To find out exactly what caused this resistance to the virus, the scientists then incubated bags containing the virus and photographed them under a microscope. They found that the virus gets stuck to receptors on the surface of the vesicles — trapping them and making it impossible for them to infect cells. In other words, the vesicles act as a kind of decoy. “Because the receptors on the vesicles are the same as those on the cells, most viruses bind to the vesicles and are destroyed before they reach the cells,” Bleier said.
In addition, the scientists also found that the stimulated vesicles contained higher amounts of microRNAs—small RNA strands—previously known to have antiviral activity.
Ultimately, the scientists wanted to see how a small temperature change could affect the quality and quantity of the secretory vesicles. To create a food-based human nose simulation, they used small pieces of mucosal tissue extracted from the noses of several patients and placed those tiny tissues, called implants, into cell culture. They then lowered the temperature from 37 to 32 degrees Celsius, stimulated TLR3 regulatory tissue, and collected secretory vesicles.
They found that cold reduces the tissue’s ability to secrete vesicles by 42 percent, and that those vesicles have 77% fewer receptors that allow them to bind to and neutralize the virus. “Even with a drop of 5 degrees for 15 minutes, it led to a really significant difference,” says Amiji.
Noam Cohen, an otolaryngologist at the University of Pennsylvania, says the work sheds light on how the virus spreads more easily in cold weather. (Cohen is not involved in this work, but previously mentored Bleier when he was a medical student.) “What this paper is demonstrating is that viruses, although they are extremely simple, but extremely cunning,” he said. “They optimized cooler temperatures for replication.”
Jennifer Bomberger, a microbiologist and immunologist at Dartmouth College, says one of the interesting points of the study is how “vesicles don’t just educate immunity,” meaning they don’t just transport transfer the instructions of the immune system. Instead, she continued, “they’re actually doing some real anti-virus on their own by binding to the virus.” However, she notes that looking at mucus from patients with real infections (rather than using virus simulations) could provide more insight into how these infections work. this blister.
The behavior of these blisters isn’t the only reason upper respiratory infections peak in winter. Before job have shown that colder temperatures also reduce the activity of antiviral molecules in the immune system called interferons. Viruses also tend to spread when people move around in the home. Social distancing during the pandemic is also likely to leave people with less immunity to the viruses that cause influenza and RSV, both of which are part of the “translate three times” that emerge this winter.
Still, Amiji says understanding exactly how the blisters change could lead to some interesting ideas for therapies — because perhaps scientists can control those changes. He envisions it as “hacking” the “tweet” bag. “How can we increase the levels of these antiviral mRNAs or other molecules to have a positive effect?” he asks.
Before the Covid-19 pandemic, the team notes that there was a practical, real-world way to help your nose protect you in cold weather: Wearing a mask. The nose can fit snugly and warmly under a mask—something any glasses wearer whose lenses are foggy from hot breath can attest. “Wearing a mask can have a dual protective role,” says Bleier. “One is to definitely block the physical breathing of [viral] particles, but also by maintaining a local temperature, at least relatively higher than that of the external environment.”
And here’s another idea to consider: Maybe it’s time to take a vacation somewhere warm.
