Genetic restrictions on cell division may be the cause of death in older adults after contracting COVID-19
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Genetic restrictions on cell division may be the cause of death in older adults after contracting COVID-19
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Genetic restrictions on cell division may be the cause of death in older adults after contracting COVID-19
Like any infection, the body’s immune system’s ability to fight COVID-19 is largely dependent on its ability to replicate immune cells that are effective at destroying the SARS-CoV-2 virus that causes the disease.
While these cloned immune cells cannot be created indefinitely, a new study from the University of Washington (UW) proposes a key hypothesis that the body’s ability to create these cloned cells declines markedly in old age.
According to a new model created by UW research professor James Anderson, this genetically predetermined restriction on the body’s immune system may be the key to COVID-19’s devastating effects on older adults. Anderson is the lead author of a paper published March 31 in The Lancet eBioMedicine detailing this model link between aging, COVID-19 and mortality.
Anderson points out that when DNA divides in cell division, the telomeres get shorter with each division, “after a cell goes through a series of replications, it becomes too short and stops dividing further. Not all cells Or all animals have this limitation, but human immune cells have this cellular longevity.” It is reported that Anderson is a biological systems modeler at the School of Aquatic and Fishery Sciences (School of Aquatic and Fishery Sciences).
Despite this limit, the average person’s immune system is well maintained until about age 50. That’s when enough of the core immune cells, or T cells, have shortened telomeres, and they can’t clone themselves quickly enough through cell division to attack and clear the COVID-19 virus — which has a dramatic Features that reduce the number of immune cells.
Additionally, Anderson added, importantly, telomere length is inherited from parents. So there are some differences in these lengths between people of each age group.
Anderson points out that the key difference between this understanding of aging—that is, there is a threshold for when the immune system runs out of collective telomere length—and the idea that all humans age over time is the most important difference in his research. Exciting discovery.
To build the model, the researchers used publicly available data on COVID-19 mortality from the U.S. Centers for Disease Control and the U.S. Census Bureau, as well as studies on telomeres.
Combining telomere length information about a person or a specific group of people could help doctors know who is less susceptible, Anderson said. They can then allocate resources such as boosters based on which groups and individuals may be more vulnerable to COVID-19.
“I’m a modeler who sees problems through mathematical equations, and I work with biologists to explain, but biologists need to see information through models to guide their research problems,” Anderson said. A modeler’s dream is Can really influence great biologists to think like modelers. But it’s harder.”
In addition, Anderson has a caveat about the model: “There’s a lot of data supporting every parameter of the model, and there’s a good logical idea of how you can model the model from the data. But it’s so simple, so intuitively appealing. , so much so that we should be skeptical of it too. As a scientist, I hope we start to learn more about the immune system and herd response as part of natural selection.”
(source:internet, reference only)
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