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Faulty gene can turn colds deadly for babies, toddlers

Rare variants hurt ability to detect, fight viruses

2:45pm, May 13, 2016
sick child

UNEASY BREATHING  Some children have rare genetic variants that can turn their first encounter with colds and other respiratory viruses deadly.

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COLD SPRING HARBOR, N.Y. — A faulty virus-sensing gene can make the common cold or respiratory syncytial virus deadly for babies and toddlers, a new study suggests.

Almost all children catch those viruses by age 2 or 3 years. Most kids quickly clear the viruses, but about one in 1,000 are admitted to the intensive care unit with severe pneumonia. The reason some tykes get really sick is in their genes, Samira Asgari, a computational biologist at the Swiss Federal Institute of Technology in Lausanne reported May 12 at the Biology of Genomes conference.

Asgari and colleagues examined protein-coding DNA of 120 otherwise healthy toddlers and babies who ended up on respirators because of colds or RSV infections. Eight had one of three rare variants in the IFIH1 gene that cause the protein that the gene produces to be shorter than normal. That affects the protein’s ability to detect double-stranded RNA made by some viruses and turn on virus-fighting defenses. As a result, the viruses can replicate better than normal, Asgari found.

Children who carry the variants have a harder time combating a first-time virus infection. If a child survives, the immune system learns to fight the virus by other means, Asgari said. The team also found mutations in other genes that may account for why other children get severely ill from common respiratory viruses.


S. Asgari et al. Loss-of-function mutations in IFIH1 predispose to severe viral respiratory infections in children. Biology of Genomes, Cold Spring Harbor, N.Y., May 12, 2016.

Further Reading

L. Sanders. Gene behavior distinguishes viral from bacterial infections. Science News. Vol. 189, January 23, 2016, p. 6.

B. Mole. Common lung infection suffocates with single protein. Science News Online, April 8, 2014.

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