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Tag: disease

  • Deer Are Beta-Testing a Nightmare Disease

    Deer Are Beta-Testing a Nightmare Disease


    Scott Napper, a biochemist and vaccinologist at the University of Saskatchewan, can easily envision humanity’s ultimate doomsday disease. The scourge would spread fast, but the progression of illness would be slow and subtle. With no immunity, treatments, or vaccines to halt its progress, the disease would eventually find just about every single one of us, spreading via all manner of body fluids. In time, it would kill everyone it infected. Even our food and drink would not be safe, because the infectious agent would be hardy enough to survive common disinfectants and the heat of cooking; it would be pervasive enough to infest our livestock and our crops. “Imagine if consuming a plant could cause a fatal, untreatable neurodegenerative disorder,” Napper told me. “Any food grown within North America would be potentially deadly to humans.”

    This nightmare illness doesn’t yet exist. But for inspiration, Napper needs to look only at the very real contagion in his own lab: chronic wasting disease (CWD), a highly lethal, highly contagious neurodegenerative disease that is devastating North America’s deer, elk, and other cervids.

    Read: An incurable disease is coming for deer

    In the half century since it was discovered in a captive deer colony in Colorado, CWD has worked its way into more than 30 U.S. states and four Canadian provinces, as well as South Korea and several countries in Europe. In some captive herds, the disease has been detected in more than 90 percent of individuals; in the wild, Debbie McKenzie, a biologist at the University of Alberta, told me, “we have areas now where more than 50 percent of the bucks are infected.” And CWD kills indiscriminately, gnawing away at deer’s brains until the tissue is riddled with holes. “The disease is out of control,” Dalia Abdelaziz, a biochemist at the University of Calgary, told me.

    What makes CWD so formidable is its cause: infectious misfolded proteins called prions. Prion diseases, which include mad cow disease, have long been known as terrifying and poorly understood threats. And CWD is, in many ways, “the most difficult” among them to contend with—more transmissible and widespread than any other known, Marcelo Jorge, a wildlife biologist at the University of Georgia, told me. Scientists are quite certain that CWD will be impossible to eradicate; even limiting its damage will be a challenge, especially if it spills into other species, which could include us. CWD is already a perfect example of how dangerous a prion disease can be. And it has not yet hit the ceiling of its destructive potential.

    Among the world’s known infectious agents, prions are an anomaly, more like zombies than living entities. Unlike standard-issue microbes—viruses, bacteria, parasites, fungi—prions are just improperly folded proteins, devoid of genetic material, unable to build more of themselves from scratch, or cleave themselves in two. To reproduce, they simply find properly formed proteins that share their base composition and convert those to their aberrant shape, through mostly mysterious means. And because prions are slightly malformed versions of molecules that our bodies naturally make, they’re difficult to defend against. The immune system codes them as benign and ignores them, even as disease rapidly unfolds. “This is an entirely new paradigm of infectious disease,” Napper told me. “It’s a part of your own body that’s turning against you.”

    And yet, we’ve managed to keep many prion diseases in check. Kuru, once common in the highlands of Papua New Guinea, was transmitted through local rituals of funerary cannibalism; the disease fizzled out after people stopped those practices. Mad cow disease (more formally known as bovine spongiform encephalopathy) was contained by culling infected animals and eliminating the suspected source, cow feed made with infected tissues. Even scrapie, a highly contagious prion disease of sheep and goats, is limited to livestock, making it feasible to pare down infected populations, or breed them toward genetic resistance.

    Read: Insomnia that kills

    CWD, meanwhile, is a fixture of wild animals, many of them migratory. And whereas most other prion diseases primarily keep quarters in the central nervous system, CWD “gets in pretty much every part of the body,” Jorge told me. Deer then pass on the molecules, often through direct contact; they’ll shed prions in their saliva, urine, feces, reproductive fluids, and even antler velvet long before they start to show symptoms. Candace Mathiason, a pathobiologist at Colorado State University, and her colleagues have found that as little as 100 nanograms of saliva can seed an infection. Her studies suggest that deer can also pass prions in utero from doe to growing fawn.

    Deer also ingest prions from their environment, where the molecules can linger in soil, on trees, and on hunting bait for years or decades. A team led by Sandra Pritzkow, a biochemist at UTHealth Houston, has found that plants can take up prions from the soil, too. And unlike the multitude of microbes that are easily done in by UV, alcohol, heat, or low humidity, prions are so structurally sound that they can survive nearly any standard environmental assault. In laboratories, scientists must blast their equipment with temperatures of about 275 degrees Fahrenheit for 60 to 90 minutes, under extreme pressure, to rid it of prions—or drench their workspaces with bleach or sodium hydroxide, at concentrations high enough to rapidly corrode flesh.

    Infected deer are also frustratingly difficult to detect. The disease typically takes years to fully manifest, while the prions infiltrate the brain and steadily destroy neural tissue. The molecules kill insidiously: “This isn’t the kind of disease where you might get a group of deer that are all dead around this watering hole,” Jorge told me. Deer drift away from the herd; they forage at odd times. They become braver around us. They drool and urinate more, stumble about, and begin to lose weight. Eventually, a predator picks them off, or a cold snap freezes them, or they simply starve; in all cases, though, the disease is fatal. Because of CWD, deer populations in many parts of North America are declining; “there is definitely some concern that local populations will disappear,” McKenzie told me. Researchers worry the disease will soon overwhelm caribou in Canada, imperiling the Indigenous communities who rely on them for food. Hunters and farmers, too, are losing vital income. Deer are unlikely to go extinct, but the disease is depriving their habitats of key grazers, and their predators of food.

    Read: America needs hunting more than it knows

    In laboratory experiments, CWD has proved capable of infecting rodents, sheep, goats, cattle, raccoons, ferrets, and primates. But so far, jumps into non-cervid species don’t seem to be happening in the wild—and although people eat an estimated 10,000 CWD-infected cervids each year, no human cases have been documented. Still, lab experiments indicate that human proteins, at least when expressed by mice, could be susceptible to CWD too, Sabine Gilch, a molecular biologist at the University of Calgary, told me.

    And the more prions transmit, and the more hosts they find themselves in, the more opportunities they may have to infect creatures in new ways. Prions don’t seem to evolve as quickly as many viruses or bacteria, Gilch told me. But “they’re not as static as we would like them to be.” She, McKenzie, and other researchers have detected a multitude of CWD strains bopping around in the wild—each with its own propensity for interspecies spread. With transmission so unchecked, and hosts so numerous, “this is kind of like a ticking time bomb,” Surachai Suppattapone, a biochemist at Dartmouth, told me.

    The world is unlikely to ever be fully rid of CWD; even the options to slow its advance are so far limited. Efforts to survey for infection depend on funding and researchers’ time, or the generosity of local hunters for samples; environmental decontamination is still largely experimental and tricky to do at scale; treatments—which don’t yet exist—would be nearly impossible to administer en masse. And culling campaigns, although sometimes quite effective, especially at the edges of the disease’s reach, often spark public backlash.

    Deer that carry certain genetic variants do seem less susceptible to prions, and progress more slowly to full-blown disease and death. But because none so far seems able to fully block infection, or completely curb shedding, prolonging life may simply prolong transmission. “Once an animal gets infected,” Abdelaziz told me, there’s almost a “hope it dies right away.” Even if sturdier prion resistance is someday found, “it’s probably just a matter of time until prions start to adapt to that as well,” Gilch said.

    Vaccines, in theory, could help, and in recent years, several research groups—including Napper’s and Abdelaziz’s—have made breakthroughs in overcoming the immune system’s inertia in attacking proteins that look like the body’s own. Some strategies try to target the problematic, invasive prions only; others are going after both the prion and the native, properly folded protein, so that the vaccine can do double duty, waylaying the infectious invader and starving it of reproductive fodder. (So far, lab animals seem to do mostly fine even when they’re bred to lack the native prion protein, whose function is still mostly mysterious.) In early trials, both teams’ vaccines have produced promising immune responses in cervids. But neither team yet fully knows how effective their vaccines are at cutting down on shedding, how long that protection might last, or whether these strategies will work across cervid species. One of Napper’s vaccine candidates, for instance, seemed to hasten the progression of disease in elk.

    Vaccines for wildlife are also tough to deliver, especially the multiple doses likely needed in this case. “It’s not like you can just run around injecting every elk and deer,” Napper told me. Instead, he and other researchers plan to compound their formula with a salty apple-cider slurry that he hopes wild cervids might eat with some regularity. “The deer absolutely love it,” he said.

    Should any CWD vaccines come to market, though, they will almost certainly be the first prion vaccines that clear the experimental stage. That could be a boon for more than just deer. Another prion disease may spill over from one species to another; others may arise spontaneously. CWD is not, and may never be, the prion disease that most directly affects us. But it is, for now, the most urgent—and the one from which we have the most to lose, and maybe gain.



    Katherine J. Wu

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  • Experimental Gene Therapy Allows Kids with Inherited Deafness to Hear

    Experimental Gene Therapy Allows Kids with Inherited Deafness to Hear

    Gene therapy has allowed several children born with inherited deafness to hear.

    A small study published Wednesday documents significantly restored hearing in five of six kids treated in China. On Tuesday, the Children’s Hospital of Philadelphia announced similar improvements in an 11-year-old boy treated there. And earlier this month, Chinese researchers published a study showing much the same in two other children.

    So far, the experimental therapies target only one rare condition. But scientists say similar treatments could someday help many more kids with other types of deafness caused by genes. Globally, 34 million children have deafness or hearing loss, and genes are responsible for up to 60% of cases. Hereditary deafness is the latest condition scientists are targeting with gene therapy, which is already approved to treat illnesses such as sickle cell disease and severe hemophilia.

    Children with hereditary deafness often get a device called a cochlear implant that helps them hear sound.

    “No treatment could reverse hearing loss … That’s why we were always trying to develop a therapy,” said Zheng-Yi Chen of Boston’s Mass Eye and Ear, a senior author of the study published Wednesday in the journal Lancet. “We couldn’t be more happy or excited about the results.”

    More From TIME

    The team captured patients’ progress in videos. One shows a baby, who previously couldn’t hear at all, looking back in response to a doctor’s words six weeks after treatment. Another shows a little girl 13 weeks after treatment repeating father, mother, grandmother, sister and “I love you.”

    All the children in the experiments have a condition that accounts for 2% to 8% of inherited deafness. It’s caused by mutations in a gene responsible for an inner ear protein called otoferlin, which helps hair cells transmit sound to the brain. The one-time therapy delivers a functional copy of that gene to the inner ear during a surgical procedure. Most of the kids were treated in one ear, although one child in the two-person study was treated in both ears.

    The study with six children took place at Fudan University in Shanghai, co-led by Dr. Yilai Shu, who trained in Chen’s lab, which collaborated on the research. Funders include Chinese science organizations and biotech company Shanghai Refreshgene Therapeutics.

    Researchers observed the children for about six months. They don’t know why the treatment didn’t work in one of them. But the five others, who previously had complete deafness, can now hear a regular conversation and talk with others. Chen estimates they now hear at a level around 60% to 70% of normal. The therapy caused no major side effects.

    Preliminary results from other research have been just as positive. New York’s Regeneron Pharmaceuticals announced in October that a child under 2 in a study they sponsored with Decibel Therapeutics showed improvements six weeks after gene therapy. The Philadelphia hospital — one of several sites in a test sponsored by a subsidiary of Eli Lilly called Akouos — reported that their patient, Aissam Dam of Spain, heard sounds for the first time after being treated in October. Though they are muffled like he’s wearing foam earplugs, he’s now able to hear his father’s voice and cars on the road, said Dr. John Germiller, who led the research in Philadelphia.

    “It was a dramatic improvement,” Germiller said. “His hearing is improved from a state of complete and profound deafness with no sound at all to the level of mild to moderate hearing loss, which you can say is a mild disability. And that’s very exciting for us and for everyone. ”

    Columbia University’s Dr. Lawrence Lustig, who is involved in the Regeneron trial, said although the children in these studies don’t wind up with perfect hearing, “even a moderate hearing loss recovery in these kids is pretty astounding.”

    Still, he added, many questions remain, such as how long the therapies will last and whether hearing will continue to improve in the kids.

    Also, some people consider gene therapy for deafness ethically problematic. Teresa Blankmeyer Burke, a deaf philosophy professor and bioethicist at Gallaudet University, said in an email that there’s no consensus about the need for gene therapy targeting deafness. She also pointed out that deafness doesn’t cause severe or deadly illness like, for example, sickle cell disease. She said it’s important to engage with deaf community members about prioritization of gene therapy, “particularly as this is perceived by many as potentially an existential threat to the flourishing of signing Deaf communities.”

    Meanwhile, researchers said their work is moving forward.

    “This is real proof showing gene therapy is working,” Chen said. “It opens up the whole field.”

    LAURA UNGAR/AP

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  • What to Know About Complementary Treatments for Lupus

    What to Know About Complementary Treatments for Lupus

    Being diagnosed with a chronic illness can be a distressing and disorienting experience. Surveys of people who have chronic diseases have found that many experience a sense of powerlessness, and that they tend to view their condition as more than a threat to their health; it’s also seen as a threat to their psychological well-being, as well as their social and personal identities.

    All of these experiences may be heightened among people with lupus, a complex autoimmune condition that tends to arise unexpectedly and in relatively young patients. The unpredictable and highly variable course of the disease can contribute to feelings of uncertainty and lack of control. Patients are likely to worry about how their life will change, or whether they’ll be able to pursue long-held ambitions. In many cases, their care provider won’t be able to give them definite answers to these questions. 

    While medication is often the cornerstone of treating the underlying disease, drugs alone can’t always address the feelings of stress and powerlessness that accompany a disease like lupus. It’s here that complementary and integrative forms of care may play an important role. “I think we have to understand the whole context of the person, and their need to manage the ups and downs of the disease,” says Dr. Carol Greco, an associate professor of psychiatry at the University of Pittsburgh Medical Center. “If something can bring a person a little more sense of control or agency, that’s huge.”

    Greco has conducted research on complementary medicine among people with lupus. She’s a member of her university health system’s Center for Integrative Medicine, and she contributed to the creation of the non-profit Society for Women’s Health Research Living Well With Lupus toolkit. Some of her work has examined how stress-reduction therapies such as meditation and relaxation training may help people with lupus manage their symptoms. “Things like meditation and biofeedback are not typically part of the traditional medicine system, but people with lupus can use these to reduce symptoms like pain, and that gives them back some confidence and a sense that they have some control,” she says. 

    Here, Greco and other experts detail how complementary and integrative medicine approaches—as part of a comprehensive care plan—can help people with lupus manage all the facets of their illness.

    Mindfulness, biofeedback, and other evidence-backed therapies

    Lupus researchers have known for decades that stress often accompanies or precedes symptom flares. One 2004 study of lupus patients found that more than 70% reported worsening symptoms on stressful days, and a 2015 study found associations between lupus flares and a certain stress-related enzyme, which corresponds with autonomic nervous system activity.  

    “We know that certain things can make lupus worse, and that includes excess fatigue and stress,” says Dr. Joseph Craft, a lupus specialist and professor of medicine and immunobiology at the Yale School of Medicine. Craft says that some complementary or lifestyle approaches can help patients manage both of these challenges and their related symptoms. “There’s no magic bullet here, but I think certainly these are things that patients can address.”

    Mindfulness is one form of stress-management therapy that has been the focus of both randomized controlled trials and smaller case series among people with lupus. So far, that work has found evidence that mindfulness can reduce sympathetic nervous system activity as well as activation of the hypothalamic-pituitary-adrenal (HPA) axis, both of which are associated with heightened stress. A 2022 research review in the journal Lupus concluded: “[Mindfulness-based interventions] have been shown to improve stress response, and potentially induce anti-inflammatory changes at an epigenetic level.” Furthermore, that review highlighted a more-robust body of work linking mindfulness to a better quality of life, as well as improved anxiety and depression scores, among people with lupus.

    Some other forms of stress reduction have also shown promise in lupus trials. “Many people in our biofeedback and stress-management program had wonderful success in reducing their pain scores,” Greco says. Biofeedback allows people to see or hear representations of their own heightened stress or anxiety—such as increases in muscle tension and heart rate—which can help them bring their stress or anxiety under control. In one of Greco’s randomized controlled trials, people with lupus who underwent a program that included biofeedback experienced significant reductions in pain, as well as improvements in physical and psychological function, compared to a control group. That trial’s program also included a progressive muscle relaxation (PMR) component. PMR is a form of relaxation therapy that involves deliberately tensing and then relaxing the body’s muscles in a programmatic way. “That program was pretty helpful for pain, but it was also helpful for mood,” Greco says. “When a patient feels better, mentally and physically, this can improve their sense of well-being and their sense of being able to do more of the things they want to do.”

    More of Greco’s work has looked into the potential benefits of acupuncture for the reduction of pain in people with lupus. Here, her group’s findings were a bit mixed, but almost half of her study’s participants experienced significant (greater than 30%) reductions in pain following 10 treatments of acupuncture, compared to no improvements among the control group. “There aren’t a lot of studies on acupuncture for lupus, but we’ve found it can have a helpful effect on pain and fatigue,” she says. 

    More research, including a 2015 study in the journal Arthritis Care and Research, has revealed that many of these same interventions also help reduce fatigue among people with lupus. So too can plain old exercise. “Exercise is really important, and we know it improves fatigue,” says Dr. Fotios Koumpouras, an associate professor of clinical medicine and director of the lupus program at Yale School of Medicine. A 2022 study in Disability and Rehabilitation found that 12 weeks of aerobic exercise (two exercise sessions per week) significantly reduced fatigue and, perhaps not surprisingly, improved motivation to exercise among women with lupus. Researchers are also exploring the benefits of yoga among people with lupus, although there isn’t much trial evidence to date. 

    Supplements are another active area of study, and some work there has found evidence of a benefit. A 2019 research review in the American Journal of the Medical Sciences found that vitamin D supplementation is associated with lower fatigue scores among patients with lupus. (Sun exposure is an established trigger for lupus flares. Since people with lupus are told to avoid exposure, vitamin D supplementation may be worthwhile even if it doesn’t lead to a reduction in symptoms.) More work in this vein has found that omega-3 supplementation may help ease inflammation in people with lupus. 

    Koumpouras says supplements—including herbal teas and maybe also CBD (which he’s looked into as a possible lupus treatment)—deserve more attention. He points out that many of the medications used to treat lupus, such as the calcineurin inhibitor voclosporin, are derived from natural agents in fungi. “As we unravel the ways the immune system functions, we will find more natural compounds that are helpful,” he says.

    Read More: The Most Exciting New Advancements in Managing and Treating Lupus

    Why doctors should support complementary therapies

    Koumpouras says that some doctors too readily dismiss the benefits of complementary approaches, and he believes this is a mistake. “I think a lot of doctors don’t appreciate how effective complementary medicines can be,” he says. “There’s of course some quackery you have to be very careful with, but I think complementary and alternative medicines have an important role in the management of rheumatic disease, including lupus.” 

    It’s important to recognize, he adds, that many patients have to walk a long and lonely path before receiving their lupus diagnosis. According to a 2021 study in Lupus, the average time between symptom onset and diagnosis among people with lupus is almost four years. “There may be some distrust among patients because they feel that their doctors weren’t listening to them, and they had an unmet need for an early and accurate diagnosis,” he says. Endorsing a patient’s interest in complementary therapies—provided those therapies are safe—may be one way to help rebuild trust.   

    Greco makes a similar point. “Sometimes patients want to do more to help themselves, and sometimes they also want to work with practitioners who can give them a lot of time and consider their health in a larger context,” she says. “An integrative-medicine or CAM practitioner may devote more time just to listening, or to addressing more of the emotional side of the illness.” That has value, she says, and traditional medical providers would do well to acknowledge and respect such complementary approaches.  

    However, the key term here is “complementary.” While patients should be encouraged to explore safe and evidence-backed treatments such as relaxation therapy and meditation, they should be warned that these are not substitutes for their medications or other formal care strategies. “We want to encourage complementary medicine without causing harm,” Koumpouras says.

    Read More: What Lupus Patients Want Their Doctor to Know

    Complementary therapies are going mainstream

    It’s worth noting that many large and progressive medical institutions are now moving toward what are known as “integrative care models.” These are multidisciplinary approaches that offer patients access to registered dietitians, physical therapists, cognitive behavioral therapists, and other specialists who may help them adopt the same lifestyle and complementary treatment strategies mentioned above. In other words, some medical systems are now bringing what were once seen as “alternative” or “non-traditional” forms of treatment into a patient’s formal care strategy, and there’s evidence that this is leading to measurable improvements.  

    “Lupus can affect any system in the body unpredictably, and because its symptoms can come and go, patients need to learn what they can do on their own to manage the ups and downs,” Greco says. 

    It would be nice if people with lupus could manage their illness solely with the help of non-drug methods. As every medical provider knows, prescription drugs—while helpful and often life-saving—cause side-effects and, in some cases, complications that may necessitate the use of yet more drugs. Every medical provider also recognizes that patients with a chronic disease often get “pill fatigue.” It’s hard to keep taking a pill (or pills) day after day, for years on end. But if those medicines are part of a more comprehensive strategy that includes other broadly healthy interventions—things like exercise or cognitive behavioral therapy—there’s evidence that patients may be more likely to take their medicines and to follow their provider’s plan.

    Any way you look at them, complementary therapies seem to have a place in the life of people living with lupus. “It’s not uncommon in places like China to use traditional and Western medicines together,” Koumpouras says. “As we deepen and expand our knowledge, I think we’ll find even better ways to use alternative and traditional therapies.”

    Markham Heid

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  • We Got Lucky With the Mystery Dog Illness

    We Got Lucky With the Mystery Dog Illness

    In late July 1980, a five-month-old Doberman pinscher puppy in Washington, D.C., started throwing up blood. It died the next day at an animal hospital, one of many pets that suffered that year from a new illness, parvovirus. “This is the worst disease I’ve ever seen in dogs,” a local veterinarian told The Washington Post, in an article describing the regional outbreak. It killed so fast that it left pet owners in disbelief, he said.

    The world was in the middle of a canine pandemic. The parvovirus, which was first recognized in 1978, can live for months outside the body, spreading not just from animal to animal but through feces, sneaking into the yards of dog owners via a bit of excrement stuck to the bottom of a person’s shoe. It quickly traveled across countries and continents, infecting thousands and possibly millions of dogs in the late ’70s and early ’80s. Essentially every dog alive at the time caught it, Colin Parrish, a virology professor at Cornell University’s College of Veterinary Medicine, told me. And untold numbers  died: A single Associated Press report from August 1980 mentions the city of Chicago losing 300 dogs by July of that year, and South Carolina losing more than 700 in just two months.

    A vaccine was quickly developed, but with doses in short supply, the outbreaks dragged on for years. Today, puppies are routinely vaccinated for parvovirus, and the 1978 canine pandemic has faded from public consciousness. Since then, no outbreak has unfolded on that scale, even as dogs have become more integrated into American households. Few people stay up at night worrying about what might happen if a new and devastating disease did appear. Yet, for a moment at the end of last year, it seemed like one might have.

    In late 2023, veterinarians started noticing something odd. They’d seen an uptick in cases of dogs sick with respiratory symptoms responding poorly to antibiotics. Some would develop severe pneumonia quickly and die. Soon, cases of this suspected illness started popping up in states across the country. Around Thanksgiving, media reports began warning dog owners about a “mystery dog illness” spreading nationwide.

    Many experts now suggest that there probably was no “mystery dog illness.” More likely, some mix of previously known illnesses were surging around the same time. Still, the case is not entirely closed, and the prospect of a deadly new disease has left dog owners fearful and jumpy: How much should they worry? Could that seemingly normal cough in the family pet actually be something much more dangerous?

    And if a new disease had started a modern dog pandemic, the world’s first in almost 50 years, what would have happened next is not entirely clear. Unlike humans and livestock, companion animals do not have sophisticated, coordinated infrastructure dedicated to monitoring and managing their diseases. The technology and science might exist to fight a dog pandemic, but any response would depend on what kind of illness we found ourselves dealing with—and whether it could infect humans as well.

    Because dogs don’t interact with one another as much as humans do, dog transmission networks are different from ours. They see one another on walks, in day cares, or in dog parks. Some might travel between states or even between countries, but many just stay in their backyard. Their cloistered networks make it hard for some viruses to move among them. In 2015 and 2016, outbreaks of a nasty canine flu called H3N2, which was traced to a single introduction in the United States from South Korea, never reached full pandemic status. “I just remember seeing so many of these pretty sick dogs, like every day,” Steve Valeika, a veterinarian and infectious-disease specialist in North Carolina, told me. “And then it just stopped.” Most of his cases were from one boarding facility.

    A disease such as parvo, which can spread without direct contact, has a better chance of circulating widely. But even then, authorities could respond quickly, maybe even quicker than in 1978. The same mRNA tools that led to the speedy development of a COVID vaccine for humans could be used in a dog pandemic; the ability to test for dog diseases has improved since parvovirus. Information travels that much faster over the internet.

    Read: COVID drugs are a miracle cure for cats

    Still, as companion animals, dogs and cats fall into an awkward space between systems. “There is no CDC for dogs,” Valeika said. “It’s all very patchwork.” Typically, animal disease is managed by agricultural agencies—in this country, the USDA. But these groups are more focused on outbreaks in livestock, such as swine flu, which threaten the food supply, the economy, or human safety. If an outbreak were to emerge in companion animals, veterinary associations, local health departments, and other dog-health groups may all pitch in to help manage it.

    The dairy and pig industries, for example, are far more coordinated. “If they said, ‘We need to get all the players together to talk about a new emerging disease issue on pigs,’ that’d be easy. They’d know who to call, and they’d be on the phone that afternoon,” Scott Weese, professor in veterinary infectious diseases at the University of Guelph, in Canada, explains. Organizing a conference call like that on the topic of a dog disease would be trickier, especially in a big country like the United States. And the USDA isn’t designed around pets, although “it’s not that they don’t care or don’t try,” he said. (The USDA did not respond to a request for comment.) No one is formally surveilling for dog disease in the way government agencies and other groups monitor for human outbreaks. At base, monitoring requires testing, which is expensive and might not change a vet’s treatment plan. “How many people want to spend $250 to get their swab tested?” Parrish asked.

    Dogs aren’t human. But they are close to humans, and it is easy to imagine that, in a dog pandemic, owners would go to great lengths to keep their pets safe. Their closeness to us, in this way, could help protect them. It also poses its own risk: If a quickly spreading dog disease jumped to humans, a different machinery would grind into gear.

    If humans could be vulnerable and certainly if they were getting sick, then the CDC would get involved. “Public health usually takes the lead on anything where we’ve got that human and animal side,” Weese told me. These groups are better funded, are better staffed, and have more expertise—but their priority is us, not our pets. The uncomfortable truth about zoonotic disease is that culling, or killing, animals helps limit spread. In 2014, after a health-care worker in Spain contracted Ebola, authorities killed her dog Excalibur as a precaution, despite a petition and protests. When the woman recovered, she was devastated. (“I’ve forgotten about everything except the death of Excalibur,” she later told CNN.) Countries routinely cull thousands of livestock animals when dealing with the spread of deadly diseases. If a new dog-borne pathogen threatened the lives of people, the U.S. would be faced with the choice of killing infected animals or dedicating resources to quarantining them.

    A scenario in which pet owners stand by while their dogs are killed en masse is hard to imagine. People love their pets fiercely, and consider them family; many would push to save their dogs. But even in a scenario where humans were safe, the systems we’ve set up might not be able to keep pets from dying on a disturbing scale. Already, there’s a nationwide shortage of vets; in a dog-health emergency, people would want access to emergency care, and equipment such as ventilators. “I am concerned that we don’t have enough of that to deal with a big pandemic as it relates to pets,” Jane Sykes, a medicine and epidemiology professor at the UC Davis School of Veterinary Medicine and the founder of the International Society for Companion Animal Infectious Diseases, told me.

    Congress has mandated that the CDC, USDA, and Department of the Interior, which oversees wildlife, work on strengthening “federal coordination and collaboration on threats related to diseases that can spread between animals and people,” Colin Basler, the deputy director of CDC’s One Health Office, wrote in an email statement. A new, deadly canine disease would almost certainly leave experts scrambling to respond, in some way. And in that scramble, pet owners could be left in a temporary information vacuum, worrying about the health of their little cold-nosed, four-legged creatures. The specifics of any pandemic story depend on the disease—how fast it moves, how it sickens and kills, and how quickly—but in almost any scenario it’s easy to imagine the moment when someone fears for their pet and doesn’t know what help will come, and how soon.

    Caroline Mimbs Nyce

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  • The Most Exciting New Advancements in Managing and Treating Lupus

    The Most Exciting New Advancements in Managing and Treating Lupus

    The case study involved just one patient: a 20-year-old woman with severe systemic lupus erythematosus (SLE). But the study’s results were so dramatic that they appeared in 2021 in the New England Journal of Medicine. 

    The woman received a type of cell therapy called CAR-T, which in the past has been used primarily to treat cancer. CAR-T cell therapy involves altering a patient’s immune cells so that they identify and attack problems or pathogens. In people with cancer, that attack is aimed at the diseased cells. But in the NEJM case study, the therapy was directed at the woman’s own B cells, which are thought to be a primary cause of inflammation and damage in patients with lupus. The results were astonishing. “Within one month, nearly all of her symptoms had calmed down,” says Dr. Michelle Petri, a professor of medicine and director of the Johns Hopkins University Lupus Center, who was not involved with the case study.

    Soon after that initial case study appeared, the same group of researchers showed that CAR-T therapy led to dramatic and lasting improvements in five additional patients with SLE. Even when the patients’ B cells returned, they did not initially display their old pattern of harmful activity. “They didn’t come back as bad lupus B cells,” Petri says. 

    While these early CAR-T results have created a lot of excitement, Petri notes that a lot more work is needed before the therapy could conceivably be rolled out to more patients. Right now, CAR-T is prohibitively expensive. (It costs roughly $400,000 per patient, she says.) CAR-T therapy is also associated with risks, including severe and systemic toxicity, which in some cases can result in coma or infection. “We need to see if the treatment is durable, which means its benefits persist for at least five years,” she says. “If the lupus comes back too soon, then we’ve spent a lot of money and exposed people to major potential for toxicity without a durable benefit.”

    The latest CAR-T work is arguably the most exciting breakthrough in the treatment of SLE. (It also holds promise for the treatment of other autoimmune conditions that feature B-cell involvement, such as Type 1 diabetes and rheumatoid arthritis.) But it’s far from the only new advancement in the treatment of lupus. In recent years, several new lupus medications have received U.S. Food and Drug Administration (FDA) approval. Many others have demonstrated benefits in early clinical trials, and there’s hope that more approvals will follow soon.

    Here’s a rundown of the latest intriguing advancements in the lupus space. From new monoclonal antibody therapies to advancements in how the disease’s activity is monitored in patients’ urine, medical science is quickly revolutionizing lupus treatment and care. 

    New and more effective drug treatments

    Lupus is a disease of immune system overactivation. “The immune system attacks the body’s own tissues, and that attack can lead to damage in many different parts of the body,” says Dr. Joseph Craft, a professor of medicine and immunobiology at the Yale School of Medicine. Craft directs a lab devoted to the study of systemic lupus erythematosus. He explains that, in some patients, lupus attacks the skin or joints. It also frequently attacks the kidneys. “That doesn’t happen in every patient, but it does happen in a significant proportion, and it can lead to kidney disease and failure,” he says. Historically, lupus has been treated with medicines that broadly suppress the immune system, such as steroids like prednisone. “Those therapies work, but they have a lot of side effects, so we don’t like to use those for long periods of time,” Craft says. (Weight gain, poor bone health, and increased risks for infections are some of the most common side effects.) 

    A lot of time and resources have been directed at the development of new lupus therapies that act more narrowly, meaning they affect only a minor element of the immune system’s operation. These so-called targeted medicines have arrived, and they’ve made a big difference. One of them is an intravenous drug called belimumab, which blocks or kills the B cells that cause tissue damage in people with lupus. “B cells produce antibodies, which are proteins that float in the blood and act against infection,” Craft explains. “In patients with lupus, the B cells are abnormally regulated, and they make antibodies that bind to self-tissues—the kidneys for example—and cause autoreactivity.” Belimumab is now FDA-approved for lupus patients with or without kidney involvement.

    Another new drug in lupus treatment is an oral medicine called voclosporin, which is a type of calcineurin inhibitor. “Calcineurin inhibitors have been used in transplant medicine in the past, and voclosporin was approved in 2021 for lupus nephritis,” says Dr. Elena Massarotti, a lupus specialist and associate professor of rheumatology at Harvard Medical School. Calcineurin inhibitors interfere with the action of a protein (calcineurin) that contributes to certain types of immune system overactivity, Massarotti explains. Voclosporin is normally given along with mycophenolate (an older immunosuppressant drug) in people who have lupus with kidney involvement, and trials have shown that it significantly outperforms standard care.

    Like all lupus medications, voclosporin is associated with risks and side-effects. A 2021 phase-three trial found that roughly 1 in 5 people on voclosporin experienced “serious” adverse events, the most common of which was pneumonia. However, that side-effect profile was on par with the risks posed by standard treatments, and the leaders of the trial determined that voclosporin has a “comparable safety profile” to the older drugs.  

    Yet another drug, anifrolumab, targets a specific type of protein receptor. “It attaches to interferon alpha receptors, which are thought to play a major role in the pathogenesis of lupus,” Massarotti says. This drug may turn out to be most helpful for people who have systemic lupus that does not feature kidney involvement, she adds.

    Read More: What Lupus Patients Want Their Doctor to Know

    More drugs in the trial pipeline

    Apart from the FDA-approved treatments mentioned above, there are a handful of new drugs that have performed well in clinical trials (though they have not yet been formally approved for the treatment of lupus). 

    One of these is a therapy called obinutuzumab. This is a monoclonal antibody treatment that works by depleting the blood’s B cells. Some research has found that it can help people with systemic lupus who have not responded well to other medications.

    Several other monoclonal antibody therapies—treatments that use specially engineered antibodies to shift the activity of the immune system—have likewise looked promising in early trials. A drug called obexelimab was found to help extend symptom remission among lupus patients who had previously taken other immunosuppressant drugs. Another new medication, daratumumab, targets long-lived white blood cells that are thought to contribute to lupus-related immune overactivity. Research has found that daratumumab may provide an advantage over existing drugs in certain patient subgroups. “However, studies with meaningfully larger groups of SLE patients are necessary to determine the efficacy and safety of daratumumab in lupus,” wrote the authors of a 2021 research review in the journal Frontiers in Medicine.

    There’s a lot more going on in this space. Many drugs—either novel medicines or treatments that have proven effective against other conditions—are now under investigation. “We have several new agents in clinical trials, and there’s active interest by academicians as well as biotech and pharmaceutical companies to develop new treatments,” Craft says. “Some of these are now moving into clinical trials.”  

    Advancements in measuring lupus activity

    In order to know if a drug is working, medical scientists and providers need dependable ways to measure the disease’s activity. Among people with forms of lupus that involve the kidneys, experts often rely on urine protein levels to assess disease activity or medication efficacy. But there’s evidence that this method is unreliable. “We use urine protein to see how active kidney lupus is, but this method may be misinforming us about 30% of the time,” says Petri. 

    Petri says that she and some of her colleagues at Johns Hopkins—namely Dr. Andrea Fava—are now focused on enhancing the science of urine proteomics, or the ways that lupus may affect the chemical composition of a patient’s urine. Already, that work has identified multiple urine proteins, including a compound called IL-16, that may be better indicators of kidney inflammation in people with systemic lupus. “Before, no one knew that interleukin-16 was a player in kidney inflammation,” Petri says. “In the future, I think we’re going to be so much better at tracking lupus, which is a dynamic process, rather than relying just on the urine protein that, some of the time, is misleading us.”

    Read More: How Changing Your Diet Could Have a Major Impact on Managing Lupus Symptoms

    What’s next

    While new or repurposed medicines are a major focus of lupus research, there’s also a lot of work being done on combination therapies. Lupus is often referred to as a multifactorial disease, meaning it’s driven by more than one underlying issue. An old saying among lupus doctors is that “no two lupus patients are identical,” and personalized approaches to care and treatment are necessary. For some people—perhaps even a majority with systemic lupus—a single drug may not be sufficient to address the heterogeneous nature of the condition, and a lot of work is now looking at how combinations of existing drugs may help patients with specific subtypes of SLE. 

    Meanwhile, so-called big-data approaches to disease mapping are also helping lupus specialists better differentiate the disease’s different subtypes in ways that may improve outcomes. Using gene-wide association studies and “gene expression profiling”—techniques that have been employed to good effect in work on other autoimmune conditions, such as Crohn’s disease—researchers are developing a clearer picture of the many faces of lupus. “Disease activity waxes and wanes, confounding attempts to determine the cause of lupus and develop effective treatments for the disease,” wrote the authors of a 2020 study in the Journal of Autoimmunity. “In the past 20 years, new technology collectively referred to as ‘Big Data’ has allowed thousands of data points to be assessed in individual patients and compared to healthy controls.” They express hope that these new analytical methods will help inform treatment models in ways that reduce side-effects and improve responses. 

    According to the U.S. Centers for Disease Control and Prevention (CDC), hundreds of thousands of Americans are living with SLE. Most are women, and the disease disproportionately affects people of color, the CDC reports. Hopefully, breakthrough cell-based treatments—such as the CAR-T therapy that recent case studies linked to radical remission—will turn out to be a true gamechanger. But even if CAR-T doesn’t pan out, many other new therapies are under investigation, and several are now improving the lives of people with SLE. For people with lupus and those who care for them, there’s a lot of reason for optimism.

    Markham Heid

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  • One of Tuberculosis’s Biggest, Scariest Numbers Is Probably Wrong

    One of Tuberculosis’s Biggest, Scariest Numbers Is Probably Wrong

    Growing up in India, which for decades has clocked millions of tuberculosis cases each year, Lalita Ramakrishnan was intimately familiar with how devastating the disease can be. The world’s greatest infectious killer, rivaled only by SARS-CoV-2, Mycobacterium tuberculosis spreads through the air and infiltrates the airways, in many cases destroying the lungs. It can trigger inflammation in other tissues too, wearing away bones and joints; Ramakrishnan watched her own mother’s body erode in this way. The sole available vaccine was lackluster; the microbe had rapidly evolved resistance to the drugs used to fight it. And the disease had a particularly insidious trait: After entering the body, the bacterium could stow away for years or decades, before erupting without warning into full-blown disease.

    This state, referred to as latency, supposedly afflicted roughly 2 billion people—a quarter of the world’s population. Ramakrishnan, now a TB researcher at the University of Cambridge, heard that fact over and over, and passed it down to her own students; it was what every expert did with the dogma at the time. That pool of 2 billion people was understood to account for a large majority of infections worldwide, and it represented one of the most intimidating obstacles to eradicating the disease. To end TB for good, the thinking went, the world would need to catch and cure every latent case.

    In the years since, Ramakrishnan’s stance on latent TB has shifted quite a bit. Its extent, she argues, has been exaggerated for a good three decades, by at least an order of magnitude—to the point where it has scrambled priorities, led scientists on wild-goose chases, and unnecessarily saddled people with months of burdensome treatment. In her view, the term latency is so useless, so riddled with misinformation, that it should disappear. “I taught that nonsense forever,” she told me; now she’s spreading the word that TB’s largest, flashiest number may instead be its greatest, most persistent myth.

    Ramakrishnan isn’t the only one who thinks so. Together with her colleagues Marcel Behr, of Quebec’s McGill University, and Paul Edelstein, of the University of Pennsylvania (“we call ourselves the three BERs,” Ramakrishnan told me), she’s been on a years-long crusade to set the record straight. Their push has attracted its fair share of followers—and objectors. “I don’t think they’re wrong,” Carl Nathan, a TB researcher at Cornell, told me. “But I’m not confident they’re right.”

    Several researchers told me they’re largely fine with the basic premise of the BERs’ argument: Fewer than 2 billion isn’t that hard to get behind. But how many fewer matters. If current latency estimates overshoot by just a smidge, maybe no practical changes are necessary. The greater the overestimate, though, the more treatment recommendations might need to change; the more research and funding priorities might need to shift; the more plans to control, eliminate, and eventually eradicate disease might need to be wholly and permanently rethought.

    Read: A historical lesson in disease containment

    The muddled numbers on latency seem to be based largely on flawed assumptions about certain TB tests. One of the primary ways to screen people for the disease involves pricking harmless derivatives of the bacterium into skin, then waiting for an inflamed lump to appear—a sign that the immune system is familiar with the microbe (or a TB vaccine), but not direct proof that the bacterium itself is present. That means that positive results can guarantee only that the immune system encountered something resembling MTB at some point—perhaps even in the distant past, Rein Houben, an epidemiologist at the London School of Hygiene & Tropical Medicine, told me.

    But for a long time, a prevailing assumption among researchers was that all TB infections had the potential to be lifelong, Behr told me. The thought wasn’t entirely far-fetched: Other microbial infections can last a lifetime, and there are historical accounts of lasting MTB infections, including a case in which a man developed tuberculosis more than 30 years after his father passed the bacterium to him. Following that logic—that anyone once infected had a good enough chance of being infected now—researchers added everyone still reacting to the bug to the pool of people actively battling it. By the end of the 1990s, Behr and Houben told me, prominent epidemiologists had used this premise to produce the big 2 billion number, estimating that roughly a third of the population had MTB lurking within.

    That eye-catching figure, once rooted, rapidly spread. It was repeated in textbooks, academic papers and lectures, news articles, press releases, government websites, even official treatment guidelines. The World Health Organization parroted it too, repeatedly calling for research into vaccines and treatments that could shrink the world’s massive latent-TB cohort. “We were all taught this dogma when we were young researchers,” Soumya Swaminathan, the WHO’s former chief scientist, told me. “Each generation passed it on to the next.”

    But, as the BERs argue, for TB to be a lifelong sentence makes very little sense. Decades of epidemiological data show that the overwhelming majority of disease arises within the first two years after infection, most commonly within months. Beyond that, progression to symptomatic, contagious illness becomes vanishingly rare.

    The trio is convinced that a huge majority of people are clearing the bug from their body rather than letting it lie indefinitely in wait—a notion that recent modeling studies support. If the bacteria were lingering, researchers would expect to see a big spike in disease late in life among people with positive skin tests, as their immune system naturally weakens. They would also expect to see a high rate of progression to full-blown TB among people who start taking immunosuppressive drugs or catch HIV. And yet, neither of those trends pans out: At most, some 5 to 10 percent of people who have tested positive by skin test and later sustain a blow to their immune system develop TB disease within about three to five years—a hint that, for almost everyone else, there may not be any MTB left. “If there were a slam-dunk experiment, that’s it,” William Bishai, a TB researcher at Johns Hopkins, told me.

    Read: Tuberculosis got to South America through … seals?

    Nathan, of Cornell, was less sold. Immunosuppressive drugs and HIV flip very specific switches in the immune system; if MTB is being held in check by multiple branches, losing some immune defenses may not be enough to set the bacteria loose. But most of the experts I spoke with are convinced that lasting cases are quite uncommon. “Some people will get into trouble in old age,” Bouke de Jong, a TB researcher at the Institute of Tropical Medicine, in Antwerp, told me. “But is that how MTB hangs out in everybody? I don’t think so.”

    If anything, people with positive skin tests might be less likely to eventually develop disease, Ramakrishnan told me, whether because they harbor defenses against MTB or because they are genetically predisposed to clear the microbe from their airway. In either case, that could radically change the upshot of a positive test, especially in countries such as the U.S. and Canada, where MTB transmission rarely occurs and most TB cases can be traced from abroad. Traditionally, people in these places with positive skin tests and no overt symptoms have been told, “‘This means you’ve got sleeping bacteria in you,’” Behr said. “‘Any day now, it may pop out and cause harm.’” Instead, he told me, health-care workers should be communicating widely that there could be up to a 95 percent chance that these patients have already cleared the infection, especially if they’re far out from their last exposure and might not need a drug regimen. TB drugs, although safe, are not completely benign: Standard regimens last for months, interact with other meds, and can have serious side effects.

    At the same time, researchers disagree on just how much risk remains once people are a couple of years past an MTB exposure. “We’ve known for decades that we are overtreating people,” says Madhu Pai, a TB researcher at McGill who works with Behr but was not directly involved in his research. But treating a lot of people with positive skin tests has been the only way to ensure that the people who are carrying viable bacteria get the drugs they need, Robert Horsburgh, an epidemiologist at Boston University, told me. That strategy squares, too, with the goal of elimination in places where spread is rare. To purge as much of the bug as possible, “clinicians will err on the side of caution,” says JoAnne Flynn, a TB researcher at the University of Pittsburgh.

    Elsewhere in the world, where MTB transmission is rampant and repeat infections are common, “to be honest, nobody cares if there’s latent TB,” Flynn told me. Many people with very symptomatic, very contagious cases still aren’t getting diagnosed or treated; in too many places, the availability of drugs and vaccines is spotty at best. Elimination remains a long-term goal, but active outbreaks demand attention first. Arguably, quibbling about latency now is like trying to snuff stray sparks next to an untended conflagration.

    Read: The dangers of ignoring tuberculosis

    One of the BERs’ main goals could help address TB’s larger issues. Despite decades of research, the best detection tools for the disease remain “fundamentally flawed,” says Keertan Dheda, a TB researcher at the London School of Hygiene & Tropical Medicine and the University of Cape Town. A test that could directly detect viable microbes in tissues, rather than an immune proxy, could definitively diagnose ongoing infections and prioritize people across the disease spectrum for treatment. Such a diagnostic would also be the only way to finally end the fuss over latent TB’s prevalence. Without it, researchers are still sifting through only indirect evidence to get at the global TB burden—which is probably still “in the hundreds of millions” of cases, Houben told me, though the numbers will remain squishy until the data improve.

    That 2 billion number is still around—though not everywhere, thanks in part to the BERs’ efforts. The WHO’s most recent annual TB reports now note that a quarter of the world’s population has been infected with MTB, rather than is infected with MTB; the organization has also officially discarded the term latent from its guidance on the disease, Dennis Falzon, of the WHO Global TB Programme, told me in an email. However subtle, these shifts signal that even the world’s biggest authorities on TB are dispensing with what was once conventional wisdom.

    Losing that big number does technically shrink TB’s reach—which might seem to minimize the disease’s impact. Behr argues the opposite. With a huge denominator, TB’s mortality rate ends up minuscule—suggesting that most infections are benign. Deflating the 2 billion statistic, then, reinforces that “this is one of the world’s nastiest pathogens, not some symbiont that we live with in peace,” Behr told me. Fewer people may be at risk than was once thought. But for those who are harboring the microbe, the dangers are that much more real.

    Katherine J. Wu

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  • You've Heard of Long COVID. Long Flu Is a Health Risk, Too

    You've Heard of Long COVID. Long Flu Is a Health Risk, Too

    Statistically, there’s a good chance you know somebody who has experienced Long COVID, the name for chronic symptoms including fatigue, brain fog, and pain following a case of COVID-19. About 14% of U.S. adults report having had Long COVID at some point, according to federal data.

    But many people don’t realize that other viruses, even very common ones, can trigger similarly long-lasting and debilitating symptoms. A study published Dec. 14 in The Lancet Infectious Diseases focuses on the risk of developing “Long flu” after a severe case of influenza.

    “We learned from COVID-19 that infections that are initially thought to cause only acute illnesses can cause chronic disease,” says co-author Dr. Ziyad Al-Aly, chief of research and development at the Veterans Affairs St. Louis Health Care System and a clinical epidemiologist at Washington University in St. Louis. That’s true of influenza as well, the new research shows.

    Al-Aly and his colleagues used records from the U.S. Department of Veterans Affairs to compare the long-term health outcomes of about 11,000 people hospitalized with influenza from 2015 to 2019 with those of about 81,000 people hospitalized with COVID-19 from 2020 to 2022. The researchers tracked how many people went on to develop any of 94 health risks associated with the two viruses in the year and a half after they were hospitalized.

    Relative to influenza survivors, people who’d had COVID-19 were at increased risk of 64 of the identified complications, including fatigue, mental-health problems, and pulmonary, gastrointestinal, and heart issue. They were also more likely to die during the study period, in keeping with other research comparing the long-term outcomes of the two illnesses.

    Influenza survivors, meanwhile, were at increased risk of only six health problems, most of them related to the respiratory and cardiovascular systems.

    “COVID is still more serious than the flu,” Al-Aly says, noting that it affects numerous organ systems while influenza is mostly a respiratory illness. But long-term health problems were common in both groups during the 18 months of follow-up. The researchers recorded about 615 health issues per 100 people in the COVID-19 group, compared to about 537 per 100 people in the influenza group. Those numbers reflect the fact that some people experience numerous chronic symptoms after an infection, Al-Aly says.

    It’s important to note that the people included in the study were all hospitalized, meaning they were very sick during the acute phases of their illnesses. The study population was also overwhelmingly male and older, with an average participant age of 70. Older adults are known to be vulnerable to the worst effects of both COVID-19 and the flu. Therefore, the results may not translate to the entire population.

    That said, previous research shows that even milder illnesses can lead to long-lasting health issues. Influenza, as well as other common viruses like Epstein-Barr (which causes mononucleosis), have long been thought to trigger myalgic encephalomyelitis/chronic fatigue syndrome, a post-infectious illness that shares many symptoms with Long COVID.

    Newer research also underscores the potential effects of even routine illnesses. In a study published in October, researchers tracked people who had gotten sick with one of a variety of respiratory diseases, including COVID-19, the flu, and the common cold, and found that lingering symptoms popped up in each group. Similarly, in one 2022 study of people with various respiratory diseases, most of whom were not hospitalized, about half of people sick with something other than COVID-19 reported ongoing issues three months later. A 2021 study looking at both hospitalized and non-hospitalized patients also found that about 40% of people with influenza experienced at least one symptom commonly associated with Long COVID in the six months after their illnesses.

    Taken together, Al-Aly says, these findings suggest that we need to start thinking of viruses differently. “Before the pandemic, I trivialized infections. [I thought] you get sick for a day or two or three, and then you bounce back, and it’s all over,” Al-Aly says. But as a growing number of studies show that’s not always the case, he has concluded that “infections deserve respect.”

    That means doing whatever possible to avoid catching and spreading them, he says, including by wearing a mask during periods of heavy transmission, getting all recommended vaccines, and staying home when you feel unwell.

    Jamie Ducharme

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  • Bird flu concerns grow in California as deadly virus infects more farms

    Bird flu concerns grow in California as deadly virus infects more farms

    Federal and state officials have confirmed outbreaks in the last few weeks of a fast-spreading avian influenza strain — commonly known as bird flu — in four new California counties, sparking concerns about the possible agricultural and financial blow of the virus.

    The “highly pathogenic” bird flu was confirmed Wednesday at two commercial farms in Stanislaus County, joining recent outbreaks at poultry farms in Fresno, San Benito and Sonoma counties, according to updates from the California Department of Food and Agriculture. The strain is easily spread among birds and often fatal for them.

    “It is important to note that [the bird flu] is widespread in California and may also be present in other counties that are not listed,” the agency said in a statement Wednesday. “Enhanced biosecurity is critical in the face of ongoing disease outbreaks.”

    Surging egg prices earlier this year were blamed on an outbreak of the bird flu that killed millions of hens and left grocers struggling to keep shelves stocked.

    California agriculture officials said that in order to protect other flocks from the disease, the farms where outbreaks were reported are being quarantined and their birds euthanized.

    After cases were confirmed earlier this week at two Sonoma County poultry farms, officials there declared a state of emergency, calling the outbreak a local disaster.

    “We need to promote and protect our local food shed and the agricultural producers who dedicate their livelihoods to producing food for our local populations and beyond,” Sonoma County Agricultural Commissioner Andrew Smith said in a statement. “These producers are integral in maintaining and increasing food security in our communities.”

    Sonoma County Supervisor David Rabbitt said he is concerned about economic and supply-chain issues that could result from the emergency, noting that south Sonoma County has about “one million farm birds within a five-mile radius” of one of the facilities hit by the outbreak, and that they provide as many as hundreds of thousands of eggs daily.

    Rabbitt also said that more than 200 employees work at the two affected Sonoma County facilities, and will be hurt by the losses.

    In October, as cases of avian flu increased nationally and the first California outbreak of the season was detected in Merced County, the state veterinarian urged that California bird farmers move their flocks indoors for now.

    The Merced County outbreak was confirmed at a commercial turkey farm, home to about 30,000 birds, according to USDA data tracking the virus’ spread.

    The most recent outbreaks confirmed in Stanislaus County were at two commercial farms that are raising about 250,000 chickens each. The infected Sonoma County farms were a duck farm with 169,000 birds, and a commercial egg producer with more than 80,000 birds.

    The San Benito and Fresno county cases also included commercial duck farms, with 5,000 birds in San Benito and 23,000 in Fresno, according to the USDA data.

    State officials did not disclose the names of the companies involved, and USDA data was limited.

    Avian infuenza can be found in both wild and domesticated fowl, including chickens, turkeys, pheasants, quail, ducks and geese, and its typically spread through bird-to-bird contact, according to the state Department of Food and Agriculture.

    There have also been confirmed cases in wild birds over the last month in Sacramento and Santa Clara counties, according to the USDA.

    Officials noted this spring that continued spread of the virus could soon become a concern for the still-endangered California condor.

    According to the federal Centers for Disease Control and Protection, this bird flu strain is considered a low risk to humans. However, the World Health Organization has said there is some cause for worry due to some reports of the virus infecting humans.

    Californians can report unusual sick or dead pets or domesticated birds via the state Department of Food and Agriculture Sick Bird Hotline at (866) 922-2473. Any unusual or dead wild birds should be reported to the state Department of Fish and Wildlife online.

    Grace Toohey

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  • UK’s First Human Case of New Swine Flu

    UK’s First Human Case of New Swine Flu

    U.K. health officials have reported a person with a flu strain typically found in pigs, marking the first time this variant has been detected in a human in the country.

    The U.K. Health Security Agency is working to determine any risks the pathogen might pose to human health, it said in a statement Monday. The person experienced only a mild illness and has fully recovered, according to the agency.

    It’s not unusual for flu viruses to jump to other species, but experts track those events closely for fear that the pathogen will adapt to the new host and become transmissible among humans. A swine flu virus sparked a pandemic in 2009 that affected millions of people globally. 

    The U.K. case was detected as part of routine surveillance and the patient’s contacts are now being followed by health authorities.

    “This is the first time we have detected this virus in humans in the U.K., though it is very similar to viruses that have been detected in pigs,” said Meera Chand, Incident Director at the Health Security Agency. “We are working rapidly to trace close contacts and reduce any potential spread.”

    The variant was first found in a minor in the U.S. state of Michigan earlier this year.

    Marthe Fourcade / Bloomberg

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  • Researchers: El Niño Could Lead to the Spread of Infectious Diseases | Entrepreneur

    Researchers: El Niño Could Lead to the Spread of Infectious Diseases | Entrepreneur

    The planet’s weather over the past three years has been dominated by a natural cycle called La Niña — an oceanic phenomenon that results in below-average sea-surface temperatures in the central and eastern tropical Pacific Ocean and lower average temperatures worldwide. But forecasters predict that, sometime between this summer and the end of the year, La Niña’s opposite extreme, El Niño, will take over.

    That seismic shift could have major implications for human health, specifically the spread of disease. El Niño will increase temperatures and make precipitation more volatile, which could fuel the spread of pathogen-carrying mosquitoes, bacteria, and toxic algae. It’s a preview of the ways climate change will influence the spread of infectious diseases.

    “The bottom line here is that there are a range of different health effects that might occur in the setting of an El Niño,” Neil Vora, a physician with the environmental nonprofit Conservation International, told Grist. “That means we have to monitor the situation closely and prepare ourselves.”

    A boon for mosquitos

    As with La Niña, the effects of an El Niño extend far beyond a patch of above-average warmth in the Pacific. Parched regions of the world — like Chile, Peru, Mexico, and the American Southwest — are often bombarded with rain and snow. Some other parts of the world, including the Northeastern U.S., the Amazon, and Southeast Asia’s tropical regions, on the other hand, don’t see much rain at all in an El Niño year.

    The planet could temporarily become 1.5 degrees Celsius (2.7 degrees Fahrenheit) warmer, on average, than in preindustrial times — a threshold scientists have long warned marks the difference between a tolerable environment and one that causes intense human suffering.

    These patterns are a boon for certain vector-borne illnesses — defined as infections transmitted by an organism (usually an arthropod, a category that includes insects and arachnids). Regions of the world that will experience longer wet seasons because of El Niño, many of which are in the tropics, may see an increase in mosquito-borne illnesses, according to Victoria Keener, a senior research fellow at the East-West Center in Honolulu, Hawaii, and a coauthor of the U.S.’s upcoming Fifth National Climate Assessment. “El Niño will mean a longer breeding season for a lot of vectors and increased malaria potential in a lot of the world,” she said.

    A 2003 study on the intersection of El Niño and infectious disease showed spikes in malaria along the coasts of Venezuela and Brazil during and after El Niño years. The study looked at more than a dozen cycles between El Niño, La Niña, and the cycle’s “neutral” phase, which taken together are known as the El Niño-Southern Oscillation, or ENSO. The researchers, who analyzed data dating back to 1899, also found an increase in malaria during or post-El Niño in Colombia, India, Pakistan, and Peru. Cases of dengue, another mosquito-borne illness, increased in 10 Pacific islands.

    The manner in which El Niño impacts mosquitos and the diseases they carry is varied and often difficult to accurately calculate, said Christopher Barker, an associate professor in the Department of Pathology, Microbiology, and Immunology of the University of California Davis School of Veterinary Medicine. Mosquitos breed in warm, wet conditions. But too much water in the form of flooding rains can wash away mosquito larvae and ultimately contribute to a decrease in mosquito populations.

    As the planet shifts into an El Niño year, Barker said the areas to keep a close eye on are ones where moderate or heavy rains are followed by dry, warm months. If the past is any indication, countries like India and Pakistan are especially at risk.

    So is California. After years of drought, recent storms in the Golden State have generated a lot of flooding and cooler-than-normal conditions. If that leads into a hotter-than-normal summer, “that may set things up for bad conditions for West Nile virus,” Barker said of the mosquito-borne illness that is becoming more prevalent in the U.S.

    El Niño is projected to bring unusual warmth to the Pacific Northwest and the northern Great Plains. Kristie L. Ebi, a professor of global health at the University of Washington, said warmth is often the determining factor in how far north vectors of disease move. “We know that mosquitoes don’t control their internal temperature,” she said. “When it’s hotter they’re going to see opportunities to move into new ranges. If the El Niño lasts long enough they get established and find habitat, then you can see an expansion in geographic range.” A study on the link between infectious disease in the U.S. and El Niño, published in 2016, found a link between tick-borne illnesses such as rickettsiosis — an infection that can damage the brain, lungs, and skin — and El Niño in the Western U.S.

    Concerns about cholera

    Vibrio cholerae, the water-borne bacteria that causes cholera, is another area of concern, experts told Grist — both in areas that see more rain during El Niño and those that see less rain. Flooding aids the spread of the cholera bacteria from open sewers and other waste containers — still prevalent in many underdeveloped parts of the world — into drinking water systems.

    Drought also leads to an uptick in cholera cases in poor countries, because restricted access to fresh water forces people to use less water for personal hygiene practices like handwashing and turn to unsafe sources of drinking water. “Cholera can be a devastating infectious disease that causes a very severe diarrhea that can dehydrate people so badly that they die,” Vora said. “In the setting of an El Niño extreme weather event, there might be impacts on sewage systems or on access to clean water, and that can lead to the spread of water-borne diseases such as cholera.”

    Research shows El Niño has had an impact on the transmission of cholera in Bangladesh and eastern India. Water-borne illnesses writ large increase in the western Pacific islands during an El Niño year, Keener said, because El Niño in that region is associated with drought. “People start conserving water and using it for drinking instead of hygiene, so you see an increase in things like pink eye, gastrointestinal issues, just a whole host of health issues,” she said.

    Poisonous algae

    Poisonous algae is a consideration in regions where El Niño spurs above-average sea-surface temperatures. Algae thrive in warm water, where their poisons accumulate in water-filtering organisms such as shellfish. Humans who consume that shellfish or are otherwise exposed to the algae can develop symptoms like abdominal cramping, rashes, vomiting, and even, in extreme cases, death. A study from 2020 links El Niño to a pair of harmful algal blooms in the southern hemisphere, commonly referred to as the “Godzilla-Red tide event,” which poisoned four people and led to massive economic losses in Australia and Chile.

    The study noted that these blooms, sparked by high sea-surface temperatures brought on by an El Niño, were a “dress rehearsal” for future outbreaks of poisonous algae influenced by climate change. The coming El Niño may bring about a Godzilla round two. “I wouldn’t be surprised with warmer temperatures if you see an association with harmful algal blooms,” Ebi said, noting that El Niño’s signature high temperatures are one of the phenomenon’s most widespread and impactful health-related consequences.

    The premise that El Niño years offer a glimpse of what a future permanently altered by climate change might look like is one governments should take seriously. Public health institutions are doing a subpar job of monitoring infectious diseases, pinpointing where they’ll crop up, and preparing communities for an uptick in environmental pathogens. The coming ENSO shift may further illuminate those weaknesses. “We have few ideas about what will move and what will pop up when there is any kind of climate or weather perturbation,” Daniel R. Brooks, coauthor of The Stockholm Paradigm: Climate Change and Emerging Disease, told Grist.

    Even public health agencies in the U.S., one of the richest countries in the world, do a poor job of assessing infectious disease risk, monitoring pathogens as they move through the environment, and testing individuals for increasingly common diseases such as the West Nile virus, especially when they’re asymptomatic. “This means the real threat is unpleasant surprise,” Brooks said. “We know a bit about some already known pathogens, but that is not good enough.”

    Grist is a nonprofit, independent media organization dedicated to telling stories of climate solutions and a just future. Learn more at Grist.org

    Zoya Teirstein

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  • Is $3.5 Million a Fair Price for a Lifesaving Gene Therapy?

    Is $3.5 Million a Fair Price for a Lifesaving Gene Therapy?

    Feb. 15, 2023 — Gene therapies have the power to cure serious, even fatal, diseases. Yet what captures public attention is often not the transformative effects but the enormous price tags. 

    At $3.5 million, Hemgenix, the new gene therapy for hemophilia B, has recently been named the most expensive drug on the planet, unseating another gene therapy, Skysona.

    “I didn’t believe the prices we’re seeing now would ever happen,” says Colin Young, PhD, director of drug development pipeline research at Tufts Medical Center. “I’m continually amazed every time a new price comes out.”

    Hemgenix is record-setting, but hardly an anomaly. Skysona, a treatment for a rare neurological disorder, launched at $3 million in September 2022. Zynteglo, a gene therapy for a genetic blood disorder, debuted just one month earlier at $2.8 million. In 2019, Zolgensma was priced at $2.1 million as a treatment for spinal muscular atrophy, a fatal genetic disease affecting infants and young children. Several other treatments land in the hundreds of thousands. 

    Yet the remarkable results lead some to call gene therapy a relative bargain. These drugs have the potential — in some cases, the proven ability — to cure illness with a single dose. This liberates patients from the physical, emotional, and financial burden of living with a serious disease, often one requiring highly expensive treatments. 

    “It’s a big paradigm shift,” says Sarah Emond, chief operating officer of the Institute for Clinical and Economic Review (ICER), a nonprofit that independently evaluates the cost of medical treatments. “Up until now, most drugs have been something that you take for chronic conditions forever.” 

    That’s because gene therapy does not treat symptoms. It targets the cause, the genetic defect behind a disease, swapping out faulty code or even inserting a gene that’s missing. Sometimes, this happens in a petri dish, and the healthy cells are transferred to the patient. Other times a vector, usually a virus, delivers the genetic material to the patient’s cells. 

    Treatment is currently confined to monogenic diseases — those caused by a single gene mutation — and the conditions are typically rare, with patient populations in the hundreds or low thousands. But treatments for more common conditions, like sickle cell disease, are on the very near horizon. 

    “This wasn’t even in my wildest imagination 20 years ago,” says Stephan Grupp, MD, PhD, medical director of the Cell and Gene Therapy Laboratory at the Children’s Hospital of Philadelphia. 

    In 2017, Kymriah — a cell-based gene therapy Grupp helped develop for a type of pediatric leukemia — was the first to be approved by the FDA. The clinical trial showed astonishing promise, with 90% of patients going into remission. 

    “There were almost 20 years of trials when nothing seemed to be working,” Grupp recalls. “And then, boom, it went from doing nothing to doing everything.” 

    One of the clinical trial patients, Emily Whitehead — now a well-known name in gene therapy — had been close to hospice. Twenty-three days after her infusion, her leukemia was gone. 

    “Some combination of disbelief and ecstasy” is how Grupp describes his reaction at the time. “We had no idea this was possible. We did mouse experiments in the lab, but that’s not guaranteed to translate into anything.” 

    Over a decade later, Emily, now 17, is still healthy. Gene therapy cured her cancer. 

    The Financial Picture

    For every successful treatment like Emily’s, dozens more fail. 

    “[Drug companies] are really lucky if 1% of their ideas actually make it to the clinic,” says Young. “Then they’re pretty lucky if 1% of those actually make it to a product. There’s a very, very high attrition rate.” 

    The few treatments that make the cut can cost up to $1 billion dollars to develop, yet they may ultimately benefit fewer than 100 patients a year.

    “Most of the companies eventually go bankrupt or get bought, even the ones that are successful,” Young says. “These things cost a hell of a lot to develop.” 

    Bluebird Bio, the company that makes Skysona and Zynteglo, is “very close to running out of money,” he says. This could threaten the launch of its sickle cell therapy regardless of the drug’s promise.

    Research and development is only one part of the financial picture. Manufacturing costs are also steep. 

    Take the viral vectors, the most common delivery system for gene therapies. Inside production facilities you’ll find towering steel vats resembling the kind you might see on a brewery tour. “They go up to the ceiling — they’re enormous,” says Nicole Paulk, PhD, a University of California San Francisco researcher who studies technologies that could make gene therapy cheaper. 

    These vats are the bioreactors where viral vectors are produced. Despite their size, each one might yield only enough vector for a few patients, “‘like single digit,” says Paulk. “It’s a super labor-intensive process.” 

    During purification, much of the virus — up to 80%  — is lost; a battery of FDA safety tests further depletes each batch.

    This is just one step in a highly complex manufacturing process — the single biggest driver of gene therapy’s cost, according to Paulk. “Every step is just very expensive. These prices sound astronomical to people. But they are justified at the moment.” 

    Production is still mostly done by humans, with drug companies relying on the same methods developed in academic labs. This inefficiency spikes costs — and creates batch-to-batch variability. Even something as small as the way a technician holds a tube could affect the end product. Automation will improve quality control and bring production costs down, enabling more drugs to enter the market. 

    Some labs are also developing “off-the-shelf” cells for certain products, like the CAR T therapies for leukemia and blood cancer. This could yield multiple treatments per batch versus the current “bespoke” method, a weeks-long process where “you have to make a fully qualified lot of drug for every single patient,” says Grupp. 

    ‘What’s the Value of a Life?’

    Even if efficiency and competition improve, not everyone is confident that will translate to lower price tags. “We haven’t seen that for any other drug,” says Young, who points out that as more CAR T products enter the market, “they come out at the same price.”

    That’s because pricing isn’t solely linked to manufacturing costs. “These companies believe the price should match the clinical benefit,” says Emond. 

    When gene therapies prove to be life-transforming — even lifesaving — that leads to a very high dollar amount. “You’re sort of deciding, ‘What’s the value of a life?’” says Young. 

    When calculating target prices, ICER incorporates a range of factors, including the economic burden the health care system can sustain without a spike in premiums. Perhaps its most critical consideration, however, is clinical benefit.

    “The magnitude of change — how much better a patient feels on the drug — comes directly from the patients in the clinical trial,” says Emond. This data is converted into “quality-adjusted life years,” or QALYs, which aims to capture both quality and quantity of life before and after treatment. The analysis includes the cost savings of treatments no longer needed.

    The latest ICER report suggests Hemgenix should be priced at around $2.9 million — some $600,000 less than its market price. A big reason for the still seven-figure price tag is the IV infusions of clotting factor that Hemgenix could eliminate. “If the gene therapy is sufficiently durable,” that is, if it works as intended,— “then it doesn’t take too many years to write off the cost of the alternative,” says Young, since earlier therapies can cost upwards of $750,000 a year. 

    Yet ICER refuses to take this number as a given, calling those other therapies “extremely overpriced.”  

    If drugs were priced strictly according to efficacy, those that confer life-changing benefits, like gene therapies, could cost seven figures without straining the system, says Emond. “We shouldn’t overpaying for drugs that bring marginal clinical benefit,” she insists. 

    The U.S. Health Care System

    Understanding the problem of pricing requires a wider view of our country’s fragmented health care system, a capitalistic model where drug prices are the highest in the world and insurers are mostly price takers. 

    Red tape notwithstanding, insurance generally covers gene therapy, leaving most people responsible for only the deductible. Still, because “there really isn’t any [payer] approaching monopoly power,” says Young, the market renders insurers essentially impotent when it comes to negotiation. 

    Drug manufacturers “try to figure out what the market will bear and just set that price. And it’s typically going to be accepted,” Young says. “You basically can’t persuade the payers in European countries to pay that much,” since there’s often a government agency deciding which drugs will be reimbursed at what price. In 2021, Bluebird Bio pulled Zynteglo from Europe after withdrawing it from Germany, where health officials rejected its target price of $1.8 million.

    But the U.S. landscape may be changing: The new Inflation Reduction Act permits Medicare, for the first time, to negotiate the prices of certain high-cost drugs that lack competition. This will go into effect in 2026, though the eligible drugs haven’t yet been announced. 

    Right now, the most urgent question is one of access. “Realistically, we’re stuck with the sort of prices we’re looking at,” says Young. “We just have to find payment mechanisms,” especially as gene therapies for more prevalent conditions advance in the development pipeline. 

    “Imagine if these therapies work for more common cancers — lung cancer, breast cancer,” Grupp says. “That would be a whole new day in therapy. But how are we going to pay for this?” 

    With an influx of eligible patients, the health care system could be seriously strained. 

    Take sickle cell disease, the most common genetic disease in the U.S., affecting one out of every 500 Black Americans. This year, the FDA is expected to approve two gene therapies for the disease. Generally, “this population has lower rates of commercial insurance than other populations that have gotten [gene therapies] until now,” says Grupp. “We’re going to have to deal with the impact of these prices on Medicaid.” 

    Moving Forward

    One possible solution is outcomes-based pricing. This refunds some or all of the treatment’s cost if results don’t last.

    “If you’re going to price these very expensive therapies for their curative potential, then if they stop working later, we have to get some of that value back,” says Grupp. An outcome-based agreement might, for example, refund a patient with hemophilia who must return to prophylaxis after receiving Hemgenix.

    This type of guarantee is already being implemented for other gene therapies. 

    If patients with leukemia aren’t in remission 30 days after receiving Kymriah, the hospital treating them isn’t billed. The maker of Luxturna, a gene therapy for a rare form of blindness, offers rebates based on light-sensitivity tests taken shortly after treatment and 2 1/2 years later. Bluebird Bio, the maker of Zynteglo, promises a refund of up to 80% if patients require red blood cell transfusions within 2 years.

    Innovative payment plans could be another answer. Bluebird Bio offers an installment option, reducing the upfront cost of gene therapy for insurers. AveXis, maker of Zolgensma, also has a pay-over-time structure, with payments spread out for as long as 5 years. Some insurers are allowing patients to pay their deductible over time rather than all at once, to reduce the impact on patients. 

    The high-risk pool model, where small insurers combine their resources and share the cost of gene therapies, could also improve patient access. 

    “If you’re a self-insured company and somebody needs a $3 million therapy, it basically kills your health plan,” says Young. Programs like Cigna’s Embarc, which allows companies to pay a flat fee per employee to guarantee coverage of gene therapy, could help solve this problem. 

    It’s this type of creative thinking that may be the key to propelling the industry forward. 

    “I totally get the gut reaction, like a million dollars is insane. That number seems fanciful to people,” says Emond. But gene therapies themselves are fanciful, offering the kinds of results researchers couldn’t fathom even 2 decades ago. 

    “We could be on the precipice of transforming the way we think about and treat disease. … We have to reward swing-for-the-fences innovation with high prices,” Emond says, then tempers her position with a blunt reminder. “Remember that price is a conscious choice.” Drugmakers choose what they charge — and how they choose could determine the future of gene therapy.

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  • Is COVID a Common Cold Yet?

    Is COVID a Common Cold Yet?

    At the start of the coronavirus pandemic, one of the worst things about SARS-CoV-2 was that it was so new: The world lacked immunity, treatments, and vaccines. Tests were hard to come by too, making diagnosis a pain—except when it wasn’t. Sometimes, the symptoms of COVID got so odd, so off-book, that telling SARS-CoV-2 from other viruses became “kind of a slam dunk,” says Summer Chavez, an emergency physician at the University of Houston. Patients would turn up with the standard-issue signs of respiratory illness—fever, coughing, and the like—but also less expected ones, such as rashes, diarrhea, shortness of breath, and loss of taste or smell. A strange new virus was colliding with people’s bodies in such unusual ways that it couldn’t help but stand out.

    Now, nearly three years into the crisis, the virus is more familiar, and its symptoms are too. Put three sick people in the same room this winter—one with COVID, another with a common cold, and the third with the flu—and “it’s way harder to tell the difference,” Chavez told me. Today’s most common COVID symptoms are mundane: sore throat, runny nose, congestion, sneezing, coughing, headache. And several of the wonkier ones that once hogged headlines have become rare. More people are weathering their infections with their taste and smell intact; many can no longer remember when they last considered the scourge of “COVID toes.” Even fever, a former COVID classic, no longer cracks the top-20 list from the ZOE Health Study, a long-standing symptom-tracking project based in the United Kingdom, according to Tim Spector, an epidemiologist at King’s College London who heads the project. Longer, weirder, more serious illness still manifests, but for most people, SARS-CoV-2’s symptoms are getting “pretty close to other viruses’, and I think that’s reassuring,” Spector told me. “We are moving toward a cold-like illness.”

    That trajectory has been forecast by many experts since the pandemic’s early days. Growing immunity against the coronavirus, repeatedly reinforced by vaccines and infections, could eventually tame COVID into a sickness as trifling as the common cold or, at worst, one on par with the seasonal flu. The severity of COVID will continue to be tempered by widespread immunity, or so this thinking goes, like a curve bending toward an asymptote of mildness. A glance at the landscape of American immunity suggests that such a plateau could be near: Hundreds of millions of people in the U.S. have been vaccinated multiple times, some even quite recently with a bivalent shot; many have now logged second, third, and fourth infections with the virus. Maybe, just maybe, we’re nearing the level of cumulative exposure at which COVID gets permanently more chill. Then again? Maybe not—and maybe never.

    Read: What does it mean to care about COVID anymore?

    The recent trajectory of COVID, at least, has been peppered with positive signs. On average, symptoms have migrated higher up the airway, sparing several vulnerable organs below; disease has gotten shorter and milder, and rates of long COVID seem to be falling a bit. Many of these changes roughly coincided with the arrival of Omicron in the fall of 2021, and part of the shift is likely attributable to the virus itself: On the whole, Omicron and its offshoots seem to prefer infecting cells in the nose and throat over those in the lungs. But experts told me the accumulation of immune defenses that preceded and then accompanied that variant’s spread are almost certainly doing more of the work. Vaccination and prior infection can both lay down protections that help corral the virus near the nose and mouth, preventing it from spreading to tissues elsewhere. “Disease is really going to differ based on the compartment that’s primarily infected,” says Stacey Schultz-Cherry, a virologist at St. Jude Children’s Research Hospital. As SARS-CoV-2 has found a tighter anatomical niche, our bodies have become better at cornering it.

    With the virus largely getting relegated to smaller portions of the body, the pathogen is also purged from the airway faster and may be less likely to be passed to someone else. On the individual level, a sickness that might have once unfurled into pneumonia now gets subdued into barely perceptible sniffles and presents less risk to others; on the population scale, rates of infection, hospitalization, and death go down.

    This is how things usually go with respiratory viruses. Repeat tussles with RSV tend to get progressively milder; post-vaccination flu is usually less severe. The few people who catch measles after getting their shots are less likely to transmit the virus, and they tend to experience such a trivial course of sickness that their disease is referred to by a different name, “modified” measles, says Diane Griffin, a virologist and an immunologist at Johns Hopkins University.

    It’s good news that the median case of COVID diminished in severity and duration around the turn of 2022, but it’s a bit more sobering to consider that there hasn’t been a comparably major softening of symptoms in the months since. The full range of disease outcomes—from silent infection all the way to long-term disability, serious disease, and death—remains in play as well, for now and the foreseeable future, Schultz-Cherry told me. Vaccination history and immunocompromising conditions can influence where someone falls on that spectrum. So too can age as well as other factors such as sex, genetics, underlying medical conditions, and even the dose of incoming virus, says Patricia García, a global-health expert at the University of Washington.

    New antibody-dodging viral variants could still show up to cause more severe disease even among the young and healthy, as occasionally happens with the flu. The BA.2 subvariant of Omicron, which is more immune-evasive than its predecessor BA.1, seemed to accumulate more quickly in the airway, and it sparked more numerous and somewhat gnarlier symptoms. Data on more recent Omicron subvariants are still being gathered, but Shruti Mehta, an epidemiologist at Johns Hopkins, says she’s seen some hints that certain gastrointestinal symptoms, such as vomiting, might be making a small comeback.

    Read: Will we get Omicron’d again?

    All of this leaves the road ahead rather muddy. If COVID will be tamed one day into a common cold, that future definitely hasn’t been realized yet, says Yonatan Grad, an epidemiologist at Harvard’s School of Public Health. SARS-CoV-2 still seems to spread more efficiently and more quickly than a cold, and it’s more likely to trigger severe disease or long-term illness. Still, previous pandemics could contain clues about what happens next. Each of the past century’s flu pandemics led to a surge in mortality that wobbled back to baseline after about two to seven years, Aubree Gordon, an epidemiologist at the University of Michigan, told me. But SARS-CoV-2 isn’t a flu virus; it won’t necessarily play by the same epidemiological rules or hew to a comparable timeline. Even with flu, there’s no magic number of shots or past infections that’s known to mollify disease—“and I think we know even less about how you build up immunity to coronaviruses,” Gordon said.

    The timing of when and how those defenses manifest could matter too. Almost everyone has been infected by the flu or at least gotten a flu shot by the time they reach grade school; SARS-CoV-2 and COVID vaccines, meanwhile, arrived so recently that most of the world’s population met them in adulthood, when the immune system might be less malleable. These later-in-life encounters could make it tougher for the global population to reach its severity asymptote. If that’s the case, we’ll be in COVID limbo for another generation or two, until most living humans are those who grew up with this coronavirus in their midst.

    COVID may yet stabilize at something worse than a nuisance. “I had really thought previously it would be closer to common-cold coronaviruses,” Gordon told me. But severity hasn’t declined quite as dramatically as she’d initially hoped. In Nicaragua, where Gordon has been running studies for years, vaccinated cohorts of people have endured second and third infections with SARS-CoV-2 that have been, to her disappointment, “still more severe than influenza,” she told me. Even if that eventually flips, should the coronavirus continue to transmit this aggressively year-round, it could still end up taking more lives than the flu does—as is the case now.

    Wherever, whenever a severity plateau is reached, Gordon told me that our arrival to it can be confirmed only in hindsight, “once we look back and say, ‘Oh, yeah, it’s been about the same for the last five years.’” But the data necessary to make that call are getting harder to collect as public interest in the virus craters and research efforts to monitor COVID’s shifting symptoms hit roadblocks. The ZOE Health Study lost its government funding earlier this year, and its COVID-symptom app, which engaged some 2.4 million regular users at its peak, now has just 400,000—some of whom may have signed up to take advantage of newer features for tracking diet, sleep, exercise, and mood. “I think people just said, ‘I need to move on,’” Spector told me.

    Mehta, the Johns Hopkins epidemiologist, has encountered similar hurdles in her COVID research. At the height of the Omicron wave, when Mehta and her colleagues were trying to find people for their community studies, their rosters would immediately fill up past capacity. “Now we’re out there for weeks” and still not hitting the mark, she told me. Even weekly enrollment for their long-COVID study has declined. Sign-ups do increase when cases rise—but they drop off especially quickly as waves ebb. Perhaps, in the view of some potential study volunteers, COVID has, ironically, become like a common cold, and is thus no longer worth their time.

    For now, researchers don’t know whether we’re nearing the COVID-severity plateau, and they’re worried it will get only more difficult to tell. Maybe it’s for the best if the mildness asymptote is a ways off. In the U.S. and elsewhere, subvariants are still swirling, bivalent-shot uptake is still stalling, and hospitalizations are once more creeping upward as SARS-CoV-2 plays human musical chairs with RSV and flu. Abroad, inequities in vaccine access and quality—and a zero-COVID policy in China that stuck around too long—have left gaping immunity gaps. To settle into symptom stasis with this many daily deaths, this many off-season waves, this much long COVID, and this pace of viral evolution would be grim. “I don’t think we’re quite there yet,” Gordon told me. “I hope we’re not there yet.”

    Katherine J. Wu

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  • How Your Voice Could Reveal Hidden Disease

    How Your Voice Could Reveal Hidden Disease

    Dec. 7, 2022 – Most of us have two voice changes in our lifetime: first during puberty, as the vocal cords thicken and the voice box migrates down the throat. Then a second time as aging causes structural changes that may weaken the voice. 

    But for some of us, there’s another voice shift, when a disease begins or when our mental health declines. 

    This is why more doctors are looking into voice as a biomarker – something that tells you that a disease is present. 

    Vital signs like blood pressure or heart rate “can give a general idea of how sick we are. But they’re not specific to certain diseases,” says Yael Bensoussan, MD, director of the University of South Florida’s Health Voice Center and the co-principal investigator for the National Institutes of Health’s Voice as a Biomarker of Health project. 

    “We’re learning that there are patterns” in voice changes that can indicate a range of conditions, including diseases of the nervous system and mental illnesses, she says. 

    Speaking is complicated, involving everything from the lungs and voice box to the mouth and brain. “A breakdown in any of those parts can affect the voice,” says Maria Powell, PhD, an assistant professor of otolaryngology (the study of diseases of the ear and throat) at Vanderbilt University in Nashville, who is working on the NIH project. 

    You or those around you may not notice the changes. But researchers say voice analysis as a standard part of patient care – akin to blood pressure checks or cholesterol tests – could help identify those who need medical attention earlier. 

    Often, all it takes is a smartphone – “something that’s cheap, off-the-shelf, and that everyone can use,” says Ariana Anderson, PhD, director of UCLA’s Laboratory of Computational Neuropsychology. 

    “You can provide voice data in your pajamas, on your couch,” says Frank Rudzicz, PhD, a computer scientist for the NIH project. “It doesn’t require very complicated or expensive equipment, and it doesn’t require a lot of expertise to obtain.” Plus, multiple samples can be collected over time, giving a more accurate picture of health than a single snapshot from, say, a cognitive test. 

    Over the next 4 years, the Voice as a Biomarker team will receive nearly $18 million to gather a massive amount of voice data. The goal is 20,000 to 30,000 samples, along with health data about each person being studied. The result will be a sprawling database scientists can use to develop algorithms linking health conditions to the way we speak.

    For the first 2 years, new data will be collected exclusively via universities and high-volume clinics to control quality and accuracy. Eventually, people will be invited to submit their own voice recordings, creating a crowdsourced dataset. “Google, Alexa, Amazon – they have access to tons of voice data,” says Bensoussan. “But it’s not usable in a clinical way, because they don’t have the health information.” 

    Bensoussan and her colleagues hope to fill that void with advance voice screening apps, which could prove especially valuable in remote communities that lack access to specialists or as a tool for telemedicine. Down the line, wearable devices with voice analysis could alert people with chronic conditions when they need to see a doctor. 

    “The watch says, ‘I’ve analyzed your breathing and coughing, and today, you’re really not doing well. You should go to the hospital,’” says Bensoussan, envisioning a wearable for patients with COPD. “It could tell people early that things are declining.” 

    Artificial intelligence may be better than a brain at pinpointing the right disease. For example, slurred speech could indicate Parkinson’s, a stroke, or ALS, among other things. 

    “We can hold approximately seven pieces of information in our head at one time,” says Rudzicz. “It’s really hard for us to get a holistic picture using dozens or hundreds of variables at once.” But a computer can consider a whole range of vocal markers at the same time, piecing them together for a more accurate assessment.

    “The goal is not to outperform a … clinician,” says Bensoussan. Yet the potential is unmistakably there: In a recent study of patients with cancer of the larynx, an automated voice analysis tool more accurately flagged the disease than laryngologists did. 

    “Algorithms have a larger training base,” says Anderson, who developed an app called ChatterBaby that analyzes infant cries. “We have a million samples at our disposal to train our algorithms. I don’t know if I’ve heard a million different babies crying in my life.” 

    So which health conditions show the most promise for voice analysis? The Voice as a Biomarker project will focus on five categories.

    Voice Disorders 

    (Cancers of the larynx, vocal fold paralysis, benign lesions on the larynx)

    Obviously, vocal changes are a hallmark of these conditions, which cause things like breathiness or “roughness,” a type of vocal irregularity. Hoarseness that lasts at least 2 weeks is often one of the earliest signs of laryngeal cancer. Yet it can take months – one study found 16 weeks was the average – for patients to see a doctor after noticing the changes. Even then, laryngologists still misdiagnosed some cases of cancer when relying on vocal cues alone. 

    Now imagine a different scenario: The patient speaks into a smartphone app. An algorithm compares the vocal sample with the voices of laryngeal cancer patients. The app spits out the estimated odds of laryngeal cancer, helping providers decide whether to offer the patient specialist care. 

    Or consider spasmodic dysphonia, a neurological voice disorder that triggers spasms in the muscles of the voice box, causing a strained or breathy voice. Doctors who lack experience with vocal disorders may miss the condition. This is why diagnosis takes an average of nearly 4½ years, according to a study in the Journal of Voice, and may include everything from allergy testing to psychiatric evaluation, says Powell. Artificial intelligence technology trained to recognize the disorder could help eliminate such unnecessary testing.

    Neurological and Neurodegenerative Disorders 

    (Alzheimer’s, Parkinson’s, stroke, ALS) 

    For Alzheimer’s and Parkinson’s, “one of the first changes that’s notable is voice,” usually appearing before a formal diagnosis, says Anais Rameau, MD, an assistant professor of laryngology at Weill Cornell Medical College and another member of the NIH project. Parkinson’s may soften the voice or make it sound monotone, while Alzheimer’s disease may change the content of speech, leading to an uptick in “umm’s” and a preference for pronouns over nouns.

    With Parkinson’s, vocal changes can occur decades before movement is affected. If doctors could detect the disease at this stage, before tremor emerged, they might be able to flag patients for early intervention, says Max Little, PhD, project director for the Parkinson’s Voice Initiative. “That is the ‘holy grail’ for finding an eventual cure.” 

    Again, the smartphone shows potential. In a 2022 Australian study, an AI-powered app was able to identify people with Parkinson’s based on brief voice recordings, although the sample size was small. On a larger scale, the Parkinson’s Voice Initiative collected some 17,000 samples from people across the world. “The aim was to remotely detect those with the condition using a telephone call,” says Little. It did so with about 65% accuracy. “While this is not accurate enough for clinical use, it shows the potential of the idea,” he says. 

    Rudzicz worked on the team behind Winterlight, an iPad app that analyzes 550 features of speech to detect dementia and Alzheimer’s (as well as mental illness). “We deployed it in long-term care facilities,” he says, identifying patients who need further review of their mental skills. Stroke is another area of interest, since slurred speech is a highly subjective measure, says Anderson. AI technology could provide a more objective evaluation. 

    Mood and Psychiatric Disorders 

    (Depression, schizophrenia, bipolar disorders) 

    No established biomarkers exist for diagnosing depression. Yet if you’re feeling down, there’s a good chance your friends can tell – even over the phone. 

    “We carry a lot of our mood in our voice,” says Powell. Bipolar disorder can also alter voice, making it louder and faster during manic periods, then slower and quieter during depressive bouts. The catatonic stage of schizophrenia often comes with “a very monotone, robotic voice,” says Anderson. “These are all something an algorithm can measure.” 

    Apps are already being used – often in research settings – to monitor voices during phone calls, analyzing rate, rhythm, volume, and pitch, to predict mood changes. For example, the PRIORI project at the University of Michigan is working on a smartphone app to identify mood changes in people with bipolar disorder, especially shifts that could increase suicide risk.

    The content of speech may also offer clues. In a UCLA study, published in the journal PLOS One, people with mental illnesses answered computer-programmed questions (like “How have you been over the past few days?”) over the phone. An app analyzed their word choices, paying attention to how they changed over time. The researchers found that AI analysis of mood aligned well with doctors’ assessments and that some people in the study actually felt more comfortable talking to a computer. 

    Respiratory Disorders 

    (Pneumonia, COPD)

    Beyond talking, respiratory sounds like gasping or coughing may point to specific conditions. “Emphysema cough is different, COPD cough is different,” says Bensoussan. Researchers are trying to find out if COVID-19 has a distinct cough. 

    Breathing sounds can also serve as signposts. “There are different sounds when we can’t breathe,” says Bensoussan. One is called stridor, a high-pitched wheezing often resulting from a blocked airway. “I see tons of people [with stridor] misdiagnosed for years – they’ve been told they have asthma, but they don’t,” says Bensoussan. AI analysis of these sounds could help doctors more quickly identify respiratory disorders. 

    Pediatric Voice and Speech Disorders 

    (Speech and language delays, autism)

    Babies who later have autism cry differently as early as 6 months of age, which means an app like ChatterBaby could help flag children for early intervention, says Anderson. Autism is linked to several other diagnoses, such as epilepsy and sleep disorders. So analyzing an infant’s cry could prompt pediatricians to screen for a range of conditions. 

    ChatterBaby has been “incredibly accurate” in identifying when babies are in pain, says Anderson, because pain increases muscle tension, resulting in a louder, more energetic cry. The next goal: “We’re collecting voices from babies around the world,” she says, and then tracking those children for 7 years, looking to see if early vocal signs could predict developmental disorders. Vocal samples from young children could serve a similar purpose.

    And That’s Only the Beginning 

    Eventually, AI technology may pick up disease-related voice changes that we can’t even hear. In a new Mayo Clinic study, certain vocal features detectable by AI – but not by the human ear – were linked to a three-fold increase in the likelihood of having plaque buildup in the arteries. 

    “Voice is a huge spectrum of vibrations,” explains study author Amir Lerman, MD. “We hear a very narrow range.” 

    The researchers aren’t sure why heart disease alters voice, but the autonomic nervous system may play a role, since it regulates the voice box as well as blood pressure and heart rate. Lerman says other conditions, like diseases of the nerves and gut, may similarly alter the voice. Beyond patient screening, this discovery could help doctors adjust medication doses remotely, in line with these inaudible vocal signals. 

    “Hopefully, in the next few years, this is going to come to practice,” says Lerman. 

    Still, in the face of that hope, privacy concerns remain. Voice is an identifier that’s protected by the federal Health Insurance Portability and Accountability Act, which requires privacy of personal health information. That is a major reason why no large voice databases exist yet, says Bensoussan. (This makes collecting samples from children especially challenging.) Perhaps more concerning is the potential for diagnosing disease based on voice alone. “You could use that tool on anyone, including officials like the president,” says Rameau. 

    But the primary hurdle is the ethical sourcing of data to ensure a diversity of vocal samples. For the Voice as a Biomarker project, the researchers will establish voice quotas for different races and ethnicities, ensuring algorithms can accurately analyze a range of accents. Data from people with speech impediments will also be gathered.

    Despite these challenges, researchers are optimistic. “Vocal analysis is going to be a great equalizer and improve health outcomes,” predicts Anderson. “I’m really happy that we are beginning to understand the strength of the voice.” 

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  • The Future of Monkeypox

    The Future of Monkeypox

    The World Health Organization has recommended a new name for monkeypox, asking countries to forget the original term in favor of a new one, “mpox,” that scientists hope will help destigmatize the disease. But in the United States, the request seems to be arriving late. The outbreak here has already been in slow retreat for months—and has already left many Americans’ minds.

    About 15 cases are now being recorded among Americans each day, less than 4 percent of the tally when the surge was at its worst. After a sluggish and bungled early rollout, tests and treatments for the virus are more available; more than a million doses of the two-shot Jynneos smallpox vaccine have found their way into arms. San Francisco and New York—two of the nation’s first cities to declare mpox a public-health emergency this past summer—have since allowed those orders to expire; so have the states of New York and Illinois. “I think this is the endgame,” says Caitlin Rivers, an infectious-disease epidemiologist at the Johns Hopkins Center for Health Security.

    But “endgame” doesn’t mean “over”—and mpox will be with us for the foreseeable future. The U.S. outbreak is only now showing us its long and ugly tail: 15 daily cases is not zero daily cases; even as the number of new infections declines, inequities are growing. Black and Latino people make up a majority of new mpox cases and are contracting the disease at three to five times the rate of white Americans, but they have received proportionately fewer vaccines. “Now it’s truly the folks who are the most marginalized that we’re seeing,” says Ofole Mgbako, a physician and population-health researcher at New York University. “Which is also why, of course, it’s fallen out of the news.” If the virus sticks around (as it very likely could), and if the disparities persist (as they almost certainly will), then mpox could end up saddling thousands of vulnerable Americans each year with yet another debilitating, stigmatized, and neglected disease.

    Read: America should have been able to handle monkeypox

    At this point, there’s not even any guarantee that this case downturn will persist. “I’m not convinced that we’re out of the woods,” says Sara Bares, an infectious-disease physician at the University of Nebraska Medical Center, in Omaha. Immunity, acquired through infection or vaccines, is now concentrated among those at highest risk, says Jay Varma, a physician and epidemiologist at Weill Cornell Medicine. But researchers still don’t know how well those defenses can stave off another infection, or how long they might last—gaps in knowledge that may be tough to fill, now that incidence is so low. And although months of advocacy and outreach from the LGBTQ community have cut down on risky sexual activities, many cautionary trends will eventually reset to their pre-outbreak norm. “We know extensively from other sexually transmissible infections that behavior change is not usually the most sustained response,” says Boghuma Kabisen Titanji, an infectious-disease physician at Emory University.

    At the same time, this year’s mpox outbreaks are stranger and more unwieldy than those that came before. A ballooning body of evidence suggests that people can become infectious before they develop symptoms, contrary to prior understanding; some physicians are concerned that patients, especially those who are immunocompromised, might remain infectious after the brunt of visible illness resolves, says Philip Ponce, an infectious-disease physician at the University of Texas Health Science Center at San Antonio and the medical director of San Antonio’s Kind Clinic. (Some 40 percent of Americans who have been diagnosed with mpox are living with HIV.) Researchers still don’t have a good grip on which bodily fluids and types of contact may be riskiest over the trajectory of a sickness. Cases are still being missed by primary-care providers who remain unfamiliar with the ins and outs of diagnosis and testing, especially in people with darker skin. And although this epidemic has, for the most part, continued to affect men who have sex with men, women and nonbinary people are getting sick as well, to an underappreciated degree.

    Read: What should worry most Americans about our monkeypox response

    Intel on the only mpox-fighting antiviral on the shelf, a smallpox drug called tecovirimat, also remains concerningly scant, even as experts worry that the virus could develop resistance. The treatment has been given a conditional greenlight for use in people who are currently, or at risk of becoming, severely sick. Anecdotally, it seems to work wonders, shaving days or weeks off the painful, debilitating course of symptoms that can send infected people into long-term isolation. But experts still lack rigorous data in humans to confirm just how well it works, Bares, who’s among the scientists involved in a nationwide study of the antiviral, told me. And although clinical trials for tecovirimat are under way, she added, in the U.S., they’re “struggling to enroll patients” now that infections have plummeted to such a sustained low. It’s a numerical problem as well as a sociocultural one. “The urgency with which people answer questions declines as case counts go down,” Varma told me.

    Recent CDC reports show that a growing proportion of new infections aren’t being reported with a known sexual-contact history, stymieing efforts at contact tracing. That might in part be a product of the outbreak’s gradual migration from liberal, well-off urban centers, hit early on in the epidemic, to more communities in the South and Southwest. “In small towns, the risk of disclosure is high,” Bares told me. In seeking care or vaccination, “you’re outing yourself.” When mpox cases in Nebraska took an unexpected nosedive earlier this fall, “a colleague and I asked one another, ‘Do you think patients are afraid to come in?’” Those concerns can be especially high in certain communities of color, Ponce told me. San Antonio’s Latino population, for instance, “tends to be much more conservative; there’s much more stigma associated with one being LGBT at all, let alone being LGBT and trying to access biomedical interventions.”

    Hidden infections can become fast-spreading ones. Monitoring an infectious disease is far easier when the people most at risk have insurance coverage and access to savvy clinicians, and when they are inclined to trust public-health institutions. “That’s predominantly white people,” says Ace Robinson, the CEO of the Pierce County AIDS Foundation, in Washington. Now that the mpox outbreak is moving out of that population into less privileged ones, Robinson fears “a massive undercount” of cases.

    Americans who are catching the virus during the outbreak’s denouement are paying a price. The means to fight mpox are likely to dwindle, even as the virus entrenches itself in the population most in need of those tools. One concern remains the country’s vaccination strategy, which underwent a mid-outbreak shift: To address limited shot supply, the FDA authorized a new dosing method with limited evidence behind it—a decision that primarily affected people near the back of the inoculation line. The method is safe but tricky to administer, and it can have tough side effects: Some of Titanji’s patients have experienced swelling near their injection site that lasted for weeks after their first dose, and now “they just don’t want to get another shot.”

    The continued shift of mpox into minority populations, Robinson told me, is also further sapping public attention: “As long as this is centered in BIPOC communities, there’s going to be less of a push.” Public interest in this crisis was modest even at its highest point, says Steven Klemow, an infectious-disease physician at Methodist Dallas Medical Center and the medical director of Dallas’s Kind Clinic. Now experts are watching that cycle of neglect reinforce itself as the outbreak continues to affect and compress into marginalized communities, including those that have for decades borne a disproportionate share of the burden of sexually associated infections such as syphilis, gonorrhea, and HIV. “These are not the groups that necessarily get people jumping on their feet,” Titanji told me.

    Some of the people most at risk are moving on as well, Robinson told me. In his community in Washington, he was disappointed to see high rates of vaccine refusal at two recent outreach events serving the region’s Black and American Indian populations. “They had no knowledge of the virus,” he told me. Titanji has seen similar trends in her community in Georgia. “There’s some sense of complacency, like, ‘It’s no longer an issue, so why do I need to get vaccinated?’” she said.

    Read: America is zooming through the pandemic panic-neglect cycle

    The tide seems unlikely to shift. Even tens of thousands of cases deep into the American outbreak, sexual-health clinics—which have been on the front lines of the mpox response—remain short on funds and staff. Although the influx of cases has slowed, Ponce and Klemow are still treating multiple mpox patients a week while trying to keep up the services they typically offer—at a time when STI rates are on a years-long rise. “We’re really assuming that this is going to become another sexually associated disease that is going to be a part of our wheelhouse that we’ll have to manage for the indefinite future,” Klemow told me. “We’ve had to pull resources away from our other services that we provide.” The problem could yet worsen if the national emergency declared in August is allowed to expire, which would likely curb the availability of antivirals and vaccines.

    Rivers still holds out hope for eliminating mpox in the U.S. But getting from low to zero isn’t as easy as it might seem. This current stretch of decline could unspool for years, even decades, especially if the virus finds a new animal host. “We’ve seen this story play out so many times before,” Varma told me. Efforts to eliminate syphilis from the U.S. in the late ’90s and early 2000s, for instance, gained traction for a while—then petered out during what could have been their final stretch. It’s the classic boom-bust cycle to which the country is so prone: As case rates fall, so does interest in pushing them further down.

    Our memories of public-health crises never seem to linger for long. At the start of this mpox outbreak, Titanji told me, there was an opportunity to shore up our systems and buffer ourselves against future epidemics, both imported and homegrown. The country squandered it and failed to send aid abroad. If another surge of mpox cases arrives, as it very likely could, she said, “we will again be going back to the drawing board.”

    Katherine J. Wu

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  • Ringleaders in massive COVID fraud extradited to US

    Ringleaders in massive COVID fraud extradited to US

    LOS ANGELES — A Los Angeles couple who fled to Europe after being convicted of running a fraud ring that stole $18 million in COVID-19 aid money were returned to the United States to face prison, authorities announced Friday.

    Richard Ayvazyan and his wife, Marietta Terabelian, were extradited from the Balkan country of Montenegro, where they were living in a luxury seaside villa before their arrest in February.

    They arrived in Los Angeles on Thursday, according to the U.S. Department of Justice.

    While they were on the run last year, a court in Los Angeles sentenced Ayvazyan to 17 years in federal prison, and Terabelian to six years.

    Prosecutors said the couple and six accomplices fraudulently applied for about 150 relief loans intended to help businesses and employees struggling during the COVID-19 pandemic and lockdown.

    They applied using fake identities or names belonging to dead or elderly people and foreign exchange students, prosecutors said.

    To back up the applications, they submitted phony tax documents and payroll records for fake businesses to lenders and the U.S. Small Business Administration, prosecutors said.

    The money was used for down payments on luxury homes in the Tarzana area of Los Angeles, suburban Glendale and the Palm Desert and to buy “gold coins, diamonds, jewelry, luxury watches, fine imported furnishings, designer handbags, clothing and a Harley-Davidson motorcycle,” said a statement from the U.S. Department of Justice.

    Ayvazyan and Terabelian were convicted in June 2021 of conspiracy to commit bank fraud and other federal crimes. Two months later, while free on bond, the couple cut off their ankle monitors and fled, leaving behind their three teenage children, authorities said.

    Unemployment fraud was a nationwide problem during the pandemic, as benefit applications overwhelmed state unemployment agencies. Criminals were able to buy stolen identity data on the dark web and use it to file a heap of phony claims.

    The federal Labor Department has said that about $87 billion in pandemic unemployment benefits could have been paid improperly nationwide, with a significant portion attributable to fraud. An Associated Press review in March 2021 found that estimates ranged from $11 billion in fraudulent payments in California to several hundred thousand dollars in states such as Alaska and Wyoming.

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  • Feature: Answers to Your Psoriasis Questions

    Feature: Answers to Your Psoriasis Questions

    If you’ve just been diagnosed with psoriasis, you may have a few questions about it. Here are answers to some of the more common ones people ask.

    What’s the difference between psoriasis and eczema?

    To an untrained eye, these conditions may seem alike. But while they’re both skin diseases, they’re not the same. In fact, “They’re 100 percent different,” says Whitney High, MD, an associate professor of dermatology and the director of the Dermatopathology Laboratory at the University of Colorado Anschutz Medical Campus.

    Psoriasis doesn’t usually affect children, High says. But eczema, or atopic dermatitis, is a childhood disease. Eczema also tends to be itchier than psoriasis. Only about a third of people who have psoriasis say they have itchiness.

    And the conditions are likely to appear in different places. Eczema often shows up on kids’ faces and buttocks and the inside of their knees and elbows. Psoriasis isn’t typically found in those places.

    Plus, “The same person that has childhood eczema doesn’t get psoriasis. And the person who has psoriasis as a young adult usually didn’t have childhood eczema,” High says.

    What causes psoriasis?

    Doctors aren’t exactly sure. “I get that a lot of times; ‘Why do I have it?’” says Melvin Chiu, a doctor of dermatology at the David Geffen Medical Center at the University of California, Los Angeles. “I don’t really … have a good answer for that. It’s a big mystery, I think, right now.”

    Chiu says researchers believe the two main culprits behind psoriasis are your genes and your environment. Scientists are still tracking down which genes are to blame, but they think that about 1 out of every 10 people got at least one of the genes that can lead to psoriasis from their parents.  But only about 3% of people who have those genes get psoriasis. That’s where the environment comes into play.

    Researchers think things like infection (especially strep throat), an injury to the skin, certain medications, smoking, and other things may trigger the condition.

    What’s the cure?

    “There is no cure at this point,” Chiu says. “It’s a chronic condition. … You may have times when it’ll be worse, and there may be times when it’ll get better.” He also says there may be some lucky people in whom it’s very minimal. Or it gets better and doesn’t get worse again. But, he says, most people “can expect it will be persistent.” Treating it can make it better. But when treatments stop, it often comes back.

    “There are some really excellent treatments,” he says. “There are newer treatments in the pipeline, and many treatments [that] are available currently … work very well.” Those treatments don’t cure the disease, he says. “But they significantly improve the disease and make [people] feel better.”

    What are the treatments?

    The most common ones are medicines prescribed by your doctor. They include foams, solutions, ointments, or creams, called topicals, that you put on your skin, along with drugs you take that affect your whole body. Your doctor also may recommend light therapy.

    “Consult with a board-certified dermatologist, and they’ll be happy to discuss any and all of these options, including over-the-counter options when they’re appropriate,” High says.

    What works for one person may not work for another. That’s why you and your doctor need to talk about what your treatment plan should be.

    Chiu says that with the treatments available now, “we can get skin a lot better.” He says that 20 to 30 years ago, psoriasis patients had much worse options and many fewer ones than people do now. “I tell people, it’s kind of an exciting time in psoriasis.”

    Can the sun help?

    Some research says a little every day can help with your symptoms. But, as always, you have to be careful not to overdo it. A sunburn may lead to a flare-up.

    Is psoriasis contagious?

    You can’t “give” it to anyone, and no one can “catch” it from you.

    “You can touch psoriasis all day long,” High says. “As a dermatologist … I see at least one person if not a few people with psoriasis [every work day], and I don’t have it.” High adds, “My wife doesn’t have it. I didn’t bring it home. I don’t do special laundry. I don’t undress in the garage or anything like that.”

    What is psoriatic arthritis?

    Up to 30% of people who have psoriasis get this condition as well. It causes inflammation and swelling in your joints that can lead to pain and stiffness.

    If you have psoriasis and feel any discomfort in your joints, tell your doctor. It’s important to treat it quickly so your joints don’t get damaged.  

    Are any other conditions linked to psoriasis?

    Research is still under way, but scientists think people with psoriasis and psoriatic arthritis may be more likely to have other serious diseases.

    “There’s an increasing appreciation that psoriasis can manifest in other ways: increased risk of cardiovascular disease, increased risk for obesity … a natural risk for diabetes,” High says. “It might impact your life in ways that you can’t even really fully predict now.”

    Besides cardiovascular diseases and obesity, psoriasis also has been linked to cancer, Crohn’s disease, depression, and liver disease, among others.

    That’s even more reason to stay in touch with your doctor and make sure you have a plan.

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