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.

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“How to Build a Life” is a column by Arthur Brooks, tackling questions of meaning and happiness. Click here to listen to his podcast series on all things happiness, How to Build a Happy Life.

I remember the night I fell in love.

The year was 1977, and I was 12 years old. A neighbor kid’s parents had bought an espresso machine—an exotic gadget in those days, even in Seattle. There was just one Starbucks in the world back then, and as luck had it, we lived within walking distance. The neighbor kid and I bought a pound of coffee and had about eight espressos each. Feeling fully alive and inspired to get closer to the universe, I climbed onto the roof of his house. In the process, I cut a gash in my stomach on his gutter. Bleeding profusely, I marveled at how intense the stars were.

Forty-five years later, not a day has gone by that I haven’t renewed my vows with the Bean. I’ve also come to understand how and why coffee captivates me.

Caffeine evolved in certain plants—including coffee shrubs, tea trees, cocoa beans, and kola nuts—as a naturally occurring pesticide to discourage insects from eating them. Stupid bugs. But that doesn’t explain why about 85 percent of Americans consume it in some form each day. (I can only assume that the other 15 percent have no quality of life whatsoever.) The reason is this: When caffeine is ingested, it quickly enters the brain, where it competes with a chemical called adenosine. One of adenosine’s most important jobs is to make you feel tired. Throughout the day, you produce a lot of it to make you eventually relax; neurons shoot it out, and then a receptor, perfectly sized to the adenosine molecule, binds to it, receiving the message that bedtime is approaching.

[From the April 2020 issue: Capitalism’s favorite drug]

That’s where caffeine comes in. It is shaped very similarly to the adenosine molecule, so it fits into the receptors. The adenosine can’t park where it’s supposed to, because caffeine is already sitting in its parking spots. (That “first sip feeling” Starbucks advertises on the side of its cups sounds a lot more appealing than “blocking morning adenosine,” but that’s what’s really happening.) In truth, caffeine doesn’t pep you up—it simply prevents you from feeling lethargic. Consume enough caffeine, and you’ll have almost no adenosine plugging into your receptors at all, so you’ll feel wired and jittery.

To get to what really matters, though: Coffee makes you happy. Writing in the journal Psychopharmacology, the researcher David M. Warburton observed what I could have told him without writing a study: A low dose of caffeine can lead to a “significant increase in … happiness and calmness and decreases in tenseness.” He also noted that, among the study participants, these effects did not come from alleviating a craving from a caffeine addiction; the effect was true, pure, and wonderful. A miracle, really.

[Read: The coffee alternative Americans just can’t get behind]

Caffeine is a gift in ways besides happiness. Combined with exercise, it can improve cognitive performance (that means it makes you smarter, in case you haven’t had your coffee yet), and if you’ve been sleeping less than optimally, it can enhance your reaction time and logical reasoning abilities. Remember this as you head out in traffic: The life your coffee saves could be your own.

It is no exaggeration to say that caffeine is a boon to humanity. As Michael Pollan argues in his audiobook Caffeine: How Coffee and Tea Created the Modern World, caffeine’s arrival into the European diet in the 17th century transformed the economy through enhanced productivity, innovation, and safety. If it weren’t for coffee, you would probably spend your days shivering in a dark cave, and die after getting a splinter. So don’t be an ungrateful wretch: If you like electricity, running water, and lifesaving medicines, give thanks for the miracle of caffeine.

Nothing in life is free, of course. Faced with the holy power of the Bean, adenosine’s malevolent forces fight back. As you consume more caffeine over time, adenosine receptors upregulate, increasing in number to accommodate the caffeine molecules and take in their intended guests as well. This leads to a state of tolerance, in which caffeine has a smaller effect after chronic use. However, this “problem” is really just an opportunity to enjoy more coffee.

[Read: The case for drinking as much coffee as you like]

Some people believe that the solution to tolerance is to hit the reset button. My wife is one of them: Recently, noticing the increases in my consumption over the years, she innocently proposed that I “take a little break” from coffee. The very suggestion made me fly into a rage. “Here’s an idea,” I replied, heart rate soaring. “Why don’t we just live apart for a year so it feels more like it did when we were first married?” An overreaction? I think not.

I’m at peace with the long-term effects of my devotion to coffee. Sure, my coffee habit is withering my hypothalamus and enervating my adrenal glands, forcing me to take in ever more caffeine as the years go by. But it is well worth it: Research from Japan shows that habitually drinking coffee reduces all-cause mortality. Studies in mice suggest that it does so by, among other things, encouraging autophagy, the biological process of cleaning out cellular trash, which naturally slows as we age. Coffee has also been found to reduce levels of fatty acid in the plasma of aged mice, which has been linked to diabetes and cancer in humans. (People say animal testing is cruel, but if it means giving mice tiny cups of coffee, I am all for it.)

Assuming that coffee does keep me alive for an extra few days or decades, I know how I’ll spend them: drinking more coffee, of darker and darker roasts, whose strong smell helps combat age-related loss of taste and smell. If Starbucks introduces a line of beans called “Indonesian Ashes,” I will be first in line to buy it.

[Read: The quest to make the best worst cup of coffee]

All the research aside, I have my own data on aging and coffee consumption. My Spanish mother-in-law, whom I loved like my own mother, died last summer at the age of 93. She was sharp as ever and the happiest person I knew, up to the very end. She also consumed multiple cups of coffee every day until her last. Our shared love of the Bean drew us together before we even spoke the same language, and sustained our relationship for more than three decades.

In her last weeks, I was lecturing in Barcelona and spending my free time with her, downing many cups and chatting about the secret to happiness. Here was her formula: el amor, la fe, y el café—love, faith, and coffee. In my unbiased opinion, that sounds exactly right.

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After three bleak years, the coronavirus pandemic is finally drawing to a close, but pandemics as a general threat very much are not. At the moment, the most pressing concern is H5N1, better known as bird flu. Public-health experts have worried for decades about the virus’s potential to spark a pandemic, and the current strain has been devastating global bird populations—not to mention spilling over into assorted mammalian hosts—for more than a year. But those worries became even more urgent in mid-October, when an outbreak of the virus on a Spanish mink farm seemed to show that the mink were not only contracting the disease but transmitting it.

Occasional spillover from birds to mammals is one thing; transmission among mammals—especially those whose respiratory tracts resemble humans’ as closely as minks’ do—is another. “I’m actually quite concerned about it,” Richard Webby, an influenza expert at St. Jude Children’s Research Hospital, told me. “The situation we’re in with H5 now, we have not been in before, in terms of how widespread it is, in terms of the different hosts it’s infecting.”

What’s hard to gauge at this point, Webby said, is the threat this spread poses to humans. That will depend on whether we can transmit the virus to one another and, if so, how efficiently. So far the risk is low, but that could change as the virus continues to spread and mutate. And the kind of research that some scientists say could allow us to get a handle on the danger is, to put it mildly, fraught. Those scientists think it’s essential to protect us from future pandemics. Others think it risks nothing less than the complete annihilation of humanity. Which way you feel—and how you think the world should approach pandemic preparedness as a whole—comes down to which type of pandemic you think we should be worried about.

The point of the research in question is to better understand pandemic threats by enhancing deadly viruses. This is done in a highly controlled laboratory setting, with the aim of better preparing for these pathogens out in the world. This type of science is often referred to as gain-of-function research. If that term sounds familiar, that’s probably because it has been invoked constantly in debates about the origins of COVID-19, to the point that it has become hopelessly politicized. On the right, gain-of-function is now a dirty word, inextricable from suspicions that the pandemic began with a lab leak at China’s Wuhan Institute of Virology, where researchers were doing experiments of just this sort. (Solid evidence points toward the competing theory: that the coronavirus jumped to people from animals. But a lab leak hasn’t totally been ruled out.)  

[Read: The lab-leak debate just got even messier]

As a category, gain-of-function actually encompasses a far broader range of research. Any experiment that genetically alters an organism so that it does something it didn’t before—that is, gains a function—is technically gain-of-function research. All sorts of experiments, including many of those used to produce antibiotics and other drugs, fall into this category. But the issue people fret about is the enhancement of pathogens that, if released into the world, could conceivably kill millions of people. When you put it that way, it’s not hard to see why this work makes some people uncomfortable.

Despite the inherent risks, some virologists told me, this sort of research is crucial to preventing future pandemics. “If we know our enemy, we can prepare defenses,” the Emory University virologist Anice Lowen told me. The research enables us to pinpoint the specific molecular changes that allow a virus capable of spreading among animals to spread among humans; our viral surveillance efforts can then be targeted to those adaptations in the wild. We can get ahead on developing countermeasures, such as vaccines and antivirals, and ascertain in advance how a virus might evolve to circumvent those defenses.

This is not merely hypothetical: In the context of the bird-flu outbreak, Lowen said, we could perform gain-of-function experiments to establish whether the adaptations that have allowed the virus to spread among mink enhance its ability to infect human cells. In fact, back in 2011, two scientists separately undertook just this sort of research, adapting H5N1 to spread among ferrets, whose respiratory tract closely resembles our own. The research demonstrated that bird flu could not only spill over into mammalian hosts but, under the proper circumstances, pass between mammalian hosts—just as it now seems to be doing—and perhaps even human ones.

[Read: Will the world’s most worrying flu virus go pandemic?]

The backlash to this research was swift and furious. Critics—and there were many—charged that such experiments were as likely to start a pandemic as to prevent one. Top flu researchers put a voluntary moratorium on their work, and the National Institutes of Health later enacted a funding moratorium of its own. With the imposition of stricter oversight regimens, both eventually lifted and the furor subsided, but researchers did not race to follow up on the two initial studies. Those follow-ups could have given us a better sense of the likelihood that H5N1 might develop the ability to transmit between humans, Angela Rasmussen, a virologist at the Vaccine and Infectious Disease Organization in Saskatchewan, Canada, told me. “That moratorium really did have a big chilling effect,” she said. “We haven’t really been looking at the determinants of mammal-to-mammal transmission, and that’s the thing that we really need in order to understand what the risk is to the human population.”

The controversy over the origins of the coronavirus pandemic has renewed calls for gain-of-function bans—or at least additional oversight. Last month, the National Science Advisory Board for Biosecurity delivered a set of recommendations that, if adopted, would tighten regulations on all sorts of virology research. Piled on top of more widespread anti-science rhetoric throughout the pandemic, the recommendations have contributed to a sense of embattlement among virologists. The advisory board is “responding to a lot of hyperbole without any real evidence,” Seema Lakdawala, a flu-transmission expert at Emory University, told me.

[Read: The pro-Trump culture war on American scientists]

But other researchers—those more on the “fear the annihilation of humanity” side of the aisle—see the recommendations as progress, important if not anywhere near sufficient.   “Laboratory accidents happen,” Richard Ebright, a molecular biologist at Rutgers University who earlier this month co-founded an anti-gain-of-function biosecurity nonprofit, told me. “They actually happen on a remarkably frequent basis.” The 1977 flu pandemic, which killed roughly 700,000 people, may well have started in a laboratory. Anthrax, smallpox, and other influenza strains have all leaked, sometimes with deadly consequences. The original SARS virus has done so too—several times, in fact, since its natural emergence in 2003. And we might never know for sure how the coronavirus pandemic began. (This lack of definitive evidence has not stopped Ebright from tweeting that NIH officials potentially share the blame for the millions of deaths COVID-19 has caused worldwide.)

To researchers in this camp, the benefits of experimenting with such dangerous pathogens simply do not justify the risks. Sure, identifying mutations that could lead to transmissibility among humans might be marginally beneficial to our surveillance efforts, Kevin Esvelt, an evolutionary biologist at MIT, told me, but viruses can make that jump via innumerable genetic pathways, and the odds of our hitting on one that’s ultimately relevant are tiny. In the case of bird flu, researchers told me, the mutations that appear to have made the virus transmissible among mink are not the mutations identified in the 2011 studies. This sort of research, Ebright said, “has existential risk, but effectively no benefit or extremely marginal benefit.”

Huge numbers of lives are at stake. The world has just lost millions to the coronavirus. Imagine the same again, or even much worse, due to our own folly. Even if we managed to swiftly contain an outbreak, Esvelt worries, the mere perception of a lab leak could irreparably damage the public trust and lead people to question far safer pandemic precautions. More doubts, more deaths. “‘Double or nothing’ doesn’t even begin to describe it,” Esvelt told me. “I’m just not comfortable risking so much of the biomedical enterprise on that toss of the dice.”

[Read: The lab-leak theory meets its perfect match]

But a lab leak isn’t Esvelt’s main concern. What really worries him is bioterrorism. Imagine that researchers identify a pandemic-capable virus and share its genome sequence, as well as all the information necessary to replicate it, with the scientific community. Other scientists begin developing countermeasures, but now hundreds or even thousands of people have the ability to make something with the potential to kill millions; it’s not exactly a well-kept secret. Someone goes rogue, replicates the virus, releases it in an international-airport terminal, and, just like that, you’ve got a pandemic. Esvelt compares the danger to that of nuclear proliferation; in his view, nothing else comes close in sheer destructive capacity.

Part of what’s so tricky about this whole debate is that, unlike most competing public-health priorities, the question of whether to conduct this research is inherently zero-sum, in the sense that we can’t have it both ways. If we do the research and publish the results, we might improve our chances of preventing natural pandemics, but we necessarily create a security risk. If we don’t do the research, we don’t create the security risk, but we also don’t reap the preventive benefits. We have to choose.

To do so with any degree of certainty, Esvelt told me, we’d need to put hard numbers to the risks and benefits of bringing a dangerous pathogen into a lab. So far, he said, few people have done that math. Plenty of researchers, he thinks, may not even realize the trade-off exists: “If you’re the kind of person that has dedicated your life to working in comparative obscurity on a shoestring budget, trying to prevent a calamity with no real hope of reward or recognition, the very possibility that humans could be malevolent enough to deliberately cause the catastrophe that you fear—honestly, I think they’re such good people that it just never occurs to them.”

[Read: The next pandemic could start with a terrorist attack]

The gain-of-function proponents I spoke with were by no means naive to the threat of bioterrorism. “It’s both presumptuous and patronizing to suggest that biosecurity risks never occur to virologists,” Rasmussen said. She pointed out that lab members undergo background checks and receive regular training on mitigating security risks (blackmail, extortion, etc.). Excessive oversight poses its own threat, her camp argues. The risk, Lowen told me, is that we “lose the war against infectious diseases by winning a battle on research safety.” “There is a great threat out there from nature,” she said. “Relative to that, the threat from laboratory accidents is small.”

Regardless of who’s right, Esvelt’s broader point is a good one: How you feel about this research—and which kind of pandemic worries you most—is, in the end, a question of how you feel about human nature and nature nature and the relation between the two. Which should we fear more—our world or ourselves?

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