Bird flu, at this point, is somewhat of a misnomer. The virus, which primarily infects birds, is circulating uncontrolled around much of the world, devastating not just birds but wide swaths of the animal kingdom. Foxes, bobcats, and pigs have fallen ill. Grizzly bears have gone blind. Sea creatures, including seals and sea lions, have died in great numbers.

But none of the sickened animals has raised as much concern as mink. In October, a bird-flu outbreak erupted at a Spanish mink farm, killing thousands of the animals before the rest were culled. It later became clear that the virus had spread between the animals, picking up a mutation that helped it thrive in mammals. It was likely the first time that mammal-to-mammal spread drove a huge outbreak of bird flu. Because mink are known to spread certain viruses to humans, the fear was that the disease could jump from mink to people. No humans got sick from the outbreak in Spain, but other infections have spread from mink to humans before: In 2020, COVID outbreaks on Danish mink farms led to new mink-related variants that spread to a small number of humans.

As mammals ourselves, we have good reason to be concerned. Outbreaks on crowded mink farms are an ideal scenario for bird flu to mutate. If, in doing so, it picks up the ability to spread between humans, it could potentially start another global pandemic. “There are many reasons to be concerned about mink,” Tom Peacock, a flu researcher at Imperial College London, told me. Right now, mink are a problem we can’t afford to ignore.

For two animals with very different body types, mink and humans have some unusual similarities. Research suggests that we share similar receptors for COVID, bird flu, and human flu, through which these viruses can gain entry into our bodies. The numerous COVID outbreaks on mink farms during the early pandemic, and the bird-flu outbreak in Spain, gravely illustrate this point. It’s “not surprising” that mink can get these respiratory diseases, James Lowe, a veterinary-medicine professor at the University of Illinois at Urbana-Champaign, told me. Mink are closely related to ferrets, which are so well known for their susceptibility to human flu that they’re the go-to model for flu research.

Mink wouldn’t get sick as often, and wouldn’t be as big an issue for humans, if we didn’t keep farming them for fur in the perfect conditions for outbreaks. Many barns used to raise mink are partially open-air, allowing infected wild birds to come in contact with the animals, sharing not only air but potentially food. Mink farms are also notoriously cramped: The Spanish farm, for example, kept tens of thousands of mink in about 30 barns. Viral transmission would be all but guaranteed in those conditions, but the animals are especially vulnerable. Because mink are normally solitary creatures, they face significant stress in packed barns, which may further predispose them to disease, Angela Bosco-Lauth, a biomedical-sciences professor at Colorado State University, told me. And because they’re often inbred so their coats look alike, an entire population may share a similar genetic susceptibility to disease. The frequency of outbreaks among mink, Bosco-Lauth said, “may actually have less to do with the animals and more to do with the fact that we raise them in the same way … we would an intensive cattle farm or chickens.”

So far, there’s no evidence that mink from the Spanish farm spread bird flu to humans: None of the workers tested positive for the virus, and since then, no other mink farms have reported outbreaks. “We’re just not very susceptible” to bird flu, Lowe said. Our bird-flu receptors are tucked deep in our lungs, but when we’re exposed, most of the virus gets caught in the nose, throat, and other parts of the upper respiratory tract. This is why bird-flu infection is less common in people but is often pneumonia-level severe when it does happen. Indeed, a few humans have gotten sick and died from bird flu in the 27 years that the current strain of bird flu, known as H5N1, has circulated. This month, a girl in Cambodia died from the virus after potentially encountering a sick bird. The more virus circulating in an environment, the higher the chances a person will get infected. “It’s a dose thing,” Lowe said.

But our susceptibility to bird flu could change. Another mink outbreak would give the virus more opportunities to keep mutating. The worry is that this could create a new variant that’s better at binding to the human flu receptors in our upper respiratory tract, Stephanie Seifert, a professor at Washington State University who studies zoonotic pathogens, told me. If the virus gains the ability to infect the nose and throat, Peacock, at Imperial College London, said, it would be better at spreading. Those mutations “would worry us the most.” Fortunately, the mutations that arose on the Spanish mink farm “were not as bad as many of us worried about,” he added, “but that doesn’t mean that the next time this happens, this will also be the case.”

Because mink carry the receptors for both bird flu and human flu, they could serve as “mixing vessels” for the viruses to combine, researchers wrote in 2021. (Ferrets, pigs, and humans share this quality too.) Through a process called reassortment, flu viruses can swap segments of their genome, resulting in a kind of Frankenstein pathogen. Although viruses remixed in this way aren’t necessarily more dangerous, they could be, and that’s not a risk worth taking. “The previous three influenza pandemics all arose due to mixing between avian and human influenza viruses,” Peacock said.

While there are good reasons to be concerned about mink, it is hard to gauge just how concerned we should be—especially given what we still don’t know about this changing virus. After the death of the young girl in Cambodia, the World Health Organization called the global bird flu situation “worrying,” while the CDC maintains that the risk to the public is low. Lowe said “it’s certainly not very risky” that bird flu will spill over into humans, but is worth keeping an eye on. H5N1 bird flu is not new, he added, and it hasn’t affected people en masse yet. But the virus has already changed in ways that make it better at infecting wild birds, and as it spreads in the wild, it may continue to change to better infect mammals, including humans. “We don’t understand enough to make strong predictions of public-health risk,” Jonathan Runstadler, an infectious-diseases professor at Tufts University, told me.

As bird flu continues to spread among birds and in domestic and wild animal populations, it will only become harder to control. The virus, formally seasonal, is already present year-round in parts of Europe and Asia, and it is poised to do the same in the Americas. Breaking the chain of transmission is vital to preventing another pandemic. An important step is to avoid situations where humans, mink, or any other animal could be infected with both human and bird flu at the same time.

Since the COVID outbreaks, mink farms have generally beefed up their biosecurity: Farm workers are often required to wear masks and protective gear, such as disposable overalls. To limit the risk to mink—and other susceptible hosts—farms need to reduce their size and density, reduce contact between mink and wild birds, and monitor the virus, Runstadler said. Some nations, including Mexico, Ecuador, have recently embraced bird-flu vaccines for poultry in light of the outbreaks. H5N1 vaccines are also available for humans, though they aren’t readily available. Still, one of the most obvious options is to shut mink farms down. “We probably should have done that after SARS-CoV-2,” Bosco-Lauth, at Colorado State, said. Doing so is controversial, however, because the global mink industry is valuable, with a huge market in China. Denmark, which produces up to 40 percent of the world’s mink pelts, temporarily banned mink breeding in 2020 after a spate of COVID outbreaks, but the ban expired last month, and farms are returning, albeit in a limited capacity.

Mink are far from the only animal that poses a bird-flu risk to humans. “Frankly, with what we’re seeing with other wildlife species, there really aren’t any mammals that I would discount at this point in time,” Bosco-Lauth said. Any mammal species repeatedly infected by the virus is a potential risk, including marine mammals, such as seals. But we should be most concerned about the ones humans frequently come into close contact with, especially animals that are raised in high density, such as pigs, Runstadler said. This doesn’t pose just a human public-health concern, he said, but the potential for “ecological disruption.” Bird flu can be a devastating disease for wildlife, killing animals swiftly and without mercy.

Whether or not bird flu makes the jump into humans, it isn’t the last virus that will threaten us—or mink. The era we live in has become known as the “Pandemicene,” as my colleague Ed Yong has called it, one defined by the regular spillover of viruses into humans, caused by our disruption of the normal trajectories of viral movement in nature. Mink may never pass bird flu to us. But that doesn’t mean they won’t be a risk the next time a novel influenza or coronavirus comes around. Doing nothing about mink essentially means choosing luck as a public-health strategy. Sooner or later, it will run out.

In the early days of the pandemic, one of the scariest and most surprising features of SARS-CoV-2 was its stealth. Initially assumed to transmit only from people who were actively sick—as its predecessor SARS-CoV did—the new coronavirus turned out to be a silent spreader, also spewing from the airways of people who were feeling just fine. After months of insisting that only the symptomatic had to mask, test, and isolate, officials scrambled to retool their guidance; singing, talking, laughing, even breathing in tight quarters were abruptly categorized as threats.

Three years later, the coronavirus is still silently spreading—but the fear of its covertness again seems gone. Enthusiasm for masking and testing has plummeted; isolation recommendations have been pared down, and may soon entirely disappear. “We’re just not communicating about asymptomatic transmission anymore,” says Saskia Popescu, an infectious-disease epidemiologist and infection-prevention expert at George Mason University. “People think, What’s the point? I feel fine.”

Although the concern over asymptomatic spread has dissipated, the threat itself has not. And even as our worries over the virus continue to shrink and be shunted aside, the virus—and the way it moves between us—is continuing to change. Which means that our best ideas for stopping its spread aren’t just getting forgotten; they’re going obsolete.

[Read: A negative COVID test has never been so meaningless]

When SARS-CoV-2 was new to the world and hardly anyone had immunity, symptomless spread probably accounted for most of the virus’s spread—at least 50 percent or so, says Meagan Fitzpatrick, an infectious-disease transmission modeler at the University of Maryland’s School of Medicine. People wouldn’t start feeling sick until four, five, or six days, on average, after being infected. In the interim, the virus would be xeroxing itself at high speed in their airway, reaching potentially infectious levels a day or two before symptoms started. Silently infected people weren’t sneezing and coughing—symptoms that propel the virus more forcefully outward, increasing transmission efficiency. But at a time when tests were still scarce and slow to deliver results, not knowing they had the virus made them dangerous all the same. Precautionary tests were still scarce, or very slow to deliver results. So symptomless transmission became a norm, as did epic superspreading events.

Now, though, tests are more abundant, presymptomatic spread is a better-known danger, and repeated rounds of vaccination and infection have left behind layers of immunity. That protection, in particular, has slashed the severity and duration of acute symptoms, lowering the risk that people will end up in hospitals or morgues; it may even be chipping away at long COVID. At the same time, though, the addition of immunity has made the dynamics of symptomless transmission much more complex.

On an individual basis, at least, silent spread could be happening less often than it did before. One possible reason is that symptoms are now igniting sooner in people’s bodies, just three or so days, on average, after infection—a shift that roughly coincided with the rise of the first Omicron variant and could be a quirk of the virus itself. But Aubree Gordon, an infectious-disease epidemiologist at the University of Michigan, told me that faster-arriving sicknesses are probably being driven in part by speedier immune responses, primed by past exposures. That means that illness might now coincide with or even precede the peak of contagiousness, shortening the average period in which people spread the virus before they feel sick. In that one very specific sense, COVID could now be a touch more flulike. Presymptomatic transmission of the flu does seem to happen on occasion, says Seema Lakdawala, a virologist at Emory University. But in general, “people tend not to hit their highest viral levels until after they develop symptoms,” Gordon told me.

Coupled with more population-level immunity, this arrangement could be working in our favor. People might be less likely to pass the virus unwittingly to others. And thanks to the defenses we’ve collectively built up, the pathogen itself is also having more trouble exiting infected bodies and infiltrating new ones. That’s almost certainly part of the reason that this winter hasn’t been quite as bad as past ones have, COVID-wise, says Maia Majumder, an infectious-disease modeler at Harvard Medical School and Boston Children’s Hospital.

That said, a lot of people are still undoubtedly catching the coronavirus from people who aren’t feeling sick. Infection per infection, the risk of superspreading events might now be lower, but at the same time people have gotten chiller about socializing without masks and testing before gathering in groups—a behavioral change that’s bound to counteract at least some of the forward shift in symptoms. Presymptomatic spread might be less likely nowadays, but it’s nowhere near gone. Multiply a small amount of presymptomatic spread by a large number of cases, and that can still seed … another large number of cases.

[Read: You probably have an asymptomatic infection right now]

There could be some newcomers to the pool of silent spreaders, too—those who are now transmitting the virus without ever developing symptoms at all. With people’s defenses higher than they were even a year and a half ago, infections that might have once been severe are now moderate or mild; ones that might have once been mild are now unnoticeable, says Seyed Moghadas, a computational epidemiologist at York University. At the same time, though, immunity has probably transformed some symptomless-yet-contagious infections into non-transmissible cases, or kept some people from getting infected at all. Milder cases are of course welcome, Fitzpatrick told me, but no one knows exactly what these changes add up to: Depending on the rate and degree of each of those shifts, totally asymptomatic transmission might now be more common, less common, or sort of a wash.

Better studies on transmission patterns would help cut through the muck; they’re just not really happening anymore. “To get this data, you need to have pretty good testing for surveillance purposes, and that basically has stopped,” says Yonatan Grad, an infectious-disease epidemiologist at Harvard’s School of Public Health.

Meanwhile, people are just straight-up testing less, and rarely reporting any of the results they get at home. For many months now, even some people who are testing have been seeing strings of negative results days into bona-fide cases of COVID—sometimes a week or more past when their symptoms start. That’s troubling on two counts: First, some legit COVID cases are probably getting missed, and keeping people from accessing test-dependent treatments such as Paxlovid. Second, the disparity muddles the start and end of isolation. Per CDC guidelines, people who don’t test positive until a few days into their illness should still count their first day of symptoms as Day 0 of isolation. But if symptoms might sometimes outpace contagiousness, “I think those positive tests should restart the isolation clock,” Popescu told me, or risk releasing people back into society too soon.

[Read: People are fed up with rapid tests]

American testing guidelines, however, haven’t undergone a major overhaul in more than a year—right after Omicron blew across the nation, says Jessica Malaty Rivera, an infectious-disease epidemiologist at Boston Children’s Hospital. And even if the rules were to undergo a revamp, they wouldn’t necessarily guarantee more or better testing, which requires access and will. Testing programs have been winding down for many months; free diagnostics are once again growing scarce.

Through all of this, scientists and nonscientists alike are still wrestling with how to define silent infection in the first place. What counts as symptomless depends not just on biology, but behavior—and our vigilance. As worries over transmission continue to falter and fade, even mild infections may be mistaken for quiet ones, Grad told me, brushed off as allergies or stress. Biologically, the virus and the disease may not need to become that much more muted to spread with ease: Forgetting about silent spread may grease the wheels all on its own.