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  • ‘We want men to heal’: Robert Marshall creates safe space for men to begin journey of healing from trauma  

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    Too many men live with unspoken wounds, sexual abuse, domestic violence, and family trauma that shape their lives but are rarely addressed. Silence and shame have kept brothers from healing for generations.

    Researchers have found that at least 1 in 6 men have experienced sexual abuse or assault, whether in childhood or as adults.

    Founder of the Survivor’s Circle and co-creator of the Brother’s Healing Male Trauma Mastermind, Robert “Dr. Rob” Marshall Jr., will be hosting Atlanta’s first-ever Male Trauma Mastermind conversation on Saturday, Dec. 13, from 11 a.m. to 2 p.m.

    This three-hour interactive experience will provide men and the women who support them with the tools, truth, and safe space needed to start or strengthen their healing journey.

    The gathering, Marshall says, is a thought-leadership and healing experience where men, particularly Black and Brown men, will openly share the stories we’ve often been forced to carry alone: childhood abuse, sexual trauma, fatherlessness, incarceration trauma, violence, emotional wounds, grief, shame, and identity struggles.

    This three-hour interactive experience will provide men and the women who support them with the tools, truth, and safe space needed to start or strengthen their healing journey. Photo by Tabius McCoy/The Atlanta Voice

    These conversations will be filmed for a national project designed to bring awareness to the silent epidemic of male trauma. But more importantly, this event is about creating tangible solutions, safe spaces, and healing pathways for our brothers.

    The idea of this event came from Marshall’s own experience with sexual abuse, fatherlessness, and realizing he never had a safe space to process.

    “I never thought I would be working with men because of my story, and I realized now, as a survivor of bullying, as a survivor of sexual abuse, as a survivor of all types of just different traumas, I’m realizing more than anything, men need a place to talk,” he said.

    Marshall says he has always asked the question, “Where do broken and hurting men go?” and the answer is always that they go to incarceration or a premature grave. With this information, he said he realized men need a space to talk and process.

    “When I say men, I mean all men. I’m not talking about just a cultural definition of what a man is,” he said. “I’m talking about a space where men from all walks of life, regardless of their religious beliefs, sexual orientation, socioeconomic background, can have a safe space to process and deal with the things they cannot talk about.”

    Photo by Tabius McCoy/The Atlanta Voice

    During the interactive experience, guests can expect a safe space to begin their journeys, Marshall says. Also, guests can expect healthcare professionals and therapists who are specifically trained for this dialogue.

    “Healing is a journey and wholeness is the destination, and we began our journey to wholeness one healing step at a time,” he said.

    To do this, Marshall says men must at least realize and be honest with themselves about where they are, what has happened to them, and what they’ve experienced.

    “What we want is this event to create a safe space where they can talk about the things they’re either demonized for talking about or they’re afraid to talk about,” he said. “For some men, they do not even know it’s happened, and they don’t know they don’t have the words for it, and a lot of times, black and brown men collectively, we experience things in our lives we don’t have verbiage for.”

    Men, Marshall says, often do not know it’s there until one day, they realize it’s affecting and changing their relationships and how they show up for work, their finances, who they love, how they love, and receive love.

    “We’re not here to fix anybody; we just want to create this space to begin that journey of healing,” Marshall said.

    Traumatologist Tray Groce, who will be at the event as well, said when starting a journey like this, there is a piece at the beginning, especially for men, which is getting them to connect with a version of themselves that society doesn’t always allow.

    “It’s the little boy in us that a lot of times society doesn’t allow us to heal,” he said. “We want to create this environment that is curated for safety because some men begin to open up in a way that their little versions of themselves that have been longing for where the trauma started, and we hope to make an atmosphere where, beyond all societal norms, can be seen at the core of who they are.”

    This event is urgent for Atlanta, Groce says, because there’s an urgency at the prevalence of what we see going on, specifically in black and brown communities.

    “Atlanta has a beautiful metropolitan DNA to it, and so with that in mind, if we can just start off with twos and threes of one man at a time, like one home, one family, one space , and allow that to multiply, healing is contagious,” he said.

    The significance of this conversation also coincides with the concept of recent holiday depression, Groce said.

    “It’s now more than ever appropriate to start hopeful conversations at a time where black and brown men are not feeling seen or heard,” he said. “There are many men out here longing for help, so we want to create this space to offer that.”

    For advice, Marshall says healing is a journey and wholeness is a destination.

    “I want men to know there’s a place called wholeness. I remember growing up thinking I would never be good enough, and I grew up in religious spaces, so I grew up believing no matter what, I was never good enough,” he said.

    He also says men will not be broken forever, and they don’t have to stay that way by finding the courage to begin their own journey.

    “It takes courage, because you must silence the voices that are in your head from your past. You must silence the fears that are trying to speak in your present, and you must combat lies that are coming from your future,” he said. “It’s never too late to become who you should have been.”

    The most dangerous man in the world, Marshall says, is a man who has hope, and the most dangerous man in the world is a man who doesn’t have hope.

    Furthermore, looking at data around Atlanta and surrounding regions, Groce says one in six men experience sexual trauma, and 39.9%, give or take, have experienced intimate partner violence. If 40% of the people in a city have gone through some form of this violence and traumatic experience, he says, the message of hope is one that needs to be resurfaced.

    Marshall says it’s one of the reasons why they are here, because of those stated statistics and how they are incorrect.

    “The Survivor’s Circle is also a research organization, and those stats are wrong because black and brown men don’t have a healthy relationship with police or the healthcare industries, which is where those data statistics come from,” he said.

    Subsequently, they believe it’s more like 80-85% of boys and men in urban communities have this worldwide, not just in Atlanta, and not just black and brown. Marshall says it’s more about urban social at lower socio-economic spaces.

    “80-85% of boys and men have experienced some form just of sexual abuse, and that’s not talking about all the other compounded trauma,” he said. “It can be sexual trauma with fatherlessness trauma compounded on top of it, or poverty, or gang violence. There’s something bigger going on here.”

    Furthermore, Marshall says he wants men to heal and begin their journeys in a safe, nonjudgmental, and supportive space.

    “We want men to heal,” he said. “I believe if you heal a man, you can heal a family. If you can heal a family, you can heal a community, and if you heal a community, we can heal the world. It takes a lot more patience, but a man, the results, and what you get out of that will change the world.”

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    Isaiah Singleton

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  • New Hampshire’s snowpack is shrinking. Researchers are still uncovering the scope of what it means.

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    Researcher Pamela Templer and her team removed snow from this study plot in Hubbard Brook Experimental Forest to simulate the increased freezing and thawing cycles created when snowpack recedes. Snowpack decline in the Northeast stresses trees and can reduce their ability to sequester carbon, Templer said. (Photo by Emerson Conrad-Rooney/Templer Lab)

    New England residents know that snow is disappearing from our landscape, and scientists have proven that climate change is to blame. But the effects of snowpack decline go far beyond what’s visible, and researchers working in the forests of New Hampshire and the Northeast are learning more about just how far the phenomenon stretches across seasons and landscapes. Their findings reveal how much tracking snow can tell us about the health of our forests and our world, and what is still to learn.

    The average amount of snow that accumulates on the ground throughout the winter season, or snowpack, is shrinking from year to year across the Northeast. While data has captured that effect (and linked it to human-caused climate change), many who live and recreate in the region have noticed it in their own lives — including the researchers who later took up the matter in their work.

    “I grew up cross-country skiing with my family,” said Emerson Conrad-Rooney, a doctoral student at Boston University whose work focuses on the effects of climate change on northern forests. Conrad-Rooney, who grew up in western Massachusetts, said the places they had grown up skiing through the winter were, in recent years, open only a handful of days all season long. “That’s been kind of separate from this research I’m doing, but just something that me and my family have seen … We’re, I think, definitely feeling that change,” they said.

    Eric Kelsey, a meteorologist and researcher at Plymouth State University, also grew up an enthusiastic winter recreator in Nashua. A love of snow and weather led Kelsey to learn more about the integral role of snowpack to the water cycle. But as he read more, Kelsey was struck by the relative lack of cohesive, long-term snowpack data, especially compared to other weather datasets tracking things like daily high and low temperatures and rainfall.

    “We just don’t have a climatology of snowpack — that was surprising to me,” Kelsey said.

    The problem, Kelsey said, was not necessarily a lack of data. For more than a century, people across the Northeast have logged information about snowfall, from dam operators attempting to predict how snowmelt would affect their rivers to farmers and ski slope proprietors.

    Appalachian Mountain Club employee Maddie Ziomek uses National Weather Service instruments to measure snowpack in the White Mountain National Forest. (Photo by Maddie Ziomek/Appalachian Mountain Club)

    Most tracked snow depth and snow water equivalent (the amount of water contained in that snow, a measure that fluctuates with snow density). Their observations, taken as a whole, are a rich collection of information about snowfall in New England, Kelsey said. But the records were also scattered and disparate, making it difficult for scientists to unlock the information they contained.

    Now, Kelsey and Plymouth State graduate student David Zywiczynski are halfway through a National Oceanic and Atmospheric Administration grant-funded effort to unify and clean that data, which includes measurements taken over yearslong periods from more than 400 sites. Then, they hope, scientists will be able to use it to make sense of long-term patterns in local snowpack, from general decline to years of snow drought — or abnormally low snowfall conditions.

    Because snowpack plays an important role in replenishing streams, lakes, and aquifers when it melts each spring, a tool to identify snow drought with more certainty could help forecasters anticipate the dry conditions that will likely persist later in the year, Kelsey said. The “snow drought index” Kelsey and Zywiczynski are working on to facilitate that may be the first tool of its kind in the nation.

    As historic data is put to work at Plymouth State, elsewhere in New Hampshire, scientists are tracking ongoing changes in forests as they unfold.

    Just beneath Mount Washington in Pinkham Notch, Appalachian Mountain Club Senior Scientist Georgia Murray oversees the collection of daily snowpack depth and snow water equivalent measurements. Data collected in the notch and above at the Mount Washington Observatory stretches back to the 1930s, Murray said, constituting one of the longer sets of continuous snowpack observations available in the region.

    Measurements from the two relatively close sites are often very different on the same day, highlighting how difficult it can be to assess snowpack, Murray said. Unlike rain, snow blows around once it falls, clearing off some areas completely and piling up in others. Having data from as many sites as possible is desirable for a more comprehensive understanding, Murray said, so she also works to encourage citizen scientists to measure and submit snowpack data across the region through a smartphone app.

    “It’s complex with snowpack, because you have, you know, nooks and crannies across the mountain, and so you have so many ways that snow is distributed differently. Having citizen science data fill in the gaps is something we really value in the mountain ecosystem, where we can’t be everywhere,” Murray said.

    Citizen science data also helps keep track of the downstream effects of snowpack decline, including its impact on plant life. Plants rely on natural cues to time their life cycles; when some cues, like the presence of snow, change while others, like day length, do not, they may be negatively impacted, Murray said.

    “In climate change, there can be these mismatches of synchronicity,” she said.

    Furthermore, as snow melts in spring, the water it releases carries nutrients through the soil, making them more available to the roots of hungry and thirsty young plants. But data shows that the timing of snow melt is changing, too, starting earlier and lasting for longer. Murray hopes citizen data will help shine a light on what that could mean for White Mountain plants, from delicate spring ephemeral wildflowers to alpine trees.

    “The snowmelt timing has a strong impact in the spring, and can have a ripple effect over the growing season,” she said.

    Understanding those and other ripple effects of snowpack decline is crucial to making informed predictions about what the future might bring for New England, researchers said.

    Pamela Templer, chair of the Biology department at Boston University and a researcher who has studied northern forests for more than two decades, established a set of three research plots at Hubbard Brook Experimental Forest, in the White Mountains, about 10 years ago. The goal of the study, entitled “Climate Change Across Seasons Experiment,” or CCASE, was to assess how seasonal changes play off each other in yearly cycles.

    Before that study, researchers had shown that in summer, temperate forests experienced some positive effects from growing seasons that were stretching longer, Templer said. Separate studies, including in Templer’s own work, had revealed the negative impacts on temperate forests from warming winters. But Templer wanted to assess those two phenomena together.

    “We didn’t know at that point what the net effect of those two changes in climate were on the forest,” Templer said.

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    To do so, Templer and her team — including Conrad-Rooney and “a village” of other researchers — simulated the freeze-thaw cycle, which can occur in the forest floor when it is not protected by an insulating layer of snow, by removing snow in some plots and heating the ground before allowing it to re-freeze. Precise measurements of the trees within the plot, taken over the 10 years the study has run so far, tracked the forest’s growth and the amount of carbon it was storing away over that period.

    The work is a demonstration of one of the many ways snowpack decline can add stress into an ecosystem, said Kelsey, who was not involved in the study.

    To a tree, damage from repeated freezing and thawing “is, you know, like getting a cut on your finger,” Kelsey said. “It hurts, it will take some resources from your body to heal it, that could be doing other things… And as we know, if there’s too many stressors on a tree, it will die. So this is just adding another stressor to the trees. That’s not good.”

    Ultimately, Templer, Conrad-Rooney, and researcher Andrew Reinmann concluded in a study published this July that the benefits to trees from longer growing seasons were outweighed by the damage those trees suffered from repeated freeze-thaw cycles in the winter. That finding, they said, reveals that previous models projecting forests’ role in helping sequester carbon may have overestimated their role in absorbing greenhouse gas.

    “If we think that forests are actually storing more carbon than is actually happening, then that means that, maybe, more carbon would be going into our atmosphere than we realize,” Conrad-Rooney said.

    This realization has implications for scientists’ ability to model ecosystem changes into the future. It could also inform land conservation decisions, Templer said.

    “We need an accurate accounting,” she said. “If we’re going to use forests as nature-based solutions to climate change in terms of sequestering carbon, then we need to know how much they’re sequestering.”

    Researchers expect that as they continue to examine historic and current snowpack data, more effects and ripples of snowpack decline will emerge.

    From its role in keeping lakes cool through the summer to protecting the landscape from wildfire, snow impacts the water cycle all year long, Kelsey said. And – as is evident both in the origin of the field’s data and its implications – the study of snow brings together many interests, including those of industry, agriculture, tourism, homeowners with wells, and more.

    “It touches our lives in so many ways,” Murray said. “… We hope that people see the science that we’re doing, so that they can understand what’s happening, and how it links to their lives and the outdoors.”

    This story was originally published by New Hampshire Bulletin. Like Maine Morning Star, New Hampshire Bulletin is part of States Newsroom, a nonprofit news network supported by grants and a coalition of donors as a 501c(3) public charity. New Hampshire Bulletin maintains editorial independence. Contact Editor Dana Wormald for questions: info@newhampshirebulletin.com.

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  • Researchers develop incredibly intelligent tech that predicts future disasters: ‘We can create simulations’

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    Floods can destroy more than property, taking away the feeling of security that comes with a home.

    Researchers from Pennsylvania State University and other institutions may have cracked a big part of the puzzle in ensuring future safety from such disasters. Their model predicts floods with more accuracy and in far less time than older tools. “With our new approach, we can create simulations using the same process, regardless of the region we are trying to simulate,” civil and environmental engineering professor Chaopeng Shen said.

    NOAA’s National Water Model is the standard hydrologists rely on. But while it’s trusted, it’s also slow. Traditional calibration involves feeding it decades of river data for every site. One site at a time. Shen described it as “time-consuming, expensive, and tedious.” The team’s new method speeds things up using artificial intelligence systems that can spot patterns in mountains of data.

    Instead of having to start over with every river basin, AI can generalize information using past readings. “Rather than approaching each site individually, the neural network applies general principles it interprets from past data to make predictions,” co-author Yalan Song said.

    The model still follows physics-based rules about how water behaves, but it quickly adapts to new areas. And while AI is great when it comes to deciphering patterns, rare storms throw a monkey wrench in the works. Song said their model keeps the water physics in place, then allows the network to learn from the messy parts.

    This method predicts extreme rainfall much better than older tools. Researchers used 15 years of river data and asked the system to replay 40 years of streamflow. Against real records, its projections landed about 30% closer across 4,000 sites.

    “With a trained neural network, we can generate parameters for the entire U.S. within minutes,” Shen said. Work that once took weeks on many supercomputers now is finished in hours on one machine.

    Similar methods have been used to design safer solid-state batteries. They can also map city vegetation for cooling plans. Labs even test AI in nuclear fusion research.

    MIT News reported that training models uses large amounts of electricity and water. A study by Hugging Face and Carnegie Mellon University found some systems can consume as much electricity as a small country. The industry, however, is moving toward renewable energy, and this could buy families time to save more than just their possessions.

    Join our free newsletter for weekly updates on the latest innovations improving our lives and shaping our future, and don’t miss this cool list of easy ways to help yourself while helping the planet.

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  • Flu Shots Need to Stop Fighting ‘Something That Doesn’t Exist’

    Flu Shots Need to Stop Fighting ‘Something That Doesn’t Exist’

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    Produced by ElevenLabs and NOA, News Over Audio, using AI narration.

    In Arnold Monto’s ideal vision of this fall, the United States’ flu vaccines would be slated for some serious change—booting a major ingredient that they’ve consistently included since 2013. The component isn’t dangerous. And it made sense to use before. But to include it again now, Monto, an epidemiologist and a flu expert at the University of Michigan, told me, would mean vaccinating people “against something that doesn’t exist.”

    That probably nonexistent something is Yamagata, a lineage of influenza B viruses that hasn’t been spotted by global surveyors since March of 2020, shortly after COVID mitigations plummeted flu transmission to record lows. “And it isn’t for lack of looking,” Kanta Subbarao, the director of the WHO’s Collaborating Centre for Reference and Research on Influenza, told me. In a last-ditch attempt to find the missing pathogen, a worldwide network of monitoring centers tested nearly 16,000 influenza B virus samples collected from February to August of last year. Not a single one of them came up Yamagata. “The consensus is that it’s gone,” Cheryl Cohen, the head of South Africa’s Centre for Respiratory Diseases and Meningitis, told me. Officially removing an ingredient from flu vaccines will codify that sentiment, effectively publishing Yamagata’s obituary.

    Read: The flu may never be the same

    Last year around this time, Subbarao told me, the WHO was already gently suggesting that the world might want to drop Yamagata from vaccines; by September, the agency had grown insistent, describing the ingredient as “no longer warranted” and urging that “every effort should be made to exclude it as soon as possible.” The following month, an advisory committee to the FDA unanimously voted to speedily adopt that same change.

    But the switch from a four-flu vaccine to a trivalent one, guarding against only three, isn’t as simple as ordering the usual, please, just hold the Yams. Trivalent vaccines require their own licensure, which some manufacturers may have allowed to lapse—or never had at all; manufacturers must also adhere to the regulatory pipelines specific to each country. “People think, ‘They change the strains every season; this should be no big deal,’” Paula Barbosa, the associate director of vaccine policy at the International Federation of Pharmaceutical Manufacturers and Associations, which represents vaccine manufacturers, told me. This situation is not so simple: “They need to change their whole manufacturing process.” At the FDA advisory-committee meeting in October, an industry representative cautioned that companies might need until the 2025–26 season to fully transition to trivalents in the Northern Hemisphere, a timeline that Barbosa, too, considers realistic. The South could take until 2026.

    In the U.S., though, where experts such as Monto have been pushing for expedient change, a Yamagata-less flu vaccine could be coming this fall. When I reached out to CSL Seqirus and GSK, two of the world’s major flu-vaccine producers, a spokesperson from each company told me that their firm was on track to deliver trivalent vaccines to the U.S. in time for the 2024–25 flu season, should the relevant agencies recommend and request it. (The WHO’s annual meeting to recommend the composition of the Northern Hemisphere’s flu vaccine isn’t scheduled until the end of February; an FDA advisory meeting on the same topic will follow shortly after.) Sanofi, another vaccine producer, was less definitive, but told me that, with sufficient notice from health authorities, its plans would allow for trivalent vaccines this year, “if there is a definitive switch.” AstraZeneca, which makes the FluMist nasal-spray vaccine, told me that it was “engaging with the appropriate regulatory bodies” to coordinate the shift to a trivalent vaccine “as soon as possible.”

    Quadrivalent flu vaccines are relatively new. Just over a decade ago, the world relied on immunizations that included two flu A strains (H1N1 and H3N2), plus one B: either Victoria or Yamagata, whichever scientists predicted might be the bigger scourge in the coming flu season. “Sometimes the world got it wrong,” Mark Jit, an epidemiologist at the London School of Hygiene & Tropical Medicine, told me. To hedge their bets, experts eventually began to recommend simply sticking in both. But quadrivalent vaccines typically cost more to manufacture, experts told me. And although several countries, including the U.S., quickly transitioned to the heftier shots, many nations—especially those with fewer resources—never did.

    Now “the extra component is a waste,” Vijay Dhanasekaran, a virologist at the University of Hong Kong, told me. It’s pointless to ask people’s bodies to mount a defense against an enemy that will never attack. Trimming Yamagata out of flu-vaccine recipes should also make them cheaper, Dhanasekaran said, which could improve global access. Plus, continuing to manufacture Yamagata-focused vaccines raises the small but serious risk that the lineage could be inadvertently reintroduced to the world, Subbarao told me, as companies grow gobs of the virus for their production pipeline. (Some vaccines, such as FluMist, also immunize people with live-but-weakened versions of flu viruses.)

    Some of the researchers I spoke with for this article weren’t ready to rule out the possibility—however slim—that Yamagata is still biding its time somewhere. (Victoria, a close cousin of Yamagata, and the other B lineage that pesters people, once went mostly quiet for about a decade, before roaring back in the early aughts.) But most experts, at this point, are quite convinced. The past couple of flu seasons have been heavy enough to offer even a rather rare lineage the chance to reappear. “If it had been circulating in any community, I’m pretty sure that global influenza surveillance would have detected it by now,” Dhanasekaran said. Plus, even before the pandemic began, Yamagata had been the wimpiest of the flu bunch, Jit told me: slow to evolve, crummy at transmitting, and already dipping in prevalence. When responses to the pandemic starved all flu viruses of hosts, he said, this lineage was the likeliest to be lost.

    Read: The pandemic broke the flu

    Eventually, companies may return to including four types of flu in their products, swapping in, say, another strain of H3N2, the most severe and fastest-evolving of the bunch—a change that Subbarao and Monto both told me might actually be preferable. But incorporating a second H3N2 is even more of a headache than returning to a trivalent vaccine: Researchers would likely first need to run clinical trials, experts told me, to ensure that the new components played nicely with each other and conferred additional benefits.

    For the moment, a slimmed-down vaccine is the quickest way to keep up with the flu’s current antics. And in doing so, those vaccines will also reflect the strange reality of this new, COVID-modified world. “A whole lineage of flu has probably been eliminated through changes in human behavior,” Jit told me. Humanity may not have intended it. But our actions against one virus may have forever altered the course of another.

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    Katherine J. Wu

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  • ‘If Exercise Could Cure This, I Would Have Been Cured So Quickly’

    ‘If Exercise Could Cure This, I Would Have Been Cured So Quickly’

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    In the weeks after she caught COVID, in May 2022, Lauren Shoemaker couldn’t wait to return to her usual routine of skiing, backpacking, and pregaming her family’s eight-mile hikes with three-mile jogs. All went fine in the first few weeks after her infection. Then, in July, hours after finishing a hike, Shoemaker started to feel off; two days later, she couldn’t make it to the refrigerator without feeling utterly exhausted. Sure it was a fluke, she tried to hike again—and this time, was out of commission for months. Shoemaker, an ecologist at the University of Wyoming, couldn’t do her alpine fieldwork; she struggled to follow a movie with a complex plot. She was baffled. Exercise, the very thing that had reliably energized her before, had suddenly become a trigger for decline.

    For the majority of people, exercise is scientifically, physiologically, psychologically good. It boosts immunity, heart function, cognition, mood, energy, even life span. Doctors routinely prescribe it to patients recovering from chronic obstructive pulmonary disease and heart attacks, managing metabolic disease, or hoping to stave off cognitive decline. Conditions that worsen when people strive for fitness are very rare. Post-exertional malaise (PEM), which affects Shoemaker and most other people with long COVID, just happens to be one of them.

    PEM, first described decades ago as a hallmark of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), is now understood to fundamentally alter the body’s ability to generate and use energy. For people with PEM, just about any form of physical, mental, or emotional exertion—in some cases, activities no more intense than answering emails, folding laundry, or digesting a particularly rare steak—can spark a debilitating wave of symptoms called a crash that may take weeks or months to abate. Simply sitting upright for too long can leave Letícia Soares, a long-hauler living in Brazil, temporarily bedbound. When she recently moved into a new home, she told me, she didn’t bother buying a dining table or chairs—“it just felt useless.”

    Read: How much less to worry about long COVID now

    When it comes to PEM, intense exercise—designed to boost fitness—is “absolutely contraindicated,” David Putrino, a physical therapist who runs a long-COVID clinic at Mount Sinai, in New York, told me. And yet, the idea that exertion could undo a person rather than returning them to health is so counterintuitive that some clinicians and researchers still endorse its potential benefits for those with PEM; it’s dogma that Shoemaker heard repeatedly after she first fell ill. “If exercise could cure this,” she told me, “I would have been cured so quickly.”

    The problem is, there’s no consensus about what people who have PEM should do instead. Backing off physical activity too much might start its own downward spiral, as people lose muscle mass and strength in a phenomenon called deconditioning. Navigating the middle ground between deconditioning and crashing is “where the struggle begins,” Denyse Lutchmansingh, a pulmonary specialist at Yale, told me. And as health experts debate which side to err on, millions of long-haulers are trying to strike their own balance.

    Though it’s now widely accepted that PEM rejiggers the body’s capacity for strain, scientists still aren’t sure of the precise biological causes. Some studies have found evidence of impaired blood flow, stymieing the delivery of oxygen to cells; others have discovered broken mitochondria struggling to process raw fuel into power. A few have seen hints of excessive inflammation, and immune cells aberrantly attacking muscles; others point to issues with recovery, perhaps via a slowdown in the clearance of lactate and other metabolic debris.

    The nature of the crashes that follow exertion can be varied, sprawling, and strange. They might appear hours or days after a catalyst. They can involve flu-like coughs or sore throats. They may crater a patient’s cognitive capacity or plague them with insomnia for weeks; they can leave people feeling so fatigued and pained, they’re almost unable to move. Some of Shoemaker’s toughest crashes have saddled her with tinnitus, numbness, and extreme sensitivity to sound and light. Triggers can also change over time; so can people’s symptoms—even the length of the delay before a crash.

    But perhaps the worst part is what an accumulation of crashes can do. Rob Wüst, who studies skeletal-muscle physiology at Amsterdam University Medical Center, told me that his team has found an unusual amount of muscle damage after exertion in people with PEM that may take months to heal. People who keep pushing themselves past their limit could watch their baseline for exertion drop, and then drop again. “Every time you PEM yourself, you travel a little further down the rabbit hole,” Betsy Keller, an exercise physiologist at Ithaca College, told me.

    Read: Long COVID has forced a reckoning for one of medicine’s most neglected diseases

    Still, the goal of managing PEM has never been to “just lay in a bed all day and don’t do anything,” Lily Chu, the vice president of the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (IACFS/ME), told me. In the 1960s, a group of scientists found that three weeks of bed rest slashed healthy young men’s capacity for exertion by nearly 30 percent. (The participants eventually trained themselves back to baseline.) Long periods of bed rest were once commonly prescribed for recovery from heart attacks, says Prashant Rao, a sports cardiologist at Beth Israel Deaconess Medical Center, in Massachusetts. But now too much rest is actively avoided, because “there’s a real risk of spiraling down, and symptoms worsening,” Rao told me. “I really fear for that, even for people with PEM.”

    There is no rulebook for threading this needle, which has led researchers to approach treatments and rehabilitation for long COVID in different ways. Some clinical trials that involve exercise as an intervention explicitly exclude people with PEM. “We did not feel like the exercise program we designed would be safe for those individuals,” Johanna Sick, a physiologist at the University of Vienna who is helping run one such trial, told me.

    Other researchers hold out hope that activity-based interventions may still help long-haulers, and are keeping patients with PEM in experiments. But some of those decisions have been controversial. The government-sponsored RECOVER trial was heavily criticized last year for its plan to enroll long-haulers in an exercise study. Scientists have since revised the trial’s design to reroute participants with moderate to severe PEM to another intervention, according to Adrian Hernandez, the Duke cardiologist leading the trial. The details are still being finalized, but the plan is to instead look at pacing, a strategy for monitoring activity levels to ensure that people stay below their crash threshold, Janna Friedly, a physiatrist at the University of Washington who’s involved in the trial, told me.

    Certain experimental regimens can be light enough—stretching, recumbent exercises—to be tolerable by many (though not all) people with PEM. Some researchers are trying to monitor participants’ heart rate, and having them perform only activities that keep them in a low-intensity zone. But even when patients’ limitations are taken into account, crashes can be hard to avoid, Tania Janaudis-Ferreira, a physiotherapist at McGill University, in Quebec, told me. She recently wrapped a clinical trial in which, despite tailoring the regimen to each individual, her team still documented several mild to moderate crashes among participants with PEM.

    Read: Long COVID is being erased—again

    Just how worrisome crashes are is another matter of contention. Pavlos Bobos, a musculoskeletal-health researcher at the University of Western Ontario, told me that he’d like to see more evidence of harm before ruling out exercise for long COVID and PEM. Bruno Gualano, a physiologist at the University of São Paulo, told me that even though crashes seem temporarily damaging, he’s not convinced that exercise worsens PEM in the long term. But Putrino, of Mount Sinai, is adamant that crashes set people back; most other experts I spoke with agreed. And several researchers told me that, because PEM seems to upend basic physiology, reduced activity may not be as worrisome for people with the condition as it is for those without.

    For Shoemaker, the calculus is clear. “Coming back from being deconditioned is honestly trivial compared to recovering from PEM,” she told me. She’s willing to wait for evidence-based therapies that can safely improve her PEM. “Whatever we figure out, if I could get healthy,” she told me, “then I can get back in shape.”

    At this point, several patients and researchers told me, most exercise-based trials for long COVID seem to be at best a waste of resources, and at worst a recipe for further harm. PEM is not new, nor are the interventions being tested. Decades of research on ME/CFS have already shown that traditional exercise therapy harms more often than it helps. (Some researchers insisted that more PEM studies are needed in long-haulers—just in case the condition diverges substantially from its manifestation in ME/CFS.) And although a subset of long-haulers could be helped by exercise, experts don’t yet have a great way to safely distinguish them from the rest.

    Even pacing, although often recommended for symptom management, is not generally considered to be a reliable treatment, which is where most long-COVID patient advocates say funds should be focused. Ideally, Putrino and others told me, resources should be diverted to trials investigating drugs that might address PEM’s roots, such as the antiviral Paxlovid, which could clear lingering virus from long-haulers’ tissues. Some researchers are also hopeful about pyridostigmine, a medication that might enhance the delivery of oxygen to tissues, as well as certain supplements that might support mitochondria on the fritz.

    Those interventions are still experimental—and Putrino said that no single one is likely to work for everyone. That only adds to the challenge of studying PEM, which has been shrouded in disbelief for decades. Despite years of research on ME/CFS, Chu, of the IACFS/ME, told me that many people with the condition have encountered medical professionals who suggest that they’re just anxious, even lazy. It doesn’t help that there’s not yet a blood test for PEM; to diagnose it, doctors must ask their patients questions and trust the answers. Just two decades ago, researchers and physicians speculated that PEM stemmed from an irrational fear of activity; some routinely prescribed therapy, antidepressants, and just pushing through, Chu said. One highly publicized 2011 study, since widely criticized as shoddy science, appeared to support those claims—influencing treatment recommendations from top health authorities such as the CDC.

    The CDC and other organizations have since reversed their position on exercise and cognitive behavioral therapy as PEM treatments. Even so, many people with long COVID and ME/CFS are still routinely told to blow past their limits. All of the long-haulers I spoke with have encountered this advice, and learned to ignore it. Fighting those calls to exercise can be exhausting in its own right. As Ed Yong wrote in The Atlantic last year, American society has long stigmatized people who don’t push their way through adversity—even if that adversity is a medically documented condition that cannot be pushed through. Reconceptualizing the role of exercise in daily living is already a challenge; it is made all the more difficult when being productive—even overworked—is prized above all else.

    Read: Fatigue can shatter a person

    Long-haulers know that tension intimately; some have had to battle it within themselves. When Julia Moore Vogel, a researcher at Scripps, developed long COVID in the summer of 2020, she was at first determined to grit her way through. She took up pilates and strength training, workouts she at the time considered gentle. But the results were always the same: horrific migraines that relegated her to bed. She now does physical therapy to keep herself moving in safe and supervised amounts. When Vogel, a former competitive runner, started her program, she was taken aback by how little she was asked to do—sometimes just two reps of chin tucks. “I would always laugh because I would be like, ‘These are not exercises,’” she told me. “I’ve had to change my whole mental model about what exercise is, what exertion is.”

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    Katherine J. Wu

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  • A Genetic Snapshot Could Predict Preterm Birth

    A Genetic Snapshot Could Predict Preterm Birth

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    This article was originally published by Knowable Magazine.

    For expectant parents, pregnancy can be a time filled with joyful anticipation: hearing the beating of a tiny heart, watching the fetus wiggling through the black-and-white blur of an ultrasound, feeling the jostling of a little being in the belly as it swells.

    But for many, pregnancy also comes with serious health issues that can endanger both parent and child. In May, for example, the U.S. Olympic sprinter Tori Bowie died while in labor in her eighth month of pregnancy. Potential factors contributing to her death included complications of preeclampsia, a pregnancy-specific disorder associated with high blood pressure. Preeclampsia occurs in an estimated 4.6 percent of pregnancies globally. Left untreated, it can lead to serious problems such as seizures, coma, and organ damage.

    Preeclampsia and preterm birth are relatively common conditions that can put both the mother and her baby at risk of health issues before and after birth. But doctors don’t have a good way to determine whether an individual will develop one of these complications, says Thomas McElrath, an ob-gyn at Brigham and Women’s Hospital, in Boston. Currently, physicians primarily look to a woman’s prior pregnancies, medical history, and factors such as age and ethnicity to determine her risk. These measures are useful but limited, and may fail to identify problems early enough to enable effective treatment, McElrath says. “They’re not as precise as I think most of us, as clinicians, would really want.”

    That may soon change. Scientists are learning that free-floating bits of genetic material found in a pregnant person’s blood may offer a way to detect complications such as preeclampsia and preterm birth—although some experts caution that it’s too early to determine how useful these tests will be in the clinic. In the meantime, the tests are providing researchers with a new way to unravel the underlying biology of these inscrutable ailments.

    All of us carry bits of our own genetic material—both DNA and its more evanescent cousin, RNA—around in our bloodstreams. During pregnancy, these free-floating fragments, known as cell-free DNA and RNA, are also released from the developing fetus into the mother’s blood, primarily via the placenta. For more than a decade, clinicians have used cell-free DNA from blood to screen the fetus for genetic abnormalities.

    But DNA provides a largely static view of the genetic content within our cells. RNA gives a snapshot of which genes are turned on or off at a specific point in time. Because gene activity varies across cells and over time, researchers realized that they could use RNA to glean a more dynamic view of the changes that occur within the mother’s body during pregnancy. RNA enables scientists to look beyond the fixed genotype to factors that change over the course of pregnancy such as prenatal complications, says Mira Moufarrej, a postdoctoral researcher at Stanford University who co-authored a paper in the 2023 Annual Review of Biomedical Data Science on noninvasive prenatal testing with circulating RNA and DNA.

    Read: The pregnancy risk that doctors won’t mention

    To screen for possible complications, scientists have been looking at cell-free RNA in pregnant women’s blood that originates from both mother and child. Some of the earliest studies of this kind emerged in the early 2000s. In 2003, for example, Dennis Lo, a chemical pathologist at the Chinese University of Hong Kong, and his colleagues reported that in a study of 22 pregnant women, a specific RNA released from the placenta was much more abundant during the third trimester in those who had preeclampsia than in those who did not. Over the years, Lo’s group and others have looked at broader changes in RNA during pregnancy in larger groups of people.

    In a 2018 study, Moufarrej, who was then a doctoral student; her adviser Stephen Quake, a biophysicist at Stanford University; and colleagues reported that cell-free RNA could help determine when labor would occur. The researchers recruited 38 pregnant women in the United States known to be at risk of preterm birth, and then drew a blood sample from each. By comparing cell-free RNA in those who eventually delivered prematurely with that in those who gave birth at full term, they were able to identify a set of RNAs that appeared up to two months prior to labor that could pinpoint about 80 percent of premature births.

    That proof-of-concept investigation spurred the researchers to look further and examine whether cell-free RNA could also predict preeclampsia. Other groups had previously reported RNA-based signatures of preeclampsia—in 2020, for instance, scientists working with the California-based biotech company Illumina reported dozens of RNA transcripts that were unique to a small cohort of pregnant women with the condition. But Moufarrej, Quake, and their colleagues wanted to track RNA changes throughout pregnancy to see whether it might be possible to identify people at risk of preeclampsia during early pregnancy, before symptoms began.

    In a study published in 2022, the researchers recruited several dozen mothers at heightened risk of preeclampsia and drew blood from them four times: at or before 12 weeks, in weeks 13 to 20, at or after 23 weeks, and after birth. Afterward, the researchers compared cell-free RNA for women who indeed developed preeclampsia against that of those who did not. The team identified RNAs corresponding to 544 genes whose activity differed in those who developed preeclampsia and those who did not. (The study did not differentiate between maternal and fetal RNA, but because the majority of cell-free RNA in a pregnant person’s blood is their own, Moufarrej says that most of these RNAs are likely maternal in origin.)

    Then, using a computer algorithm, the researchers developed a test based on 18 genes measured prior to 16 weeks of pregnancy that could be used to predict a woman’s risk of developing preeclampsia months later. The test correctly identified all of the women who would later develop preeclampsia—and, equally important, all of the women who the test predicted wouldn’t develop preeclampsia did in fact escape the disease. (About a quarter of the women who were predicted to develop preeclampsia did not get the disease.) The same 18-gene panel also correctly predicted most cases of preeclampsia in two other groups totaling 118 women.

    The team also took a closer look at which tissues the RNA of interest originated from. This included the usual suspects, such as the lining of the blood vessels (also known as the endothelium), which scientists already know is associated with preeclampsia, as well as other, more unexpected sources, such as the nervous and muscular systems. The authors note that, in the future, this information could be used both to understand how preeclampsia affects different parts of the body and to assess which organs are at highest risk of damage in a particular patient.

    According to Quake, studies like these from both his team and others are starting to reveal the diversity of changes throughout the body that contribute to pregnancy complications—and providing evidence for something that clinicians and researchers have long suspected: that both preeclampsia and preterm birth are conditions with a range of underlying causes and outcomes. “There are now strong indications that you should be defining multiple subtypes of preeclampsia and preterm birth with molecular signatures,” says Quake. “That could really transform the way physicians approach the disease.”

    Research teams elsewhere are also looking at other pregnancy complications such as reduced fetal growth, which can cause infants to be at higher risk of problems such as low blood sugar and a reduced ability to fight infections. Some of these tests are now being validated in large studies, while others are still in the early days of development.

    RNA-based tests for both preeclampsia and preterm-birth risk are inching their way toward the clinic. Mirvie, a company co-founded by Quake in South San Francisco, is focused on developing both. Last year, the company published a study of a preterm-birth test with hundreds of pregnant individuals as well as one on a preeclampsia test with samples from more than 1,000 women. Both studies had promising results. The company is now in the middle of an even larger study of the preeclampsia test that will include 10,000 pregnancies, Quake says. (Quake and Moufarrej are both shareholders of Mirvie.)

    Cell-free RNA-based tests for preeclampsia are leading the way, says McElrath, likely because preterm birth has more subtypes and more potential causes—including carrying multiples, chronic health conditions such as diabetes, and preeclampsia—which make it a more complicated issue to address. (McElrath is involved in validating Mirvie’s tests; he serves as a scientific adviser to the company and has a financial stake in it.)

    Read: Childbirth is no fun. But an extremely fast birth can be worse.

    Still, questions about these tests remain. An important next step, says Moufarrej, is determining what’s behind the RNA changes associated with a heightened risk for these pregnancy complications. All of the studies conducted to date have been correlative—linking patterns in RNA with risk—but to provide effective treatment, it will be important to determine the cause of these changes, she adds. Another open question is how important maternal versus fetal RNAs are to determining the risk of pregnancy complications. To date, most studies have not distinguished between these two sources. “This remains an active area of investigation,” McElrath says.

    Erik Sistermans, a human geneticist at Amsterdam UMC, says that although  researchers can learn a lot from cell-free RNA, it’s still too early to judge what the power of these RNA-based tests will be in clinical practice. He notes that he and other researchers are also investigating the possibility of using cell-free DNA to determine the risk of pregnancy complications such as preeclampsia. For example, some groups are looking at chemical modifications to DNA known as epigenetic changes, which occur in response to age, environment, and other factors.

    Yalda Afshar, a maternal- and fetal-medicine physician at UCLA, agrees that it’s still unclear whether these tests will provide benefits not available from existing screening methods such as looking for the presence of risk factors. For these screening tests to truly benefit patients, clinicians will first need to understand the underlying biology of these complications—and have effective treatments to offer patients found to be at risk, she adds. (Afshar is an unpaid consultant for Mirvie.)

    There are also ethical questions to consider. Screening tests provide only an estimate of risk, not a definitive diagnosis, Sistermans notes. Before these tests are rolled out to the public, it will be crucial to consider how best to communicate test results, and what next steps to take for individuals who are identified as being in a high-risk category, he says. For preeclampsia, low-dose aspirin can help prevent or delay its onset, while the hormone progesterone may help prevent some cases of preterm birth. But every additional test added to a prenatal screen makes decisions more complicated and potentially stressful for pregnant women. “You shouldn’t underestimate the amount of anxiety these kinds of tests may cause,” Sistermans says.

    Still, researchers are optimistic about the future of cell-free RNA-based tests. The tests for preeclampsia are already more accurate than currently available tests for the condition, according to McElrath. And if researchers succeed in predicting other complications, he adds, future patients will benefit not just from additional information about their pregnancies, but also from the opportunity to receive more personalized care. “Once we start to see success in early preeclampsia prediction,” McElrath says, “it will quickly spread out from there.”

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    Diana Kwon

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  • An Adorable Way to Study How Kids Get Each Other Sick

    An Adorable Way to Study How Kids Get Each Other Sick

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    At the start of 2022, as the Omicron variant of the coronavirus blazed across the United States, Seema Lakdawala was in Pittsburgh, finalizing plans to open a brand-new day care. She had found the perfect facility and signed the stack of paperwork; she had assembled a hodgepodge of plushies, puzzles, and toys. It was the perfect setup, one that “I’ve been dreaming about for years,” Lakdawala, a virologist at Emory University, told me. She couldn’t help but swell with pride, later that spring, when she ushered in her establishments’ first attendees: five young ferrets—including one deliberately infected with the flu.

    Over the next several months, Lakdawala and her colleagues watched several cohorts of ferrets ping-pong flu viruses back and forth as they romped and wrestled and frolicked inside of a shared playpen. The researchers meticulously logged the ferrets’ movements; they took note of the surfaces and other animals that each one touched. Their early findings, now being prepared for publication in a scientific journal, could help researchers figure out how flu viruses most efficiently spread in group settings—not just among ferrets, but among human kids.

    Aerosols, droplets, face-to-face contact, contaminated surfaces—there are plenty of ways for flu viruses to spread. But the nitty-gritty of flu transmission remains “pretty much a black box,” says Aubree Gordon, an epidemiologist at the University of Michigan. Despite decades of research, “we really don’t know the relative importance of each potential route.” Now, though, ferrets in playpens could help researchers to tease out those dynamics—and even, someday, to design flu-blocking measures for bona fide day cares.

    Ferrets have long been the “gold standard for influenza infection and transmission,” says Nicole Rockey, an environmental engineer at Duke University who led the experiments with Lakdawala. The animals’ airway architecture is uncannily similar to ours, and unlike most lab mice, ferrets are vulnerable to catching and passing on flu viruses—even developing the same coughy, sniffly symptoms that so many humans do. But most flu-transmission experiments in ferrets remain limited to artificial circumstances: pairs of animals in tiny cages with dividers between them, where scientists ogle them inhaling each other’s air for days or even weeks. That’s not how animals catch one another’s infections in the wild, and it’s certainly not how human outbreaks unfold. “We don’t interact with each other for 48 hours straight through a perforated wall,” Rockey told me.

    A giant playpen outfitted with toys, air samplers, and video cameras isn’t exactly a natural habitat for a ferret. But the setup does tap into many of the animals’ impish instincts. Domesticated by humans over thousands of years, ferrets “are a very playful species, and they love to be social,” says Alice Dancer, an animal-welfare researcher at the University of London’s Royal Veterinary College. That makes them great models for not just flu transmission, but flu transmission among kids, who are thought to be major drivers of outbreaks. In their day care, the ferrets squabble over toys, clamber up play structures, and canoodle plush snakes; they chase one another around, and nap in big piles when they get tuckered out; they exchange affectionate nuzzles, bonks, and little play bites. Every interaction represents a potential transmission event; so, too, do the surfaces they touch, and the shared pockets of air from which they all breathe.

    Read: The flu may never be the same

    Already, the researchers have collected some results that, Lakdawala told me, are “changing the way I think about transmission a little bit.” In one early experiment, involving an infected animal cavorting with four uninfected ones, they were surprised to find that the ferret with the least direct contact with the flu “donor” was the only “recipient” in the room who got sick. It seemed counterintuitive, Lakdawala told me, until video footage revealed that the newly sickened recipient had been copying everything that the donor did—chewing the toys it chewed, rolling the balls it rolled, swiping the surfaces it swiped. It was as if the first ferret was leaving a trail of infectious breadcrumbs for the second one to snarf. If that finding holds up in other experiments, which the researchers are analyzing now, it could suggest that contaminated surfaces, or fomites, are playing a larger-than-expected role in passing the virus around, Rockey told me.

    Another of the team’s early findings points to a similar notion. When the researchers cranked up the ventilation in their ferret day cares, hoping to clear virus particles out of the air, they found that the same proportion of uninfected ferrets ended up catching the virus. This was disappointing, but not a total shock given how paws-on ferrets—and kids, for that matter—are with one another and their surroundings. It didn’t matter if the air in the room was being exchanged more than once every three minutes. Whenever the ferrets had their run of the room, the researchers would find virus particles smeared on the toys, the snack station, and the playpen walls.

    Ventilation wasn’t totally useless: More air exchanges, the team found, did seem to reduce the concentration of flu genetic material in the air, and the ferrets who got infected under those conditions were slower to start shedding the virus—a hint, Lakdawala thinks, that they might have taken in a lower infectious dose. Among humans, that might translate into less severe cases of disease, Gordon told me, though that would need to be confirmed.

    Whatever upshots Rockey and Lakdawala’s ferret findings might have for human day cares won’t necessarily apply to other venues. In offices, hospitals, and even schools for older kids, people are generally a lot less tactile with one another, and a lot better versed on hygiene. Plus, adult bodies just aren’t built like kids’, says Cécile Viboud, an epidemiologist at the Fogarty International Center at the National Institutes of Health. Their airways are bigger, stronger, and more developed—and some experiments suggest that, for at least some respiratory viruses, the older and larger people are, the more infectious aerosols they might expel. For adults, ventilation may matter all the more.

    Lakdawala and her colleagues are still mulling some other interventions that might work better for ferrets, and eventually kids: humidifiers, air purifiers, targeted cleaning, maybe even keeping individuals from crowding too closely into a portion of the playpen. (They don’t plan to experiment with handwashing or masking; imagine the difficulty of strapping an N95 to a ferret’s face.) Lakdawala is also mulling whether surfaces made of copper—which her team has shown can render flu viruses inactive within minutes—could play a protective role.

    But everything that happens in the ferrets’ playpens will still come with caveats. “It’s still an animal model, at the end of the day,” Viboud told me. For all the similarities between the ferret airway and ours, the way their little noses and snouts are shaped could affect how they cough and sneeze. And the researchers haven’t yet studied spread among ferrets with preexisting immunity to flu, which some day-care attendees will have. Ferrets are also more inclined to bite, wrestle, and defecate wherever they please than the average (potty-trained) kid.

    Still, for the most part, Lakdawala delights in how childlike the ferrets can be. They’re affectionate and mischievous; they seem to bubble with energy and glee. After discovering that the air-sampling robot stationed in the center of their day care was mobile, several of the ferrets began to take it for rides. In watching and sharing the footage at conferences, Lakdawala has received one piece of feedback, over and over again: Oh yeah, parents tell her. My kids do that too.

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    Katherine J. Wu

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  • The Republican Lab-Leak Circus Makes One Important Point

    The Republican Lab-Leak Circus Makes One Important Point

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    For more than three hours yesterday, the House Select Subcommittee on the Coronavirus Pandemic grilled a pair of virologists about their participation in an alleged “cover-up” of the pandemic’s origins. Republican lawmakers zeroed in on evidence that the witnesses, Kristian Andersen and Robert Garry, and other researchers had initially suspected that the coronavirus spread from a Chinese lab. “Accidental escape is in fact highly likely—it’s not some fringe theory,” Andersen wrote in a Slack message to a colleague on February 2, 2020. When he laid out the same concern to Anthony Fauci in late January, that some features of the viral genome looked like they might be engineered, Fauci told him to consider going to the FBI.

    But days later, Andersen, Garry, and the other scientists were starting to coalesce around a different point of view: Those features were more likely to have developed via natural evolution. The scientists wrote up this revised assessment in an influential paper, published in the journal Nature Medicine in March 2020, called “The Proximal Origin of SARS-CoV-2.” The virus is clearly “not a laboratory construct or a purposefully manipulated virus,” the paper said; in fact, the experts now “did not believe that any type of laboratory-based scenario is plausible,” and that the pandemic almost certainly started with a “zoonotic event”—which is to say, the spillover of an animal virus into human populations. That analysis would be cited repeatedly by scientists and media outlets in the months that followed, in support of the idea that the lab-leak theory had been thoroughly debunked.

    The researchers’ rapid and consequential change of heart, as revealed through emails, witness interviews, and Slack exchanges, is now a wellspring for Republicans’ suspicions. “All of a sudden, you did a 180,” Representative Nicole Malliotakis of New York said yesterday morning. “What happened?”

    Based on the available facts, the answer seems clear enough: Andersen, Garry, and the others looked more closely at the data, and decided that their fears about a lab leak had been unwarranted; the viral features were simply not as weird as they’d first thought. The political conversation around this episode is not so easily summarized, however. Yesterday’s hearing was less preoccupied with the small, persistent possibility that the coronavirus really did leak out from a lab than with the notion of a conspiracy—a cover-up—that, according to Republicans, involved Fauci and others in the U.S. government swaying Andersen and Garry to leave behind their scientific judgment and endorse “pro-China talking points” instead. (Fauci has denied that he tried to disprove the lab-leak theory.)

    Read: If the lab-leak theory is right, what next?

    Barbed accusations of this kind have only added headaches to the question of how the pandemic really started. For all of its distractions, though, the House investigation still serves a useful purpose: It sheds light on how discussions of the lab-leak theory went so very, very wrong, and turned into an endless, stultifying spectacle. In that way, the hearing—and the story that it tells about the “Proximal Origin” paper—gestures not toward the true origin of COVID, but toward the origin of the origins debate.

    From the start, the problem has been that a “lab leak” could mean many things. The term may refer to the release of a manufactured bioweapon, or to an accident involving basic-science research; it could involve a germ with genes deliberately inserted, or one that was rapidly evolved inside a cage or in a dish, or even a virus from the wild, brought into a lab and released by accident (in unaltered form) in a city like Wuhan. Yet all these categories blurred together in the early days of the pandemic. The confusion was made plain when Senator Tom Cotton of Arkansas, a hard-core China hawk, aired a proto-lab-leak theory in a February 16, 2020 interview with Fox News. “This virus did not originate in the Wuhan animal market,” he told the network. He later continued, “just a few miles away from that food market is China’s only biosafety-level-4 super-laboratory that researches human infectious diseases. Now, we don’t have evidence that this disease originated there, but because of China’s duplicity and dishonesty from the beginning, we need to at least ask the question.”

    Cotton did not specifically suggest that the Chinese “super-laboratory” was weaponizing viruses, nor did he say that any laboratory accident would necessarily have involved a genetically engineered virus, as opposed to one that had been cultured or collected from a bat cave. Nevertheless, The New York Times and The Washington Post reported that the senator had repeated a “fringe theory” about the coronavirus that was going around in right-wing circles at the time, that it had been manufactured by the Chinese government as a bioweapon. It was hard for reporters to imagine that Cotton could have been suggesting anything but that: The idea that Chinese scientists might have been collecting wild viruses, and doing research just to understand them, was not yet thinkable in that chaotic, early moment of pandemic spread. “Lab leak” was simply understood to mean “the virus is a bioweapon.”

    Scientists knew better. On the same day that Cotton gave his interview, one of Andersen and Garry’s colleagues posted the “Proximal Origin” paper on the web as an unpublished manuscript. (“Important to get this out,” Garry wrote in an email sent to the group the following morning. He included a link to the Washington Post article about Cotton described above.) In this version, the researchers were quite precise about what, exactly, they were aiming to debunk: The authors said, specifically, that their analysis clearly showed the virus had not been genetically engineered. It might well have been produced through cell-culture experiments in a lab, they wrote, though the case for this was “questionable.” And as for the other lab-leak possibilities—that a Wuhan researcher was infected by the virus while collecting samples from a cave, or that someone brought a sample back and then accidentally released it—the paper took no position whatsoever. “We did not consider any of these scenarios,” Andersen explained in his written testimony for this week’s hearing. If a researcher had indeed been infected in the field, he continued, then he would not have counted it as a “lab leak” to begin with—because that would mean the virus jumped to humans somewhere other than a lab.

    Read: There is no evidence strong enough to end the pandemic-origins debate

    Rather than settling the matter, however, all this careful parsing only led to more confusion. In the early days of the pandemic, and in the context of the Cotton interview and its detractors, too much specificity was deemed a fatal flaw. On February 20, Nature decided to reject the manuscript, at least partly on account of its being too soft in its debunking. A month later, when their paper finally did appear in Nature Medicine, a new sentence had been added near the end: the one discounting “any type of laboratory-based scenario.” At this crucial moment in the pandemic-origins debate, the researchers’ original, narrow claim—that SARS-CoV-2 had not been purposefully assembled—was broadened to include a blanket statement that could be read to mean the lab-leak theory was wrong in all its forms.

    Over time, this aggressive phrasing would cause problems of its own. At first, its elision of several different possible scenarios served the mainstream narrative: We know the virus wasn’t engineered; ergo, it must have started in the market. More recently, the same confusion has served the interests of the lab-leak theorists. Consider a report from the Office of the Director of National Intelligence on pandemic origins, declassified last month. American intelligence agencies have determined that SARS-CoV-2 was not developed as a bioweapon, it explains, and they are near-unanimous in saying that it was not genetically engineered. (This confirms what Andersen and colleagues said in the first version of their paper, way back in February 2020.) “Most” agencies, the report says, further judge that the virus was not created through cell-culture experiments. Yet the fact that two of the nine agencies nonetheless believe that “a laboratory-associated incident” of any kind is the most likely cause of the first human infection has been taken as a sign that all lab-leak scenarios are still on the table. Thus Republicans in Congress can rail against Facebook for removing posts about the “lab-leak theory,” while ignoring the fact that the platform’s rules only ever prohibited one particular and largely discredited idea, that SARS-CoV-2 was “man-made or manufactured.” (In any case, that prohibition was reversed some three months later.)

    Where does this leave us? The committee’s work does not reveal a cover-up of COVID’s source. At the same time, it does show that the authors of the “Proximal Origin” paper were aware of how their work might shape the public narrative. (In a Slack conversation, one of them referred to “the shit show that would happen if anyone serious accused the Chinese of even accidental release.”) At first they strived to phrase their findings as clearly as they could, and to separate the strong evidence against genetic engineering of the virus—and what Garry called “the bio weapon scenario”—from the lingering possibility that laboratory science might have been involved in some other way. In the final version of their paper, though, they added in language that was rather less precise. This may have helped to muffle the debate in early 2020, but the haze it left behind was noxious and long-lasting.

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    Daniel Engber

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  • A Major Clue to COVID’s Origins Is Just Out of Reach

    A Major Clue to COVID’s Origins Is Just Out of Reach

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    Updated at 2:45 p.m. on March 21, 2023

    Last week, the ongoing debate about COVID-19’s origins acquired a new plot twist. A French evolutionary biologist stumbled across a trove of genetic sequences extracted from swabs collected from surfaces at a wet market in Wuhan, China, shortly after the pandemic began; she and an international team of colleagues downloaded the data in hopes of understanding who—or what—might have ferried the virus into the venue. What they found, as The Atlantic first reported on Thursday, bolsters the case for the pandemic having purely natural roots: The genetic data suggest that live mammals illegally for sale at the Huanan Seafood Wholesale Market—among them, raccoon dogs, a foxlike species known to be susceptible to the virus—may have been carrying the coronavirus at the end of 2019.

    But what might otherwise have been a straightforward story on new evidence has rapidly morphed into a mystery centered on the origins debate’s data gaps. Within a day or so of nabbing the sequences off a database called GISAID, the researchers told me, they reached out to the Chinese scientists who had uploaded the data to share some preliminary results. The next day, public access to the sequences was locked—according to GISAID, at the request of the Chinese researchers, who had previously analyzed the data and drawn distinctly different conclusions about what they contained.

    Read: The strongest evidence yet that an animal started the pandemic

    Yesterday evening, the international team behind the new Huanan-market analysis released a report on its findings—but did not post the underlying data. The write-up confirms that genetic material from raccoon dogs and several other mammals was found in some of the same spots at the wet market, as were bits of SARS-CoV-2’s genome around the time the outbreak began. Some of that animal genetic material, which was collected just days or weeks after the market was shut down, appears to be RNA—a particularly fast-degrading molecule. That strongly suggests that the mammals were present at the market not long before the samples were collected, making them a plausible channel for the virus to travel on its way to us. “I think we’re moving toward more and more evidence that this was an animal spillover at the market,” says Ravindra Gupta, a virologist at the University of Cambridge, who was not involved in the new research. “A year and a half ago, my confidence in the animal origin was 80 percent, something like that. Now it’s 95 percent or above.”

    For now, the report is just that: a report, not yet formally reviewed by other scientists or even submitted for publication to the journal—and that will remain the case as long as this team continues to leave space for the researchers who originally collected the market samples, many of them based at the Chinese Center for Disease Control and Prevention, to prepare a paper of their own. And still missing are the raw sequence files that sparked the reanalysis in the first place—before vanishing from the public eye.

    Every researcher I asked emphasized just how important the release of that evidence is to the origins investigation: Without data, there’s no base-level proof—nothing for the broader scientific community to independently scrutinize to confirm or refute the international team’s results. Absent raw data, “some people will say that this isn’t real,” says Gigi Gronvall, a senior scholar at the Johns Hopkins Center for Health Security, who wasn’t involved in the new analysis. Data that flicker on and off publicly accessible parts of the internet also raise questions about other clues on the pandemic’s origins. Still more evidence might be out there, yet undisclosed.

    Transparency is always an essential facet of research, but all the more so when the stakes are so high. SARS-CoV-2 has already killed nearly 7 million people, at least, and saddled countless people with chronic illness; it will kill and debilitate many more in the decades to come. Every investigation into how it began to spread among humans must be “conducted as openly as possible,” says Sarah Cobey, an infectious-disease modeler at the University of Chicago, who wasn’t involved in the new analysis.

    The team behind the reanalysis still has copies of the genetic sequences its members downloaded earlier this month. But they’ve decided that they won’t be the ones to share them, several of them told me. For one, they don’t have sequences from the complete set of samples that the Chinese team collected in early 2020—just the fraction that they spotted and grabbed off GISAID. Even if they did have all of the data, the researchers contend that it’s not their place to post them publicly. That’s up to the China CDC team that originally collected and generated the data.

    Part of the international team’s reasoning is rooted in academic decorum. There isn’t a set-in-stone guidebook among scientists, but adhering to unofficial rules on etiquette smooths successful collaborations across disciplines and international borders—especially during a global crisis such as this one. Releasing someone else’s data, the product of another team’s hard work, is a faux pas. It risks misattribution of credit, and opens the door to the Chinese researchers’ findings getting scooped before they publish a high-profile paper in a prestigious journal. “It isn’t right to share the original authors’ data without their consent,” says Niema Moshiri, a computational biologist at UC San Diego and one of the authors of the new report. “They produced the data, so it’s their data to share with the world.”

    If the international team released what data it has, it could potentially stoke the fracas in other ways. The World Health Organization has publicly indicated that the data should come from the researchers who collected them first: On Friday, at a press briefing, Tedros Adhanom Ghebreyesus, the WHO’s director-general, admonished the Chinese researchers for keeping their data under wraps for so long, and called on them to release the sequences again. “These data could have and should have been shared three years ago,” he said. And the fact that it wasn’t is “disturbing,” given just how much it might have aided investigations early on, says Gregory Koblentz, a biodefense expert at George Mason University, who wasn’t involved in the new analysis.

    Publishing the current report has already gotten the researchers into trouble with GISAID, the database where they found the genetic sequences. During the pandemic, the database has been a crucial hub for researchers sharing viral genome data; founded to provide open access to avian influenza genomes, it is also where researchers from the China CDC published the first whole-genome sequences of SARS-CoV-2, back in January 2020. A few days after the researchers downloaded the sequences, they told me, several of them were contacted by a GISAID administrator who chastised them about not being sufficiently collaborative with the China CDC team and warned them against publishing a paper using the China CDC data. They were in danger, the email said, of violating the site’s terms of use and would risk getting their database access revoked. Distributing the data to any non-GISAID users—including the broader research community—would also be a breach.

    This morning, hours after the researchers released their report online, many of them found that they could no longer log in to GISAID—they received an error message when they input their username and password. “They may indeed be accusing us of having violated their terms,” Moshiri told me, though he can’t be sure. The ban was instated with absolutely no warning. Moshiri and his colleagues maintain that they did act in good faith and haven’t violated any of the database’s terms—that, contrary to GISAID’s accusations, they reached out multiple times with offers to collaborate with the China CDC, which has “thus far declined,” per the international team’s report.

    GISAID didn’t respond when I reached out about the data’s disappearing act, its emails to the international team, and the group-wide ban. But in a statement released shortly after I contacted the database—one that echoes language in the emails sent to researchers—GISAID doubled down on accusing the international team of violating its terms of use by posting “an analysis report in direct contravention of the terms they agreed to as a condition to accessing the data, and despite having knowledge that the data generators are undergoing peer review assessment of their own publication.”

    Maria Van Kerkhove, the WHO’s COVID-19 technical lead, told me that she’s learned that the China CDC researchers recently provided a fuller data set to GISAID—more complete than the one the international team downloaded earlier this month. “It’s ready to go,” she told me. GISAID just needs permission, she said, from the Chinese researchers to make the sequences publicly available. “I reach out to them every day, asking them for a status update,” she added, but she hasn’t yet heard back on a definitive timeline. In its statement, GISAID also “strongly” suggested “that the complete and updated dataset will be made available as soon as possible,” but gave no timeline. I asked Van Kerkhove if there was a hypothetical deadline for the China CDC team to restore access, at which point the international team might be asked to publicize the data instead. “This hypothetical deadline you’re talking about? We’re way past that,” she said, though she didn’t comment specifically on whether the international team would be asked to step in. “Data has been uploaded. It is available. It just needs to be accessible, immediately.”

    Why, exactly, the sequences were first made public only so recently, and why they have yet to reappear publicly, remain unclear. In a recent statement, the WHO said that access to the data was withdrawn “apparently to allow further data updates by China CDC” to its original analysis on the market samples, which went under review for publication at the journal Nature last week. There’s no clarity, however, on what will happen if the paper is not published at all. When I reached out to three of the Chinese researchers—George Gao, William Liu, and Guizhen Wu—to ask about their intentions for the data, I didn’t receive a response.

    “We want the data to come out more than anybody,” says Saskia Popescu, an infectious-disease epidemiologist at George Mason University and one of the authors on the new analysis. Until then, the international team will be fielding accusations, already flooding in, that it falsified its analyses and overstated its conclusions.

    Researchers around the world have been raising questions about these particular genetic sequences for at least a year. In February 2022, the Chinese researchers and their close collaborators released their analysis of the same market samples probed in the new report, as well as other bits of genetic data that haven’t yet been made public. But their interpretations deviate pretty drastically from the international team’s. The Chinese team contended that any shreds of virus found at the market had most likely been brought in by infected humans. “No animal host of SARS-CoV-2 can be deduced,” the researchers asserted at the time. Although the market had perhaps been an “amplifier” of the outbreak, their analysis read, “more work involving international coordination” would be needed to determine the “real origins of SARS-CoV-2.” When reached by Jon Cohen of Science magazine last week, Gao described the sequences that fleetingly appeared on GISAID as “[n]othing new. It had been known there was illegal animal dealing and this is why the market was immediately shut down.”

    There is, then, a clear divergence between the two reports. Gao’s assessment indicates that finding animal genetic material in the market swabs merely confirms that live mammals were being illegally traded at the venue prior to January 2020. The researchers behind the new report insist that the narrative can now go a step further—they suggest not just that the animals were there, but that the animals, several of which are already known to be vulnerable to SARS-CoV-2, were there, in parts of the market where the virus was also found. That proximity, coupled with the virus’s inability to persist without a viable host, points to the possibility of an existing infection among animals, which could spark several more.

    The Chinese researchers used this same logic of location—multiple types of genetic material pulled out of the same swab—to conclude that humans were carrying around the virus at Huanan. The reanalysis confirms that there probably were infected people at the market at some point before it closed. But they were unlikely to be the virus’s only chauffeurs: Across several samples, the amount of raccoon-dog genetic material dwarfs that of humans. At one stall in particular—located in the sector of the market where the most virus-positive swabs were found—the researchers discovered at least one sample that contained SARS-CoV-2 RNA, and was also overflowing with raccoon-dog genetic material, while containing very little DNA or RNA material matching the human genome. That same stall was photographically documented housing raccoon dogs in 2014. The case is not a slam dunk: No one has yet, for instance, identified a viral sample taken from a live animal that was swabbed at the market in 2019 before the venue was closed. Still, JHU’s Gronvall told me, the situation feels clearer than ever. “All of the science is pointed” in the direction of Huanan being the pandemic’s epicenter, she said.

    To further untangle the significance of the sequences will require—you guessed it—the now-vanished genetic data. Some researchers are still withholding their judgment on the significance of the new analysis, because they haven’t gotten their hands on the genetic sequences themselves. “That’s the whole scientific process,” Van Kerkhove told me: data transparency that allows analyses to be “done and redone.”

    Van Kerkhove and others are also wondering whether more data could yet emerge, given how long this particular set went unshared. “This is an indication to me in recent days that there is more data that exists,” she said. Which means that she and her colleagues haven’t yet gotten the fullest picture of the pandemic’s early days that they could—and that they won’t be able to deliver much of a verdict until more information emerges. The new analysis does bolster the case for market animals acting as a conduit for the virus between bats (SARS-CoV-2’s likeliest original host, based on several studies on this coronavirus and others) and people; it doesn’t, however, “tell us that the other hypotheses didn’t happen. We can’t remove any of them,” Van Kerkhove told me.

    More surveillance for the virus needs to be done in wild-animal populations, she said. Having the data from the market swabs could help with that, perhaps leading back to a population of mammals that might have caught the virus from bats or another intermediary in a particular part of China. At the same time, to further investigate the idea that SARS-CoV-2 first emerged out of a laboratory mishap, officials need to conduct intensive audits and investigations of virology laboratories in Wuhan and elsewhere. Last month, the U.S. Department of Energy ruled that such an accident was the likelier catalyst of the coronavirus outbreak than a natural spillover from wild animals to humans. The ruling echoed earlier judgments from the FBI and a Senate minority report. But it contrasted with the views of four other agencies, plus the National Intelligence Council, and it was made with “low confidence” and based on “new” evidence that has yet to be declassified.

    Read: The lab leak will haunt us forever

    The longer the investigation into the virus’s origins drags on, and the more distant the autumn of 2019 grows in our rearview, “the harder it becomes,” Van Kerkhove told me. Many in the research community were surprised that new information from market samples collected in early 2020 emerged at all, three years later. Settling the squabbles over SARS-CoV-2 will be especially tough because the Huanan market was so swiftly shut down after the outbreak began, and the traded animals at the venue rapidly culled, says Angela Rasmussen, a virologist at the University of Saskatchewan and one of the researchers behind the new analysis. Raccoon dogs, one of the most prominent potential hosts to have emerged from the new analysis, are not even known to have been sampled live at the market. “That evidence is gone now,” if it ever existed, Koblentz, of George Mason University, told me. For months, Chinese officials were even adamant that no mammals were being illegally sold at the region’s wet markets at all.

    So researchers continue to work with what they have: swabs from surfaces that can, at the very least, point to a susceptible animal being in the right place, at the right time, with the virus potentially inside it. “Right now, to the best of my knowledge, this data is the only way that we can actually look,” Rasmussen told me. It may never be enough to fully settle this debate. But right now, the world doesn’t even know the extent of the evidence available—or what could, or should, still emerge.

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    Katherine J. Wu

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  • The Strongest Evidence Yet That an Animal Started the Pandemic

    The Strongest Evidence Yet That an Animal Started the Pandemic

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    For three years now, the debate over the origins of the coronavirus pandemic has ping-ponged between two big ideas: that SARS-CoV-2 spilled into human populations directly from a wild-animal source, and that the pathogen leaked from a lab. Through a swirl of data obfuscation by Chinese authorities and politicalization within the United States, and rampant speculation from all corners of the world, many scientists have stood by the notion that this outbreak—like most others—had purely natural roots. But that hypothesis has been missing a key piece of proof: genetic evidence from the Huanan Seafood Wholesale Market in Wuhan, China, showing that the virus had infected creatures for sale there.

    This week, an international team of virologists, genomicists, and evolutionary biologists may have finally found crucial data to help fill that knowledge gap. A new analysis of genetic sequences collected from the market shows that raccoon dogs being illegally sold at the venue could have been carrying and possibly shedding the virus at the end of 2019. It’s some of the strongest support yet, experts told me, that the pandemic began when SARS-CoV-2 hopped from animals into humans, rather than in an accident among scientists experimenting with viruses.

    “This really strengthens the case for a natural origin,” says Seema Lakdawala, a virologist at Emory who wasn’t involved in the research. Angela Rasmussen, a virologist involved in the research, told me, “This is a really strong indication that animals at the market were infected. There’s really no other explanation that makes any sense.”

    The findings won’t fully silence the entrenched voices on either side of the origins debate. But the new analysis may offer some of the clearest and most compelling evidence that the world will ever get in support of an animal origin for the virus that, in just over three years, has killed nearly 7 million people worldwide.

    Read: The lab leak will haunt us forever

    The genetic sequences were pulled out of swabs taken in and near market stalls around the pandemic’s start. They represent the first bits of raw data that researchers outside of China’s academic institutions and their direct collaborators have had access to. Late last week, the data were quietly posted by researchers affiliated with the country’s Center for Disease Control and Prevention, on an open-access genomic database called GISAID. By almost pure happenstance, scientists in Europe, North America, and Australia spotted the sequences, downloaded them, and began an analysis.

    The samples were already known to be positive for the coronavirus, and had been scrutinized before by the same group of Chinese researchers who uploaded the data to GISAID. But that prior analysis, released as a preprint publication in February 2022, asserted that “no animal host of SARS-CoV-2 can be deduced.” Any motes of coronavirus at the market, the study suggested, had most likely been chauffeured in by infected humans, rather than wild creatures for sale.

    The new analysis, led by Kristian Andersen, Edward Holmes, and Michael Worobey—three prominent researchers who have been looking into the virus’s roots—shows that that may not be the case. Within about half a day of downloading the data from GISAID, the trio and their collaborators discovered that several market samples that tested positive for SARS-CoV-2 were also coming back chock-full of animal genetic material—much of which was a match for the common raccoon dog. Because of how the samples were gathered, and because viruses can’t persist by themselves in the environment, the scientists think that their findings could indicate the presence of a coronavirus-infected raccoon dog in the spots where the swabs were taken. Unlike many of the other points of discussion that have been volleyed about in the origins debate, the genetic data are “tangible,” Alex Crits-Christoph, a computational biologist and one of the scientists who worked on the new analysis, told me. “And this is the species that everyone has been talking about.”

    Finding the genetic material of virus and mammal so closely co-mingled—enough to be extracted out of a single swab—isn’t perfect proof, Lakdawala told me. “It’s an important step, I’m not going to diminish that,” she said. Still, the evidence falls short of, say, isolating SARS-CoV-2 from a free-ranging raccoon dog or, even better, uncovering a viral sample swabbed from a mammal for sale at Huanan from the time of the outbreak’s onset. That would be the virological equivalent of catching a culprit red-handed. But “you can never go back in time and capture those animals,” says Gigi Gronvall, a senior scholar at the Johns Hopkins Center for Health Security. And to researchers’ knowledge, “raccoon dogs were not tested at the market and had likely been removed prior to the authorities coming in,” Andersen wrote to me in an email. He underscored that the findings, while an important addition, are still not “direct evidence of infected raccoon dogs at the market.”

    Still, the findings don’t stand alone. “Do I believe there were infected animals at the market? Yes, I do,” Andersen told me. “Does this new data add to that evidence base? Yes.” The new analysis builds on extensive previous research that points to the market as the source of the earliest major outbreak of SARS-CoV-2: Many of the earliest known COVID-19 cases of the pandemic were clustered roughly in the market’s vicinity. And the virus’s genetic material was found in many samples swabbed from carts and animal processing equipment at the venue, as well as parts of nearby infrastructure, such as storehouses, sewage wells, and water drains. Raccoon dogs, creatures commonly bred for sale in China, are also already known to be one of many mammal species that can easily catch and spread the coronavirus. All of this left one main hole in the puzzle to fill: clear-cut evidence that raccoon dogs and the virus were in the exact same spot at the market, close enough that the creatures might have been infected and, possibly, infectious. That’s what the new analysis provides. Think of it as finding the DNA of an investigation’s main suspect at the scene of the crime.

    The findings don’t rule out the possibility that other animals may have been carrying SARS-CoV-2 at Huanan. Raccoon dogs, if they were infected, may not even be the creatures who passed the pathogen on to us. Which means the search for the virus’s many wild hosts will need to plod on. “Do we know the intermediate host was raccoon dogs? No,” Andersen wrote to me, using the term for an animal that can ferry a pathogen between other species. “Is it high up on my list of potential hosts? Yes, but it’s definitely not the only one.”

    On Tuesday, the researchers presented their findings at a hastily scheduled meeting of the World Health Organization’s Scientific Advisory Group for the Origins of Novel Pathogens, which was also attended by several of the Chinese researchers responsible for the original analysis, according to multiple researchers who were not present but were briefed about it before and after by multiple people who were there.

    Shortly after the meeting, the Chinese team’s preprint went into review at a Nature Research journal—suggesting that a new version was being prepared for publication. (I reached out to the WHO for comment and will update the story when I have more information.)

    At this point, it’s still unclear why the sequences were posted to GISAID last week. They also vanished from the database shortly after appearing, without explanation. When I emailed George Gao, the former China CDC director-general and the lead author on the original Chinese analysis, asking for his team’s rationale, I didn’t immediately receive a response. Given what was in the GISAID data, it does seem that raccoon dogs could have been introduced into and clarified the origins narrative far sooner—at least a year ago, and likely more.

    China has, for years, been keen on pushing the narrative that the pandemic didn’t start within its borders. In early 2020, a Chinese official suggested that the novel coronavirus may have emerged from a U.S. Army lab in Maryland. The notion that a dangerous virus sprang out from wet-market mammals echoed the beginnings of the SARS-CoV-1 epidemic two decades ago—and this time, officials immediately shut down the Huanan market, and vehemently pushed back against assertions that live animals being sold illegally in the the country were to blame; a WHO investigation in March 2021 took the same line. “No verified reports of live mammals being sold around 2019 were found,” the report stated. But just three months later, in June 2021, a team of researchers published a study documenting tens of thousands of mammals for sale in wet markets in Wuhan between 2017 and late 2019, including at Huanan. The animals were kept in largely illegal, cramped, and unhygienic settings—conditions conducive to viral transmission—and among them were more than 1,000 raccoon dogs. Holmes himself had been at the market in 2014 and snapped a photo at Stall 29, clearly showing a raccoon dog in a cage; another set of images from the venue, captured by a local in December 2019 and later shared on Weibo, caught the animals on film as well—right around the time that the first recorded SARS-CoV-2 infections in humans occurred.

    And yet, Chinese researchers maintained their stance. As Jon Cohen reported for Science magazine last year, scientists from several of China’s largest academic institutions posted a preprint in September 2021 concluding that a massive nationwide survey of bats—the likeliest original source of the coronavirus before it jumped into an intermediate host, such as raccoon dogs, and then into us—had turned up no relatives of SARS-CoV-2. The implication, the team behind the paper asserted, was that relatives of the coronavirus were “extremely rare” in the region, making it unlikely that the pandemic had started there. The findings directly contradicted others showing that cousins of SARS-CoV-2 were indeed circulating in China’s bats. (Local bats have also been found to harbor viruses related to SARS-CoV-1.)

    The original Chinese analysis of the Huanan market swabs, from February 2022, also stuck with China’s party line on the pandemic. One of the report’s graphs suggested that viral material at the market had been mixed up with genetic material of multiple animal species—a data trail that should have led to further inquiry or conclusions, but which the Chinese researchers appear to have ignored. Their report noted only humans as being linked to SARS-CoV-2, stating that its findings “highly” suggested that any viral material at the market came from people (at least one of whom, presumably, picked it up elsewhere and ferried it into the venue). The Huanan market, the study’s authors wrote, “might have acted as an amplifier” for the epidemic. But “more work involving international coordination” would be needed to suss out the “real origins of SARS-CoV-2.”

    The wording of that report baffled many scientists in Europe, North America, and Australia, several of whom had, almost exactly 24 hours after the release of the China CDC preprint, published early versions of their own studies, concluding that the Huanan market was the pandemic’s probable epicenter—and that SARS-CoV-2 might have made its hop into humans from the venue twice at the end of 2019. Itching to get their hands on China CDC’s raw data, some of the researchers took to regularly trawling GISAID, occasionally at odd hours—the only reason that Florence Débarre, an evolutionary biologist at the French National Centre for Scientific Research, spotted the sequences pinging onto the server late last Thursday night with no warning or fanfare.

    Within hours of downloading the data and starting their own analysis, the researchers found their suspicions confirmed. Several surfaces in and around one stall at the market, including a cart and a defeathering machine, produced virus-positive samples that also contained genetic material from raccoon dogs—in a couple of cases, at higher concentrations than of human genomes. It was Stall 29—the same spot where Holmes had snapped the photo of the raccoon dog, nearly a decade before.

    Slam-dunk evidence for a raccoon-dog host—or another animal—could still emerge. In the hunt for the wild source of MERS, another coronavirus that caused a deadly outbreak in 2012, researchers were eventually able to identify the pathogen in camels, which are thought to have caught their initial infection from bats—and which still harbor the virus today; a similar story has played out for Nipah virus, which hopscotched from bats to pigs to us.

    Read: Bird flu leaves the world with an existential choice

    Proof of that caliber, though, may never turn up for SARS-CoV-2. (Nailing wild origins is rarely simple: Despite a years-long search, the wild host for Ebola still has not been definitively pinpointed.) Which leaves just enough ambiguity to keep debate about the pandemic’s origins running, potentially indefinitely. Skeptics will likely be eager to poke holes in the team’s new findings—pointing out, for instance, that it’s technically possible for genetic material from viruses and animals to end up sloshed together in the environment even if an infection didn’t take place. Maybe an infected human visited the market and inadvertently deposited viral RNA near an animal’s crate.

    But an infected animal, with no third-party contamination, still seems by far the most plausible explanation for the samples’ genetic contents, several experts told me; other scenarios require contortions of logic and, more important, additional proof. Even prior to the reveal of the new data, Gronvall told me, “I think the evidence is actually more sturdy for COVID than it is for many others.” The strength of the data might even, in at least one way, best what’s available for SARS-CoV-1: Although scientists have isolated SARS-CoV-1-like viruses from a wet-market-traded mammal host, the palm civet, those samples were taken months after the outbreak began—and the viral variants found weren’t exactly identical to the ones in human patients. The versions of SARS-CoV-2 tugged out of several Huanan-market samples, meanwhile, are a dead ringer for the ones that sickened humans with COVID early on.

    The debate over SARS-CoV-2’s origins has raged for nearly as long as the pandemic itself—outlasting lockdowns, widespread masking, even the first version of the COVID vaccines. And as long as there is murkiness to cling to, it may never fully resolve. While evidence for an animal spillover has mounted over time, so too have questions about the possibility that the virus escaped from a laboratory. When President Biden asked the U.S. intelligence community to review the matter, four government agencies and the National Intelligence Council pointed to a natural origin, while two others guessed that it was a lab leak. (None of these assessments were made with high confidence; a bill passed in both the House and Senate would, 90 days after it becomes a law, require the Biden administration to declassify underlying intelligence.)

    If this new level of scientific evidence does conclusively tip the origins debate toward the animal route, it will be, in one way, a major letdown. It will mean that SARS-CoV-2 breached our borders because we once again mismanaged our relationship with wildlife—that we failed to prevent this epidemic for the same reason we failed, and could fail again, to prevent so many of the rest.

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    Katherine J. Wu

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  • I Was Allergic to Cats. Until Suddenly, I Wasn’t.

    I Was Allergic to Cats. Until Suddenly, I Wasn’t.

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    Of all the nicknames I have for my cat Calvin—Fluffernutter, Chonk-a-Donk, Fuzzy Lumpkin, Jerky McJerkface—Bumpus Maximus may be the most apt. Every night, when I crawl into bed, Calvin hops onto my pillow, purrs, and bonks his head affectionately against mine. It’s adorable, and a little bit gross. Tiny tufts of fur jet into my nose; flecks of spittle smear onto my cheeks.

    Just shy of a decade ago, cuddling a cat this aggressively would have left me in dire straits. From early childhood through my early 20s, I nursed a serious allergy that made it impossible for me to safely interact with most felines, much less adopt them. Just a few minutes of exposure was enough to make my eyes water and clog my nasal passages with snot. Within an hour, my throat would swell and my chest would erupt in crimson hives.

    Then, sometime in the early 2010s, my misery came to an abrupt and baffling end. With no apparent interventions, my cat allergy disappeared. Stray whiffs of dander, sufficient to send my body into conniptions mere months before, couldn’t even compel my nose to twitch. My body just up and decided that the former bane of its existence was suddenly totally chill.

    What I went through is, technically speaking, “completely weird,” says Kimberly Blumenthal, an allergist and immunologist at Massachusetts General Hospital. Some allergies do naturally fade with time, but short of allergy shots, which don’t always work, “we think of cat allergy as a permanent diagnosis,” Blumenthal told me. One solution that’s often proposed? “Get rid of your cat.”

    My case is an anomaly, but its oddness is not. Although experts have a broad sense of how allergies play out in the body, far less is known about what causes them to come and go—an enigma that’s becoming more worrying as rates of allergy continue to climb. Nailing down how, when, and why these chronic conditions vanish could help researchers engineer those circumstances more often for allergy sufferers—in ways that are actually under our control, and not just by chance.

    All allergies, at their core, are molecular screwups: an immune system mistakenly flagging a harmless substance as dangerous and attacking it. In the classic version, an allergen, be it a fleck of almond or grass or dog, evokes the ire of certain immune cells, prompting them to churn out an antibody called IgE. IgE drags the allergen like a hostage over to other defensive cells and molecules to rile them up too. A blaze of inflammation-promoting signals, including histamine, end up getting released, sparking bouts of itching, redness, and swelling. Blood vessels dilate; mucus floods out in gobs. At their most extreme, these reactions get so gnarly that they can kill.

    Just about every step of this chain reaction is essential to produce a bona fide allergy—which means that intervening at any of several points can shut the cascade down. People whose bodies make less IgE over time can become less sensitive to allergens. The same seems to be true for those who start producing more of another antibody, called IgG4, that can counteract IgE. Some people also dispatch a molecule known as IL-10 that can tell immune cells to cool their heels even in the midst of IgE’s perpetual scream.

    All this and more can eventually persuade a body to lose its phobia of an allergen, a phenomenon known as tolerance. But because there is not a single way in which allergy manifests, it stands to reason that there won’t be a single way in which it disappears. “We don’t fully understand how these things go away,” says Zachary Rubin, a pediatrician at Oak Brook Allergists, in Illinois.

    Read: What they aren’t telling you about hypoallergenic dogs

    Tolerance does display a few trends. Sometimes, it unfurls naturally as people get older, especially as they approach their 60s (though allergies can appear in old age as well). Other diagnoses can go poof amid the changes that unfold as children zip through the physiological and hormonal changes brought on by toddlerhood, adolescence, and the teen years. As many as 60 to 80 percent of milk, wheat, and egg allergies can peace out by puberty—a pattern that might also be related to the instability of the allergens involved. Certain snippets of milk and egg proteins, for instance, can unravel in the presence of heat or stomach acid, making the molecules “less allergenic,” and giving the body ample opportunity to reappraise them as benign, says Anna Nowak-Węgrzyn, a pediatric allergist and immunologist at NYU Langone Health. About 80 to 90 percent of penicillin allergies, too, disappear within 10 years of when they’re first detected, more if you count the ones that are improperly diagnosed, as Blumenthal has found.

    Other allergies are more likely to be lifers without dedicated intervention—among them, issues with peanuts, tree nuts, shellfish, pollen, and pets. Part of the reason may be that some of these allergens are super tough to neutralize or purge. The main cat allergen, a protein called “Fel d 1” that’s found in feline saliva, urine, and gland secretions, can linger for six months after a cat vacates the premises. It can get airborne, and glom on to surfaces; it’s been found in schools and churches and buses and hospitals, “even in space,” Blumenthal told me.

    Read: The next weird way we’re changing cats

    For hangers-on like these, allergists can try to nudge the body toward tolerance through shots or mouth drops that introduce bits of an allergen over months or years, basically the immunological version of exposure therapy. In some cases, it works: Dosing people with Fel d 1 can at least improve a cat allergy, but it’s hardly a sure hit. Researchers haven’t even fully sussed out how allergy shots induce tolerance—just that “they work well for a lot of patients,” Rubin told me. The world of allergy research as a whole is something of a Wild West: Some people are truly, genuinely, hypersensitive to water touching their skin; others have gotten allergies because of organ transplants, apparently inheriting their donor’s sensitivity as amped-up immune cells hitched a ride.

    Part of the trouble is that allergy can involve just about every nook and cranny of the immune system; to study its wax and wane, scientists have to repeatedly look at people’s blood, gut, or airway to figure out what sorts of cells and molecules are lurking about, all while tracking their symptoms and exposures, which doesn’t come easy or cheap. And fully disentangling the nuances of bygone allergies isn’t just about better understanding people who are the rule. It’s about delving into the exceptions to it too.

    How frustratingly little we know about allergies is compounded by the fact that the world is becoming a more allergic place. A lot of the why remains murky, but researchers think that part of the problem can be traced to the perils of modern living: the wider use of antibiotics; the shifts in eating patterns; the squeaky-cleanness of so many contemporary childhoods, focused heavily on time indoors. About 50 million people in the U.S. alone experience allergies each year—some of them little more than a nuisance, others potentially deadly when triggered without immediate treatment. Allergies can diminish quality of life. They can limit the areas where people can safely rent an apartment, or the places where they can safely dine. They can hamper access to lifesaving treatments, leaving doctors scrambling to find alternative therapies that don’t harm more than they help.

    But if allergies can rise this steeply with the times, maybe they can resolve rapidly too. New antibody-based treatments could help silence the body’s alarm sensors and quell IgE’s rampage. Some researchers are even looking into how fecal transplants that port the gut microbiome of tolerant people into allergy sufferers might help certain food sensitivities subside. Anne Liu, an allergist and immunologist at Stanford, is also hopeful that “the incidence of new food allergies will decline over the next 10 years,” as more advances come through. After years of advising parents against introducing their kids to sometimes-allergenic substances such as milk and peanuts too young, experts are now encouraging early exposures, in the hopes of teaching tolerance. And the more researchers learn about how allergies naturally abate, the better they might be able to safely replicate fade-outs.

    One instructive example could come from cases quite opposite to mine: longtime pet owners who develop allergies to their animals after spending some time away from them. That’s what happened to Stefanie Mezigian, of Michigan. After spending her entire childhood with her cat, Thumper, Mezigian was dismayed to find herself sneezing and sniffling when she visited home the summer after her freshman year of college. Years later, Mezigian seems to have built a partial tolerance up again; she now has another cat, Jack, and plans to keep felines in her life for good—both for companionship and to wrangle her immune system’s woes. “If I go without cats, that seems to be when I develop problems,” she told me.

    It’s a reasonable thought to have, Liu told me. People in Mezigian’s situation probably have the reactive IgE bopping around their body their entire life. But maybe during a fur-free stretch, the immune system, trying to be “parsimonious,” stops making molecules that rein in the allergy, she said. The immune system is nothing if not malleable, and a bit diva-esque: Set one thing off kilter, and an entire network of molecules and cells can revamp its approach to the world.

    I may never know why my cat allergy ghosted me. Maybe I got infected by a virus that gently rewired my immune system; maybe my hormone levels went into flux. Maybe it was the stress, or joy, of graduating college and starting grad school; maybe my diet or microbiome changed in just the right way, at just the right time. Perhaps it’s pointless to guess. Allergy, like the rest of the immune system, is a hot, complicated mess—a common fixture of modern living that many of us take for granted, but that remains, in so many cases, a mystery. All I can do is hope my cat allergy stays gone, though there’s no telling if it will. “I have no idea,” Nowak-Węgrzyn told me. “I’m just happy for you. Go enjoy your cats.”

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    Katherine J. Wu

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  • Enago to Provide English Editing Services to AAAS Authors

    Enago to Provide English Editing Services to AAAS Authors

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    With this collaboration, Enago to support AAAS authors in ensuring language accuracy of their research documents

    Press Release
    –


    updated: Apr 11, 2017


    New York, USA , April 11, 2017 (Newswire.com)
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     Enago, a leading provider of language editing solutions for scientific researchers, has entered into a publishing service collaboration (non-exclusive) with the American Association for the Advancement of Science (AAAS), the world’s largest multidisciplinary scientific society and a leading publisher of cutting-edge research through its Science family of journals. AAAS has individual members in more than 91 countries around the globe.

    Under the partnership, Science Journals’ authors will be able to avail Enago’s manuscript preparation services at pre-submission stage. AAAS authors will receive special 20% discount as part of this collaboration. 

    “We are always looking for new tools and services to help the research community and we see the Enago’s language editing service doing just that. We hope that Enago will provide AAAS authors with access to a reliable language editing option, ensuring that author documents are clean and grammatically correct.”

    Hannah Hecker, Product Development (AAAS)

    Hannah Hecker, Product Development (AAAS), said, “We are always looking for new tools and services to help the research community and we see the Enago’s language editing service doing just that. We hope that Enago will provide AAAS authors with access to a reliable language editing option, ensuring that author documents are clean and grammatically correct.” 

    “Enago is delighted to be collaborating with AAAS to help serve the needs of Science Journals authors by providing easy access to high quality manuscript preparation services,” said Tony O’Rourke, Strategic Alliances-Europe, Enago. “This non-exclusive collaboration with AAAS is one of the several partnerships through which Enago brings forward its manuscript preparation services to help publishers get closer to their authors.” 

    About Enago

    Enago is the trusted name in author services for the global research community. Since 2005, we have worked with researchers in more than 125 countries — improved the communication of their research and helped them achieve publication success. Enago is a preferred partner for leading publishers, societies, as well as universities worldwide. We have offices in Tokyo, Seoul, Beijing, Shanghai, Istanbul, and New York. Enago operates globally with regional teams supporting researchers locally.

    To learn more about Enago, please visit: enago.com

    About AAAS

    The American Association for the Advancement of Science (AAAS) is the world’s largest multidisciplinary scientific society and a leading publisher of cutting-edge research through its Science family of journals. AAAS has individual members in more than 91 countries around the globe. AAAS seeks to “advance science, engineering, and innovation throughout the world for the benefit of all people.”

    To learn more about AAAS, please visit: aaas.org

    Source: Enago

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  • QS Partners With Enago to Offer Manuscript Preparation and Author Education Services

    QS Partners With Enago to Offer Manuscript Preparation and Author Education Services

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    Enago to Support QS Partner Universities Improve Their International Research Output

    Press Release
    –


    updated: Apr 5, 2017


    London, UK , April 5, 2017 (Newswire.com)
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    Quacquarelli Symonds (QS) today announced their partnership with Enago, a leading author service provider that specifically caters to the large section of the global research community for whom English is a second language (ESL).

    QS was founded in 1990 and has established itself as a leading global provider of specialist higher education and career information and solutions. QS activities span across 50 countries, working with over 2000 of the world’s leading higher education institutions. Enago is the trusted name in author services for the global research community. Since 2005, Enago worked with 100,000+ researchers in 125+ countries improving the communication of their research and helping them to achieve success in international publication. Enago is the preferred partner for leading academic publishers, societies and universities worldwide. Enago has offices in Tokyo, Seoul, Beijing, Shanghai, Istanbul and New York, and operates globally with regional teams supporting researchers locally.

    “QS has always advised higher education institutions to improve their international research output as part of overall globalization and we are pleased to now offer comprehensive support by partnering with Enago. We encourage the importance of publishing cutting-edge research and opinions from across the globe, and are happy that we are now able to increase our support for our partner universities.”

    Jason Newman, Global Commercial Director, QS Intelligence Unit

    “QS has always advised higher education institutions to improve their international research output as part of overall globalization and we are pleased to now offer comprehensive support by partnering with Enago,” commented Jason Newman, Global Commercial Director, QS Intelligence Unit. “We encourage the importance of publishing cutting-edge research and opinions from across the globe, and are happy that we are now able to increase our support for our partner universities.”

    “Enago is delighted to be collaborating with a forward-thinking organization like QS to improve universities’ research output,” said Rajiv Shirke, VP Global Operations, Enago. “Having easy access to the manuscript preparation services provided by Enago will not only accelerate the process of publishing high-impact research but also ensure that specific author needs are taken care of during the editorial process.”

    For more details please visit QS-Enago website: https://www.enago.com/qs/ 

    About Enago

    Enago is the trusted name in author services for the global research community. Since 2005, we have worked with researchers in more than 125 countries—improved the communication of their research and helped them achieve publication success. Enago is a preferred partner for leading publishers, societies, as well as universities worldwide. We have offices in Tokyo, Seoul, Beijing, Shanghai, Istanbul, and New York. Enago operates globally with regional teams supporting researchers locally.

    To learn more about Enago, please visit: enago.com

    About Quacquarelli Symonds

    QS was founded in 1990 and has established itself as the leading global provider of specialist higher education and careers information and solutions. At QS we believe that education and career decisions are too important to leave to chance, we want to ensure candidates have access to the best tools and the best independent expert information before making a decision. Our activities span across 50 countries, working with over 2000 of the world’s leading higher education institutions and over 12,000 employers. We provide services at each key career stage; first degree, Masters, PhD, MBA, and executive-level.

    To learn more about QS, please visit: qs.com

    Source: Enago

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  • IFCU Partners With Enago to Offer Manuscript Preparation and Author Education Services

    IFCU Partners With Enago to Offer Manuscript Preparation and Author Education Services

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    IFCU Member Universities to Benefit from Enago’s English Editing and Publication Support Services

    Press Release
    –


    updated: Mar 30, 2017


    New York, NY, March 30, 2017 (Newswire.com)
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     Enago, an internationally trusted name in author services for the global research community, has recently signed an agreement with the International Federation of Catholic Universities (IFCU), one of the world’s largest international alliances of universities. Comprising over 200 universities throughout the globe, IFCU facilitates research, partnership and exchange programmes between Catholic institutes of education. With this agreement, Enago will provide English editing services to researchers and scientists at IFCU member universities. The resulting collaboration will see IFCU recommending Enago’s services exclusively to researchers and scientists at its member universities.

    This mutual agreement will support IFCU researchers and scientists in polishing their research content. Enago provides English language editing services to researchers for whom English is not their first language, thereby improving their chances of publication in international peer-reviewed journals. With an editorial team of professional subject-matter experts, Enago is highly equipped to offer the highest standard of English editing and publication support services to IFCU researchers.

    “This agreement will accelerate author access to quality editing services across the Federation. It will help us immensely in fulfilling our mission of fostering academic cooperation in the field of research. We believe that this association will empower our researchers to share their research with decision-making communities across the globe.”

    Montserrat Alom, Project Chief of the Centre for Coordination of Research, IFCU

    “This agreement will accelerate author access to quality editing services across the Federation. It will help us immensely in fulfilling our mission of fostering academic cooperation in the field of research. We believe that this association will empower our researchers to share their research with decision-making communities across the globe,” said Montserrat Alom, Project Chief of the Centre for Coordination of Research, IFCU.

    “Both IFCU and Enago are committed to supporting the research community, thereby fostering academic collaboration and an effective exchange of ideas. As their partner, we are delighted to provide IFCU researchers with our best-in-class editorial services to enhance the overall quality of their research output. Over the years, Enago has steadily built its credibility and reputation in delivering exceptional quality author support services to researchers worldwide. We understand completely what it takes to make a research paper “publication ready” and look forward to assisting IFCU members with our expertise,” said Tony O’Rourke, who manages Strategic Alliances for Enago. 

    For more details please visit www.enago.com

    About Enago:

    Enago is the trusted name in author services for the global research community. Since 2005, we have worked with researchers in more than 125 countries — improved the communication of their research and helped them achieve publication success. Enago is a preferred partner for leading publishers, societies, as well as universities worldwide. We have offices in Tokyo, Seoul, Beijing, Shanghai, Istanbul, and New York. Enago operates globally with regional teams supporting researchers locally.

    To learn more about Enago, please visit www.enago.com

    About IFCU:

    The IFCU represents one of the largest international alliances of universities in the world, comprising over 200 universities throughout the globe. The IFUC facilitates, research, partnership and exchange programmes between catholic institutes of education. Originally created by a Papal Decree in 1948 when it was known as the Fœderatio Universitatum Catholicarum, it became the International Federation of Catholic Universities in 1965. The federation has its origins in collaboration in 1924 between the Università Cattolica del Sacro Cuore in Milan and the Catholic university of Nijmegen in the Netherlands. Today, the secretariat is based in Paris at the Institut Catholique de Paris. 

    To learn more about IFCU, please visit www.fiuc.org

    Source: Enago

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  • National Council of University Research Administrators (NCURA) Partners With Enago to Offer Manuscript Preparation and Author Education Services

    National Council of University Research Administrators (NCURA) Partners With Enago to Offer Manuscript Preparation and Author Education Services

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    A Partnership to Empower Researchers Improve Their Chances of Publication Success

    Press Release
    –


    updated: Mar 24, 2017


    New York, USA, March 24, 2017 (Newswire.com)
    –
    NCURA today announced its new partnership with Enago, a leading author service provider that specifically caters to the large section of the global research community for whom English is a second language (ESL). Founded in 1959, NCURA is the leading professional association for university research administrators. NCURA serves its members and advances the field of research administration through education and professional development programs, the sharing of knowledge and experience, and by fostering a professional, collegial, and respected community. Enago is the trusted name in author services for the global research community. Since 2005, Enago has worked with 100,000+ researchers in 125+ countries in improving the communication of their research and helping them to achieve success in international publication. Enago is the preferred partner for leading academic publishers, societies, and universities worldwide. Enago has offices in Tokyo, Seoul, Beijing, Shanghai, Istanbul, and New York, and operates globally with regional teams supporting researchers locally.

     “NCURA’s members include the world’s top research institutions, and as such, their faculty and researchers are increasingly a part of global research consortia.  For this reason, it is important for us to continue to offer additional services to our members and their faculty partnering with Enago,” commented Jesse Szeto, Global Operations Director, NCURA. “We recognize the importance of publishing cutting-edge research results from across the globe, and we are pleased that this partnership will increase our support for the research community.”

    “NCURA’s members include the world’s top research institutions, and as such, their faculty and researchers are increasingly a part of global research consortia. For this reason, it is important for us to continue to offer additional services to our members and their faculty partnering with Enago, We recognize the importance of publishing cutting-edge research results from across the globe, and we are pleased that this partnership will increase our support for the research community.”

    Jesse Szeto, Global Operations Director, NCURA

    “Enago is delighted to be collaborating with a forward-thinking organization like NCURA to improve universities’ research output.” said Rajiv Shirke, VP Global Operations, Enago. “Having easy access to the manuscript preparation services provided by Enago will not only accelerate the process of publishing high-impact research but also ensure that specific author needs are taken care of during the editorial process.”

    For more details please visit NCURA-Enago landing page: http://university.enago.com/ncura  

    About Enago:

    Enago is the trusted name in author services for the global research community. Since 2005, we have worked with researchers in more than 125 countries — improved the communication of their research and helped them achieve publication success. Enago is a preferred partner for leading publishers, societies, as well as universities worldwide. We have offices in Tokyo, Seoul, Beijing, Shanghai, Istanbul, and New York. Enago operates globally with regional teams supporting researchers locally.

    To learn more about Enago, please visit www.enago.com. 

    About NCURA:

    NCURA serves its members and advances the field of research administration through education and professional development programs, the sharing of knowledge and experience, and by fostering a professional, collegial, and respected community.

    To learn more about NCURA, please visit www.ncura.edu

    Source: Enago

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  • Enago Conducts a Series of Workshops in Lithuania

    Enago Conducts a Series of Workshops in Lithuania

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    Enago conducted a series of author workshops to introduce researchers in Lithuania to publishing in international peer-reviewed journals

    Press Release
    –

    Sep 30, 2016


    Kaunas, Lithuania, September 30, 2016 (Newswire.com)
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    ​​​​Enago, in collaboration with Vilnius Gediminas Technical University (VGTU) and Kaunas University of Technology (KTU), organized a series of workshops for researchers across Lithuania. The workshop sessions were attended by over 450+ researchers and professors from different research backgrounds.

    The first session on Academic Publishing touched on the importance of publishing papers in English, before presenting practical advice and quick tips on effectively using academic English to write better scientific manuscripts. Other points addressed in detail included the importance of a good literature review, effective planning and preparation of manuscripts for publication, selecting the right journal, and correctly structuring papers and references before initial submission.

    English is the international language of science. The expertise shared by Enago has given Lithuanian academics the opportunity to increase their international publishing potential, and therefore, will reaffirm Lithuania’s standing on the scientific stage

    Dr. Ieva Cesevièiute, Head of Research Information Services, Kaunas University of Technology

    The next session was on How to Deal with Journal Rejection, where the audience was explained why manuscripts are rejected by journals and clarifying how the peer review process works, along with listing the obvious mistakes authors should avoid in order to prevent a rejection. The ultimate aim of this session was to help researchers maintain a positive outlook while dealing with journal rejection, equipping them with the tools to resubmit with confidence.

    “This interactive workshop was specifically designed for Lithuanian researchers to gain better understanding of academic publishing and learn the nuances of the various stages involved in order to increase their chances of publication in the English language,” said Rajiv Shirke, Vice President, Global Operations, Enago.

    Eleonora Dagienė, Director of VGTU Press, commented, “We appreciate Enago for organising such successful workshops here in Lithuania. It was truly a pleasure to be a part of it. The topic covered was a crucial one and the participants did not have a notion of the aspects involved in the publication process. This has also raised the overall level of inquisitiveness, which is always beneficial as VGTU maintains its educational role while VGTU Press works on ensuring the quality of publications. The positive feedback and acknowledgement continues to flow in, and I can surmise that the objective has been fully accomplished.”

    Dr. Ieva Cesevièiute, Head of Research Information Services, KTU added, “English is the international language of science. The expertise shared by Enago has given Lithuanian academics the opportunity to increase their international publishing potential, and therefore, will reaffirm Lithuania’s standing on the scientific stage.”   

    About the Speaker: Duncan Nicholas, Publication and Training Consultant for Enago Academy, is a distinguished publishing expert, consultant, and trainer. As Managing Editor at the Taylor and Francis Group, he helped establish editorial and peer review processes for a variety of journals. He is also a member of ISMTE and EASE, which focus on increasing professional networking within the scholarly publishing community as well as help establish best practices amongst publishers and journals. He has conducted numerous training programs on various topics related to scholarly publishing, including open science, journal metrics, publication ethics, peer review, and challenges in academic writing for ESL authors.

    About Enago: Enago is the flagship brand of Crimson Interactive Inc., an award-winning language solutions company that serves academia and industry through three main entities: Enago (English Editing and Publication Support), Ulatus (Translation), and Voxtab (Transcription). Enago employs one of the market’s largest teams of editors (850+) who are proven language and subject matter experts in more than 1,100 disciplines. To date, the company’s talented pool of specialists has helped more than 81,000 authors share their research in the most impactful journals across the globe. Crimson has a local presence in Japan, China, Taiwan, Turkey, Korea, Brazil, Germany, Russia, India, and the United States.

    Source: Enago

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