The ability of the immune system to fight COVID-19, like any infection, depends largely on its ability to replicate immune cells that are effective in killing the SARS-CoV-2 virus..

These cloned immune cells cannot be created indefinitely, and a key hypothesis from a new University of Washington study is that the body's ability to create these cloned cells declines significantly in old age.. The information was shared by the publication MedicalXpress.

According to a model created by UW research professor James Anderson, this genetically predetermined limit to your immune system may be the key to why COVID-19 is having such a devastating effect on older adults.. Anderson is the lead author of a paper published in the Lancet EBioMedicine that details this modeled association between aging, COVID-19 and mortality..

“When DNA is cleaved during cell division, the end cap, called the telomere, gets a little shorter with each division,” explains Anderson Michelle Kellett and James Anderson/University of Washington. – After a series of replications, the cell becomes too short and stops further division. Not all cells or all animals have this limit, but human immune cells have this kind of cellular life.”.

The average person's immune system holds up pretty well despite this limit, until about age 50.. That's when basic immune cells are enough Anderson says T cells have shortened telomeres and can't rapidly clone themselves by cell division in large enough numbers to attack and clear the COVID-19 virus, which has the property of drastically reducing immune cells.. It's important to note, he added, that telomere length is inherited from your parents.. Therefore, there are some differences in these lengths between people at each age, as well as how old a person becomes before these lengths are mostly used up..

Anderson said the key difference between this understanding of aging, which has a threshold when your immune system has exhausted its collective telomere length, and the idea that we all age sequentially over time, is the "

“Depending on your parents and very little on how you live, your longevity or, as our newspaper claims, your response to COVID-19 depends on who you were when you were born,” he said, “which is very.

To build this model, the researchers used publicly available data on COVID-19 deaths from the Centers for Disease Control and the US Census Bureau, as well as telomere studies, many of which were published by co-authors over the past two decades.. Gathering information about telomere length about an individual or a specific demographic can help doctors know who is less susceptible, he says.. And then they could allocate resources, like booster shots, whereby populations and individuals can be more susceptible to COVID-19..

One of Anderson's caveats about this model is that it can explain too much..

“There is a lot of data supporting every parameter of the model, and there is a good logical flow of thought about how you go from data to model,” he said of the power of the model.. “But it’s so simple and intuitively appealing that we should also be suspicious of it.”. As a scientist, my hope is that we will begin to better understand the immune system and population responses as part of natural selection.”.

medical-heal. en.