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Ah-choo: Tiny components in white blood cells could make a cold more likely

Andrew Russell | Tribune-Review
Sheldon Cohen, professor of psychology at Carnegie Mellon University, talks on Monday, February 18, 2013, about a study being published on Wednesday in the American Journal of Medicine linking genetics with a person's susceptibility to colds.

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Tuesday, Feb. 19, 2013, 4:00 p.m.
 

Tiny components of white blood cells can predict who is susceptible to catching a cold, according to a study led by a Carnegie Mellon University scientist and being published on Wednesday in the Journal of the American Medical Association.

Lead investigator Sheldon Cohen, a Carnegie Mellon researcher and psychology professor, joined experts from the University of Virginia, the University of California at San Francisco and Children's Hospital of Pittsburgh on the three-year project.

It found that the length of telomeres, the DNA-based caps at the end of chromosomes of white blood cells, can predict who will come down with a cold. In the study, those with shorter telomeres were more susceptible to the virus.

Prior research identified telomere length as an age-associated biological marker. Shorter telomeres in people older than 60 are associated with cancer, heart disease and various infectious diseases.

“Our work suggests telomere length is a relatively consistent marker across the lifespan, and that it can start predicting disease susceptibility in young adulthood,” Cohen said.

His interest in how stress affects the body led to the new study.

“We became interested in the idea that telomeres might be unique biopathways through which stress can influence disease outcome,” Cohen said.

Earlier research led by Elissa Epel, a University of California at San Francisco scientist who collaborated on this study, suggested stress resulted in shorter telomeres in healthy mothers taking care of chronically ill children.

Epel calls telomere length a kind of “canary in the coal mine.”

Short telomeres, she said, are not a marker of a specific disease, but one that “makes us vulnerable to disease.”

From 2008 to 2011, Cohen said researchers looked at 152 healthy adults, ages 18 to 55. After lab work and telomere measurements, participants were quarantined and exposed to a cold virus in a controlled setting.

“We extended our knowledge to suggest that telomere length might be important as far back as young adulthood and that age matters,” Cohen said. “For the youngest participants, the 18- to 22-year-olds, there is no association with telomere length. But it starts growing at age 22 and, by the time you are 35 to 40 years old, there is a substantial association (between susceptibility and telomere length).”

Cohen said the team's work is preliminary.

Epel said scientists before were not certain there was value in monitoring telomere length in young adults.

“We know that telomere length in mid-life predicts timing of disease onset decades later, and even early mortality, in a handful of studies. But whether it predicts how well our immune system is able to fight off infections — that has been a big question mark.”

Debra Erdley is a staff writer for Trib Total Media. She can be reached at 412-320-7996 or derdley@tribweb.com.

 

 

 
 


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