Model finds key for COVID-19 deaths in the elderly

A person’s ability to fight COVID-19, like other infections, depends to a large extent on the ability of their immune system to replicate the immune cells that are effective in destroying the SARS-CoV-2 virus. that causes the disease.

These cloned immune cells can not be produced indefinitely, and an important hypothesis of a new University of Washington study is that the body’s ability to make these cloned cells decreases significantly with age.

This genetically predetermined limit on your immune system may be the key to why COVID-19 has such a devastating effect on the elderly, according to a model created by UW research professor James Anderson.

“When DNA splits into cell division, the end cap – called a telomere – becomes a little shorter with each division,” said Anderson, who is a model of biological systems at the School of Aquatic and Fisheries Sciences.

“After a series of replications of a cell, it becomes too short and the further distribution stops. Not all cells or all animals have this limit, but immune cells in humans have this cell life.

The average person’s immune system is doing quite well despite this limit up to about 50 years old. This is when enough nuclear immune cells, called T cells, have shortened telomeres and cannot quickly clone themselves via cellular division in large enough numbers to attack and eradicate the COVID-19 virus, which has the property of sharply reducing immune cells numbers, Anderson said.

Importantly, he said, telomere lengths are inherited from your parents. As a result, there are some differences in these lengths between people at any age, such as how old a person gets before these lengths are most commonly used.

Anderson said the main difference between this notion of aging, which has a threshold for when your immune system has run out of collective telomere length, and the idea that we are all consistently aging over time is the “most exciting “discovery of his research.

“Depending on your parents and very little on how you live, your longing or, as our paper claims, your reaction to COVID-19 is a function of who you were when you were born, what a kind of is a big problem, “he said.

To build this model, the researchers used publicly available data on COVID-19 mortality from the Center for Disease Control and the U.S. Census Bureau, and studies on telomeres, many of which were published by the co-authors over the past two decades.

Gathering telomere length information about a person or specific demographic, he said, could help doctors know who was less sensitive. And then they could allocate resources, such as boostershots, according to which populations and individuals may be more sensitive to COVID-19.

“I’m a model and I see things through mathematical equations that I interpret by working with biologists, but biologists have to look at the information through the model to guide their research questions,” Anderson said.

“The dream of a model is to actually influence the great biologists to think like model workers. That’s harder, “he added.

One caution he has about this model is that it may explain too much.

“There is a lot of data that supports every parameter of the model and there is a pretty logical thought for how you get from the data to the model,” he said.

“But it is so simple and so intuitively appealing that we should also be suspicious of it. As a scientist, my hope is that we begin to further understand the immune system and the reactions of the population as part of natural selection.

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Model finds key for COVID-19 deaths in the elderly

Source link Model finds key for COVID-19 deaths in the elderly

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