The scientists incubated the virus-laden vesicles and examined them under microscope to determine what was going on. They found that the viruses got stuck to receptors on the vesicles’ surface—trapping them and rendering them incapable of infecting cells. The vesicles had been acting as decoys. “Because the same receptors are on the vesicles as are on the cells, most of the viruses get bound to the vesicle and killed before they ever get to the cells,” Bleier says. 

In addition, the scientists also found that the stimulated vesicles contained higher quantities of microRNA—small strands of RNA—previously known to have antiviral activity.

Scientists wanted to find out how small changes in temperature might alter the amount and quality of the secreted Vesicles. To create a dish-based mimic of the human nose, they used small pieces of mucosal tissue extracted from a few patients’ noses and placed those little tissues, known as explants, into cell culture. They then lowered the temperature to 37 degrees Celsius and stimulated TLR3 to increase its regulation. Finally, they collected secreted vesicles.

They found that the cold caused a 42 percent drop in the tissues’ ability to secrete vesicles, and those vesicles had 77 percent fewer of the receptors that would let them bind to and neutralize a virus. “Even in that 5-degree drop for 15 minutes, it resulted in a really dramatic difference,” Amiji says. 

Noam Cohen, an otorhinolaryngologist at the University of Pennsylvania, says that this work sheds light on the mechanics of how viruses spread more easily in cold weather. Bleier was Bleier’s mentor when he was medical student, and Cohen was not affiliated with the work. “What this paper is demonstrating is that viruses, even though they’re incredibly simplistic, are incredibly crafty,” he says. “They’ve optimized a cooler temperature to replicate.”  

Jennifer Bomberger, a microbiologist and immunologist at Dartmouth College, says that one of the study’s interesting points was how the “vesicles weren’t just immune-education,” meaning they weren’t just ferrying immune system instructions. Instead, she continues, “they were actually carrying out some of the actual antiviral effects themselves by binding to the virus.” She notes, though, that looking at mucus from patients with real infections (rather than using a virus-mimic) might provide additional insights into how these vesicles work.

These vesicles’ behavior is not the only reason upper respiratory infections spike in winter. Previous work has shown that colder temperatures also diminish the work of immune system antiviral molecules called interferons. People who move inside are more likely to contract viruses. Social distancing during the pandemic has also potentially left people with less built-up immunity to the viruses that cause the flu and RSV, both part of the “tripledemic” that emerged this winter.  

Still, Amiji says that understanding exactly how the vesicles change could lead to some interesting ideas for therapies—because perhaps scientists can control those changes. He visualizes it as “hacking” the vesicle “tweets.” “How can we 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’s already a practical real-world way to help your nose defend you in cold weather: Masking. Noses can stay snug and cozy under a mask—as any glasses-wearer whose lenses have fogged from their warm breath can attest. “Wearing masks may have a dual protective role,” says Bleier. “One is certainly preventing physical inhalation of the [viral] particles, but also by maintaining local temperatures, at least at a relatively higher level than the outside environment.”

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