• HOME
  • NEWS
    • BIOENGINEERING
    • SCIENCE NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • FORUM
    • INSTAGRAM
    • TWITTER
  • CONTACT US
Wednesday, May 18, 2022
BIOENGINEER.ORG
No Result
View All Result
  • Login
  • HOME
  • NEWS
    • BIOENGINEERING
    • SCIENCE NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
        • Lecturer
        • PhD Studentship
        • Postdoc
        • Research Assistant
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • FORUM
    • INSTAGRAM
    • TWITTER
  • CONTACT US
  • HOME
  • NEWS
    • BIOENGINEERING
    • SCIENCE NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
        • Lecturer
        • PhD Studentship
        • Postdoc
        • Research Assistant
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • FORUM
    • INSTAGRAM
    • TWITTER
  • CONTACT US
No Result
View All Result
Bioengineer.org
No Result
View All Result
Home NEWS Science News Chemistry

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

Bioengineer by Bioengineer
May 6, 2022
in Chemistry
0
Share on FacebookShare on TwitterShare on LinkedinShare on RedditShare on Telegram

Your immune system’s ability to combat COVID-19, like any infection, largely depends on its ability to replicate the immune cells effective at destroying the SARS-CoV-2 virus that causes the disease. These cloned immune cells cannot be infinitely created, and a key hypothesis of a new University of Washington study is that the body’s ability to create these cloned cells falls off significantly in old age.

Illustration of model finding

Credit: Michele Kellett and James Anderson/University of Washington

Your immune system’s ability to combat COVID-19, like any infection, largely depends on its ability to replicate the immune cells effective at destroying the SARS-CoV-2 virus that causes the disease. These cloned immune cells cannot be infinitely created, and a key hypothesis of a new University of Washington study is that the body’s ability to create these cloned cells falls off significantly in old age.

According to a model created by UW research professor James Anderson, this genetically predetermined limit on your immune system may be the key to why COVID-19 has such a devastating effect on the elderly. Anderson is the lead author of a paper published March 31 in The Lancet eBioMedicine detailing this modeled link between aging, COVID-19 and mortality. 

“When DNA split in cell division, the end cap — called a telomere — gets a little shorter with each division,” explains Anderson, who is a modeler of biological systems in the School of Aquatic and Fishery Sciences. “After a series of replications of a cell, it gets too short and stops further division. Not all cells or all animals have this limit, but immune cells in humans have this cell life.” 

The average person’s immune system coasts along pretty good despite this limit until about 50 years old. That’s when enough core immune cells, called T cells, have shortened telomeres and cannot quickly clone themselves through cellular division in big enough numbers to attack and clear the COVID-19 virus, which has the trait of sharply reducing immune cell numbers, Anderson said. Importantly, he added, telomere lengths are inherited from your parents. Consequently, there are some differences in these lengths between people at every 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 for when your immune system has run out of collective telomere length, and the idea that we all age consistently over time is the “most exciting” discovery of his research.

“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.”  

Co-authors include Ezra Susser, Mailman School of Public Health, Columbia University; Konstantin Arbeev and Anatoliy Yashin, Social Science Research Institute, Duke University; Daniel Levy, National Heart, Lung, and Blood Institute, National Institutes of Health; Simon Verhulst, University of Groningen, Netherlands; Abraham Aviv, New Jersey Medical School, Rutgers University.

###

For more information, contact Anderson at [email protected] 



Journal

EBioMedicine

DOI

10.1016/j.ebiom.2022.103978

Method of Research

Data/statistical analysis

Subject of Research

Cells

Article Title

Telomere-length dependent T-cell clonal expansion: A model linking ageing to COVID-19 T-cell lymphopenia and mortality

Article Publication Date

31-Mar-2022

Share12Tweet8Share2ShareShareShare2

Related Posts

Schematic illustration of common CLC superstructures and opposite-chirality-coexisted superstructures.

Pancharatnam–Berry phase reversal via opposite-chirality-coexisted superstructures

May 18, 2022
Derek T. Anderson and Matt Maschmann

How to build an ‘explainable AI’ framework to speed up the innovation process

May 17, 2022

SPIE-CLP journal Advanced Photonics announces annual best papers recognition

May 17, 2022

Meteorological mechanisms behind severe drought in southwestern China during spring 2021 differ from similar historical events

May 17, 2022

POPULAR NEWS

  • Weybourne Atmospheric Observatory

    Breakthrough in estimating fossil fuel CO2 emissions

    46 shares
    Share 18 Tweet 12
  • Hidden benefit: Facemasks may reduce severity of COVID-19 and pressure on health systems, researchers find

    44 shares
    Share 18 Tweet 11
  • Discovery of the one-way superconductor, thought to be impossible

    43 shares
    Share 17 Tweet 11
  • Sweet discovery could drive down inflammation, cancers and viruses

    42 shares
    Share 17 Tweet 11

About

We bring you the latest biotechnology news from best research centers and universities around the world. Check our website.

Follow us

Tags

Weather/StormsUrbanizationVaccinesVirusWeaponryUrogenital SystemVaccineZoology/Veterinary ScienceViolence/CriminalsVirologyUniversity of WashingtonVehicles

Recent Posts

  • Pancharatnam–Berry phase reversal via opposite-chirality-coexisted superstructures
  • Reliable diagnostics at the tip of your finger
  • Seafloor animal cued to settle, transformed by a bacterial compound
  • Tooth unlocks mystery of Denisovans in Asia
  • Contact Us

© 2019 Bioengineer.org - Biotechnology news by Science Magazine - Scienmag.

No Result
View All Result
  • Homepages
    • Home Page 1
    • Home Page 2
  • News
  • National
  • Business
  • Health
  • Lifestyle
  • Science

© 2019 Bioengineer.org - Biotechnology news by Science Magazine - Scienmag.

Welcome Back!

Login to your account below

Forgotten Password?

Retrieve your password

Please enter your username or email address to reset your password.

Log In
Posting....