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 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.

Here are a few The world was worried about monkeypox becoming the next pandemic for several weeks during this summer. At the peak in early August the US was recording 600 cases a day, and the health authorities’ fumbling response echoed the early days of Covid-19. Vaccines were slow to arrive and in short supply for most of the fall. Testing was bottlenecked. Antiviral drugs, though they existed, were almost unobtainable because they hadn’t been federally authorized for the disease. Although most of the cases involved gay or bisexual men and can last for weeks, it was possible that this rarely fatal, but sometimes very painful, infection could spread to other people. 

The world is very different today, at least temporarily. The spread of mpox had slowed dramatically by mid-December. The US, which had recorded 29,740 cases as of December 21—more than a third of the global total—was registering barely a handful each day. 

One reason was that vaccines were more readily available and that testing proved to be easier. Another is that Covid is much harder to pass than mpox. But the most important, according to most, is the fact that those most at-risk took control of their safety in the early weeks, when authorities were struggling. “The success was the community mobilization,” says Joseph Osmundson, a queer activist, molecular microbiologist, and clinical assistant professor at New York University.

Osmundson assisted in brokering what may be considered a symbol for the response to mpox. A fleet of white-painted vans, with privacy-masked windows, was assembled by Osmundson. The vans contained mobile clinics for vaccines, which were operated by New York City’s health department. These vans were parked at night in bars, clubs, and other establishments that cater to bisexual and gay men between Labor Day and Thanksgiving. Many parties that were held there were shut down for some time. According to the queer community, the location owners were able to identify the most vulnerable areas and agreed to park the vans outside. More than 3000 doses were administered by the van vaccination program.

The program showed a health department being smart about where to find people who needed help, but just as much, it represented a community that wasn’t willing to wait for the health bureaucracy to find them. Gay and bi men, as well as other members of the queer community, reached out to each other, badgered and agitated from the very beginning. Some who had caught the disease posted online videos or gave press interviews describing their symptoms in intimate detail, defying the risk of social shaming (“He caught monkeypox, guess what he’s been up to”) to warn others about the risks. Information was shared via WhatsApp and social media about the availability of vaccines at clinics. how to When most doctors hadn’t seen any cases of mpox, they were able to diagnose the patient. The few who received antiviral therapies before they became generally available were given advice to share with their doctor about how to navigate the bureaucratic maze that is required to authorise an individual.

Most everyone is unanimous in their belief that gay men with many sexual partners are responsible for the decline in ski slope cases. As research by the US Centers for Disease Control and Prevention demonstrated in the fall, men who felt at risk voluntarily abstained from sex, kept to one or a small number of partners, signed out of hook-up apps, or skipped the kind of parties where group sex happens.