combat COVID-19, like any infection, largely depends on the replication of the immune cells effective at destroying the SARS-CoV-2 virus that causes the disease.
The study, published recently in The Lancet biomedicine journal, suggests that the body’s ability to produce these cloned immune cells, which cannot be infinitely created, falls off significantly in old age.
”When DNA split in cell division, the end cap — called a telomere — gets a little shorter with each division,” said professor James Anderson, a modeler of biological systems at UW.
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The average person’s immune system coasts along pretty well despite this limit until about 50 years old, the researchers said.
That is when enough core immune cells, called T cells, have shortened telomeres and cannot quickly clone themselves through cellular division in big enough numbers to attack and clear the COVID-19 virus, which has the trait of sharply reducing immune cell numbers, they said.
According to Anderson, telomere lengths are inherited from parents.
There are some differences in these lengths between people at every age as well as how old a person becomes before these lengths are mostly used up.
”Depending on your parents and very little on how you live, your longevity or, as our paper claims, your response to COVID-19 is a function of who you were when you were born,” he said.
To build their model, the researchers used publicly available data on COVID-19 mortality from the Center for Disease Control and US Census Bureau and studies on telomeres, many of which were published by the co-authors over the past two decades.
Assembling telomere length information about a person or specific demographic could help doctors know who was less susceptible, the researchers said.
The doctors could allocate resources, such as booster shots, according to which populations and individuals may be more susceptible to COVID-19, they added.