Model finds COVID-19 deaths among elderly may be due to genetic limit on cell division

This comparison represents the basic principle in a new genetic engineering study led by the University of Washington: Circles represent the aging of the immune system, in which the ability to make new vaccines remains permanent until the person (who human represents) reaches the middle. age or age and then it falls sharply. The central blue pattern represents a virus or challenge to the immune system. Credit: Michele Kellett and James Anderson / University of Washington

The ability of your immune system to fight COVID-19, like any other infection, depends on its ability to make effective copies of the virus that destroys the SARS-CoV-2 virus that causes the disease. These infinite immune systems cannot be invented, and an important predictor of a new study by the University of Washington is that the body’s ability to produce these cloned cells falls sharply in old age.

According to a role model Created by UW research professor James Anderson immune system may be the main reason why COVID-19 has such a negative effect on the elderly. Anderson is the lead author of a paper published March 31 in Lancet eBioMedicine details this collaborative approach designed for aging, COVID-19 and mortality.

“When DNA is separated cell division, The endpoint — called the telomere — is slightly shorter with each region, “said Anderson, who is a biologist at the School of Marine Science and Fisheries. short and stops further distribution. Not all Cells “Or all animals have this limit, but the cells in humans have the same cell life.”

The average personThe body’s immune system works well despite this limit up to 50 years. That’s enough to reach the core antibiotics, called T cells, shortened the telomeres and could not carry themselves rapidly by dividing the cell in large quantities to attack and eliminate the COVID-19 virus, which has a tendency to reduce the number of bacteria, said Anderson. Importantly, he added, the telomere length is inherited from your parents. Therefore, there are some differences in these heights between people at any age and age before this length is used.

Anderson says the big difference between this understanding of aging, which has the door to when your immune system ends is the telomere length of the joint, and the idea that we are all getting older over time is “the most interesting” “find out his findings.

“It depends a little on your parents’ lifestyle, longevity or, as our paper claims, your response to COVID-19 is the work of who you were when you were born,” he said. kind. great thing. “

To construct this model the researchers used publicly available data on COVID-19 mortality from the US Centers for Disease Control and Prevention and the telomeres study, published by several authors in twenty years ago.

Combining long telomere data about a person or specific population, he said, could help doctors identify which one is less common. They can also isolate resources, such as stimulants, depending on how much the population and individuals are exposed to COVID-19.

“I am a calculator and I see things through my calculations that I translate by working with biologists, but biologists need to look at the data through the model to guide their research questions,” Anderson says, acknowledging that “someone else’s dream. modeler is to be able to make a real impact for the great biologists to think like designers. This is even more difficult.”

One of the great caveats that Anderson has on this model is that it can explain a lot.

“There is a lot of data that supports every model of design and there is a good thinking process for how you get from data to model,” says the strength of the model. “But it is a simple and interesting thing that we should not doubt about it either. As a scientist, my hope is to begin to understand the immune system and the public’s response as part of natural selection. ”

Co-authors include Ezra Susser, Mailman School of Public Health, Columbia University; Konstantin Arbeev and Anatoliy Yashin, Center for the Study of Social Sciences, Duke University; Daniel Levy, Heart of the Heart, Lung, and Blood Center, National Institutes of Health; Simon Verhulst, University of Groningen, Netherlands; Abraham Aviv, New Jersey School of Medicine, Rutgers University.

Studies have linked telomere length to death risk from COVID-19

Learn more:
James J. Anderson et al, T-cell clonal Dependence on Telomere Length: A mechanism that linked aging to COVID-19 T-cell lymphopenia and mortality, eBioMedicine (2022). DOI: 10.1016 / j.ebiom.2022.103978

hintModel detected COVID-19 mortality among the elderly may be due to genetic limitations on cell division (2022, May 7) retrieved 7 May 2022 from covid-deaths-elderly-due -genetic.html

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Model finds COVID-19 deaths among elderly may be due to genetic limit on cell division Source link Model finds COVID-19 deaths among elderly may be due to genetic limit on cell division

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