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.

The metaphor for changing is powerful. But when it comes to the future and how we want to change, we can find many models in the natural world. 

“What about the lowly cockroach or the lowly earwig?” says Jessica Ware, an associate curator of invertebrates at the American Museum of Natural History, rolling her eyes. (Or Imbler’s gum-leaf skeletonizer.) By some estimates, around  60 percent of all animals go through what scientists call holometabolism—a fancy word for reforming your entire body like butterflies do. Ladybugs, beetles, bees, lacewings, and flies all wrap themselves up and go through an incredible transformation. “You know, there’s a lot of really cool insects out there, but they get no press, they get no greeting cards. It’s all butterflies, butterflies, butterflies,” Ware says.

Stories of collaboration and transformation are common in the natural world. These stories are ones we can all likely learn from. 

For example, some sea slugs eat algae, and then extract the chloroplasts and make it into their own photosynthesis. Others sea slugs, which eat poisonous sponges, store the poison in their body to protect themselves. Spade sees this as a connection to Spade’s belief that groups could benefit from each other’s different attributes and skill sets. “We could all get skilled up, and we could gain the most interesting skills that various people in the group have brought.” For Dean, it’s a reminder that “we are each a very small part of something very big.”

For Liz Neeley, a science communicator and founder of the firm Liminal, it’s a giant, dorky-looking fish that offers a metaphor for change. She points to the mola mola—also known as the giant ocean sunfish. And giant is no overstatement—by the time they’re adults, these fish can weigh over 4,000 pounds. They are not born this large. When they’re born, they’re 3 millimeters long—about half the length of a grain of rice. The mola mola’s total body weight increases by 60 million over the course of their lives. That changes everything. “Your ability to perceive your environment, the things you find frightening, even how much effort it takes to move through water,” says Neeley. “At that size, water is heavy, it’s thick, it’s gloppy. You’re kind of swimming through syrup.”

That car-sized giant fish can now be seen swimming across the sea with an inkling of how it felt to be small and vulnerable as it fought against all the water. “I don’t know exactly what size I am as a fish,” says Neeley. “But I hope I can continue to build a practice of revisiting those core assumptions I have about myself in the world and what’s a threat to me and how I move through it.”

This is all because my podcast fundamentally, Flash forwardIt was all about transformation. Is it possible to make a difference in the future? How do we get to the tomorrows we want and not the ones we don’t? A key piece to that answer has to do the way that insects turn into goo. To get the future we desire, must we completely dissolve our bodies and world? Is it necessary to completely destroy the world and build new ones? Are we able to change slowly and incrementally? 

The life expectancy is Since the 1800s, the number of countries that perform best has increased by 3 months each year. Throughout most of human history, you had a roughly 50–50 chance of making it into your twenties, mainly due to deaths from infectious diseases and accidents. Thanks to medical advances, we’ve gradually found ways to avoid and treat such causes of death; the end result is perhaps humanity’s greatest ever achievement—we’ve literally doubled what it means to be human, increasing lifespans from 40 to 80 years. On the other hand, this has allowed one scourge to rise above all the others to become the world’s largest cause of death: aging.

Aging is now responsible for over two-thirds of deaths globally—more than 100,000 people every day. This is because, counterintuitive though it may sound, the chief risk factor for most of the modern world’s leading killers is the aging process itself: Cancer, heart disease, dementia, and many more health problems become radically more common as we get older. Although smoking and poor nutrition can all increase your risk for chronic diseases such as heart disease, diabetes, or other serious illnesses, these factors are minor in comparison to the effects of aging. High blood pressure increases the risk of having heart attacks by twofold, while being older than 40 makes your risk increase by ten. The number of deaths and suffering that aging causes will increase as the world population age.

But this isn’t my prediction—apart from being depressing, extrapolating a two-century trend for a further year is hardly groundbreaking. What’s far more exciting is that, in 2023, we may see the first drug that targets the biology of aging itself.

Scientists now have a good handle on what causes us to age, biologically speaking: The so-called “hallmarks” of the aging process range from damage to our DNA—the instruction manual within each of our cells—to proteins that misbehave because of alterations to their chemical structure. The best part is that we have now ideas about how to Treat them.

By the end of 2023, it’s likely that one of these ideas will be shown to work in humans. One strong contender is “senolytics,” a class of treatments that targets aged cells—which biologists call senescent cells—that accumulate in our bodies as we age. These cells seem to drive the aging process—from causing cancers to neurodegeneration—and, conversely, removing them seems to slow it down, and perhaps even reverse it.

In 2018, a 2018 study showed that mice treated with senolytic cocktails of quercetin and dasatinib, a cancer drug, not only lived longer but were also less likely to develop diseases such as cancer. They could even run faster and farther on tiny treadmills designed for mice.

Over two dozen companies are searching for ways to safely and effectively eliminate these senescent human cells. Unity Biotechnology is the largest company. It was founded by Mayo Clinic scientists and investors, including Jeff Bezos. They are currently testing a variety of senolytic medications against lung diseases such as macular degeneration, which can cause blindness, and lung fibrosis. There are many approaches under investigation, including small proteins that target senescent cells, vaccines to encourage the immune system to clear them out, and even gene therapy by a company called Oisín Biotechnologies, named after an Irish mythological character who travels to Tir na nÓg, the land of eternal youth.

Senolytics aren’t the only contenders, either: Others currently in human trials include Proclara Biosciences’ protein GAIM, which clears up sticky “amyloid” proteins, or Verve Therapeutics’ gene therapy to reduce cholesterol by modifying a gene called PCSK9. It is likely that the first anti-aging drug will target an individual age-related condition, not aging in general. We will soon be able to look at this goal if we see a drug which targets an aspect of aging through clinical trials.

These treatments may be the catalyst for the biggest medical revolution since the invention of antibiotics in 2023. Rather than going to the doctor when we’re sick and picking off age-related problems like cancer and dementia in their late stages when they’re very hard to fix, we’ll intervene preventively to stop people getting ill in the first place—and, if those treadmill-shredding mice are anything to go by, we’ll reduce frailty and other problems that don’t always elicit a medical diagnosis at the same time.