Why do you get sick in winter? blame your nose

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To figure out what exactly was causing this antiviral ability, the scientists then incubated the vesicles with the viruses and imaged them under a microscope. They found that the viruses stuck to receptors on the surface of the vesicles, trapping them and making them unable to infect cells. In other words, the vesicles acted as a sort of decoy. Because the same receptors are on the vesicles as on the cells, most viruses bind to the vesicle and are killed before they even reach the cells, Bleier says.

Additionally, the scientists also found that the stimulated vesicles contained higher amounts of microRNA, small strands of RNA previously known to have antiviral activity.

Finally, the scientists wanted to see how a small change in temperature could affect the quality and quantity of secreted vesicles. To create a flat-based mimic of the human nose, they used small pieces of mucous tissue taken from the noses of a few patients and placed these small tissues, called explants, in cell culture. Then they lowered the temperature from 37 to 32 degrees Celsius, stimulated the tissue to upregulate TLR3, and collected the secreted vesicles.

They found that the cold caused a 42% drop in the ability of tissues to secrete vesicles, and that these vesicles had 77% fewer receptors that would allow them to bind to a virus and neutralize it. Even in that 5 degree drop for 15 minutes, it made a really dramatic difference, Amiji says.

Noam Cohen, an otolaryngologist at the University of Pennsylvania, says the work sheds light on the mechanisms of easier virus spread in cold weather. (Cohen was not affiliated with this work, but had previously mentored Bleier when he was a medical student.) What this article demonstrates is that viruses, while incredibly simplistic, are incredibly cunning, he said. They optimized a colder temperature to replicate.

Jennifer Bomberger, a microbiologist and immunologist at Dartmouth College, says one of the interesting points of the study was how the vesicles weren’t just immune education, meaning they weren’t just carrying instructions from the immune system. Instead, she continues, they themselves achieved some of the actual antiviral effects by binding to the virus. She notes, however, that examining mucus from patients with real infections (rather than using a virus mimic) could provide additional information about how these vesicles work.

The behavior of these vesicles is not the only reason why upper respiratory tract infections peak during the winter. Previous work has shown that colder temperatures also decrease the work of antiviral immune system molecules called interferons. Viruses also tend to spread when people move indoors. Social distancing during the pandemic has also potentially left people with less developed immunity to the viruses that cause influenza and RSV, both part of the tripledemic that emerged this winter.

Still, Amiji says understanding exactly how the vesicles change could lead to interesting ideas for therapies, because maybe scientists can control those changes. He visualizes it as the hacking of the gall tweets. How to increase the content of these antiviral mRNAs or other molecules to have a positive effect? he asks.

In light of the Covid-19 pandemic, the team notes that there is already a practical and concrete way to help your nose defend you in cold weather: masking. Noses can stay toasty warm under a mask, as any eyeglass wearer whose lenses fog up from their hot breath can attest. Wearing masks can have a dual protective role, Bleier says. One is certainly to prevent the physical inhalation of the [viral] particles, but also by maintaining local temperatures, at least at a level relatively higher than the external environment.

And here’s another idea to consider: Maybe it’s just time for a vacation somewhere warm.

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