Maybe Mom was right all along.
Although generations of parents have warned their children that venturing into the cold without a hat will make them sick, scientists have long understood that viruses cause the common cold, and that they can strike in all seasons.
Now, however, new research suggests that cool temperatures may indeed play a role in fostering colds.
In a paper published this week in the Proceedings of the National Academy of Sciences, a group of Yale University researchers reported that cooler temperatures greatly inhibit the natural virus-fighting ability of cells in the nose — or at least in the noses of mice.
Rhinoviruses are the most frequent cause of the common cold, and they can also trigger asthma attacks. So in a series of experiments, researchers exposed the rodents to a special mouse-adapted rhinovirus and observed how the infection spread at different temperatures.
They discovered that when a virus invaded cells warmed to the normal body temperature of 98.6 degrees Fahrenheit, the cells fought back in prime fashion: Enzyme sensors within the cells detected the intruding rhinovirus, prompting the cells to emit an interferon alarm that alerted immune cells to the problem.
But things progressed very differently when they examined cells at cooler temperatures.
At 91 degrees, the virus replicated in a very “robust” fashion, the study authors found. It appeared the cells not only failed to detect the invading virus, but they also failed to release interferons.
“It was a double whammy,” said senior author Akiko Iwasaki, an immunobiologist at the Yale School of Medicine.
Iwasaki and her colleagues wrote that mouse cells in the lungs are at core body temperature, while temperatures are lower for cells in the nose. That raises the intriguing possibility that “inhaling cool air might diminish resistance to respiratory virus infections by lowering the temperature of potential host cells lining the nasal cavity.”
But just because something happens in mice doesn’t mean it will also happen in people.
UC Irvine microbiologist Bert Semler, who was not involved in the study, noted that the process of altering a rhinovirus so that it was adapted to mice might account for the fact that the cells responded differently at different temperatures.
Iwasaki conceded that the experiment was not proof that the mechanism applied to humans. She said she and her colleagues hoped soon to test their hypothesis on human cell lines.
“Obviously, mice are not humans,” Iwasaki said. “But now that we’ve got the basic understanding of this, we would love to know how it works in the human system.”
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