Biology

Genetic Limit on Cell Division Could Explain COVID-19 Deaths Among Elderly

This illustration represents the core theory in a new modeling study led by the University of Washington: The circles represent the immune system’s aging, in which its ability to make new immunity cells remains constant until a person (represented by the human figures) reaches middle- age or older and then falls off significantly. The central blue figure represents an immune system T cell that attacks the virus. Credit: Michele Kellett and James Anderson/University of Washington

Your immune system’s ability to fight[{” attribute=””>COVID-19, like any infection, largely depends on its ability to replicate the immune cells effective at destroying the

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“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, “which is kind of a big deal.”

To build this 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, he said, could help doctors know who was less susceptible. And then they could allocate resources, such as booster shots, according to which populations and individuals may be more susceptible to COVID-19.

“I’m a modeler and see things through mathematical equations that I am interpreting by working with biologists, but the biologists need to look at the information through the model to guide their research questions,” Anderson said, admitting that “the dream of a modeler is to be able to actually influence the great biologists into thinking like modelers. That’s more difficult.”

One caution Anderson has about this model is that it might explain too much.

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

Reference: “Telomere-length dependent T-cell clonal expansion: A model linking ageing to COVID-19 T-cell lymphopenia and mortality” by James J. Anderson, Ezra Susser, Konstantin G. Arbeev, Anatoliy I. Yashin, Daniel Levy, Simon Verhulst and Abraham Aviv, 31 March 2022, EBioMedicine.
DOI: 10.1016/j.ebiom.2022.103978

Co-authors include Ezra Susser, Mailman School of Public Health,

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