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To find out what exactly caused this antiviral ability, the scientists then incubated the vesicles with viruses and imaged them under a microscope. They found that the viruses were trapped in receptors on the surface of the vesicles – making it impossible for them to catch on and infect cells. In other words, vesicles act as a form of decomposition. “Because vesicles have the same receptors as cells, most viruses bind to the vesicles and are killed before they reach the cells,” says Bleier.
In addition, the scientists found that the induced vesicles contained high levels of microRNA—small strands of RNA—previously known to have antiviral activity.
Finally, the scientists wanted to see how a small temperature change might affect the quality and quantity of secretory vesicles. To create a dish-based replica of the human nose, they used small pieces of mucosal tissue extracted from the noses of a few patients and placed those small pieces of tissue, called explants, in cell culture. They then lowered the temperature to 37 to 32°C, stimulated the tissue to upregulate TLR3, and collected the secretory vesicles.
They found that the common cold caused a 42 percent drop in the tissue’s ability to secrete vesicles, and those vesicles had 77 percent fewer receptors that allow them to bind and neutralize the virus. “Even with that 5-degree drop for 15 minutes, it really made a dramatic difference,” Amiji says.
Noam Cohen, an otorhinolaryngologist at the University of Pennsylvania, says the work sheds light on the dynamics of how viruses spread more easily in cold weather. (Cohen was unrelated to the work, but had previously mentored Bleier when he was a medical student.) “What this paper demonstrates is that viruses are incredibly simple, but they’re also incredibly tricky,” he says. “They’ve evolved colder temperatures to replicate.”
Jennifer Bamberger, a microbiologist and immunologist at Dartmouth College, says one of the interesting points of the study is that “vesicles are not just immuno-educational,” meaning they don’t just carry immune system instructions. Instead, he continues, “they actually exerted some real antiviral effects by binding to the virus.” However, he notes that looking at mucus from patients with real infections (rather than using a virus-mimic) might provide more insights into how these vesicles work.
The behavior of these vesicles is not the only reason why upper respiratory infections peak in winter. previous Work Cold temperatures have been shown to reduce the work of immune system antiviral molecules called interferons. Viruses also spread when people go indoors. Social distancing during pandemics has left people with less immunity to the viruses that cause influenza and RSV.Triple” That Emerged this winter.
However, Amiji says that understanding how the vesicles change could lead to some interesting ideas for treatment — because scientists can control those changes. He visualises it as vesicle “tweeting” “hacking”. “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 protect your nose in cold weather: masking. Nosepieces can be snug and comfortable under a mask—any goggle-wearer can make sure the fog is sealed off from their hot breath. “Wearing masks may have a dual protective role,” says Bleier. “One certainly prevents the body from inhaling [viral] particles, but by maintaining a local temperature, at least relatively higher than the external environment
And here’s an idea to consider: Maybe it’s time for a vacation somewhere warm.
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