El límite genético en la división celular podría explicar las muertes por COVID-19 entre los ancianos

Esta ilustración representa la teoría central en un nuevo estudio de modelado dirigido por la Universidad de Washington: Los círculos representan el envejecimiento del sistema inmunitario, en el que su capacidad para producir nuevas células inmunitarias permanece constante hasta que una persona (representada por figuras humanas) alcanza la edad media. edad o mayor y luego se cae significativamente. La figura azul central representa una célula T del sistema inmunitario que ataca al virus. Crédito: Michele Kellet y James Anderson/Universidad de Washington

La capacidad de su sistema inmunitario para combatir[{” attribute=””>COVID-19, like any infection, largely depends on its ability to replicate the immune cells effective at destroying the


“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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