For millions of people, COVID-19 doesn’t end with a negative test. Weeks or months after traces of the virus disappear from noses and throats, symptoms can persist or come back. New ones might pop up and stick around for months. People suffering from long COVID are unwillingly in it for the long haul — and it’s still unclear who’s at the highest risk for the condition.

Researchers don’t yet have an official definition for long COVID, and its symptoms are wide-ranging (SN: 7/29/22). Some people struggle with extreme fatigue that interferes with their daily lives. Others can’t concentrate or struggle with memory amid thick brain fog. Still others have organ damage or a persistent cough and difficulty breathing.
“There are a variety of different kinds of ways that people can have long COVID. It’s not just the one thing,” says Leora Horwitz, an internal medicine physician at New York University Langone Health. “That’s what makes it so hard to study.”

This spectrum of symptoms makes pinning down who’s at high risk for long-term health problems from the disease especially hard. Some post-COVID conditions may stem from virus-induced damage or from the stress of being hospitalized with severe disease. In other cases, the body’s own immune response to the virus could drive the damage. Or the virus may be hiding somewhere in the body, possibly the gut, helping symptoms to persist (SN: 11/24/20). Different causes may have different risk groups, says Hannah Davis, cofounder of the Patient-Led Research Collaborative, a research and advocacy group studying long COVID.

There are some broad hints about who’s at risk. Studies suggest that women are more likely than men to have lingering symptoms. COVID-19 patients with more than five symptoms in the first week of infection or preexisting health conditions such as asthma may be more likely to develop long COVID. Age also appears to be a risk factor, though results are mixed regarding whether the burden falls on older people or middle-aged people. Populations that were disproportionally hit by COVID-19 overall — including Black and Hispanic people — may similarly face disparities for long COVID. And while vaccination seems to protect people from developing long COVID, Horwitz says, it’s still unclear by how much.

Age is a risk factor for severe COVID-19, and the U.S. Centers for Disease Control and Prevention lists more than 30 health problems, including cancer and lung disease, that also raise the risk. “So many researchers assume that those [risk factors] will be the same for long COVID and there’s no scientific basis for that,” Davis says. There are many more that researchers could be missing when it comes to long COVID.

Using health records and exams, and knowledge of ailments with symptoms similar to long COVID, experts are on the hunt for those risk factors.

Examining health
When it comes to getting a better handle on who’s at risk for long COVID — which also goes by the wonky alias Post-Acute Sequelae of SARS-CoV-2 infection — electronic health records may hold important clues.

Horwitz is part of the U.S. National Institutes of Health’s RECOVER initiative that aims to understand the long-term impacts of COVID-19. One arm of the study involves mining millions of electronic health records to find potential patterns.

Studying millions of these records should pinpoint potential risk factors that are rare in the population overall but perhaps more common for people with long COVID, Horwitz says. “That’s hard even in a cohort study of thousands.”

But health records aren’t perfect: They depend on physicians logging that patients are having trouble sleeping or focusing, or that they’re exhausted. “The things people are complaining about, we’re really bad at writing down those diagnoses on the record,” Horwitz says. “So we miss that.”
To account for health records’ deficiencies, Horwitz and colleagues are also directly studying thousands of people. Participants answer a questionnaire every three months so that the team can identify what kinds of symptoms people have and whether they’re getting better or worse.

Then blood, urine, stool and saliva samples can reveal what’s happening in the body. Tests on those samples can uncover if the coronavirus is still around and causing trouble, or if the immune system has learned to attack the body itself. Participants with abnormal test results will undergo additional, targeted testing.

“Unlike electronic health records where it’s hit or miss, like somebody might have had a CAT scan or might not, here we say, ‘OK, you have trouble breathing. We will take a look at your lungs,’” Horwitz says.

The study includes a range of participants: adults and kids, pregnant people, those currently with COVID-19 and people who died after having the disease.

Some of the potential risk factors that the team is looking for include autoimmune diseases and other viral infections. The list may grow as more people join the study. “We’re trying to balance the fishing versus making sure that we’re at least fishing for things that could be in the water,” Horwitz says.

Among short supply, though, are people who never caught the virus — important “controls” to highlight what’s different about people who got COVID-19.

So far, more than 7,000 people have signed up, and the group plans to recruit around 10,000 more. It’s a lot of data, but early results may soon start coming in.

“We’ll probably try to do an interim peek at those data this fall,” Horwitz says. “It’s tricky because we deliberately wanted to enroll 18,000 people so we would have enough power to really look at the things we care about. I don’t want to cheat and look too early, but we also know that there’s a lot of interest.”

Striking similarities
Some long COVID symptoms — brain fog, fatigue and trouble sleeping — mirror another illness: myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS. Other long COVID symptoms, such as rapid heartbeat and dizziness, fall in the category of nervous system disorders called dysautonomia. Similar symptoms could belie similar risk factors.

Yet potential risk factors for those conditions are largely missing from long COVID research, says Davis, who has had long COVID since March 2020. Among the possibilities that scientists are considering are things like Epstein-Barr virus, migraines and some autoimmune diseases.

Epstein-Barr virus could be a big one, Davis says. Infections last a lifetime because the virus can go into hiding in the body and possibly reemerge. That virus has been linked to ME/CFS for decades, though its role in the disease remains unclear, Davis says.
Some early hints of a link between Epstein-Barr virus and long COVID already exist. Multiple studies have found evidence in blood samples from some long COVID patients that the immune system recently battled with Epstein-Barr virus, which can cause infectious mononucleosis, a disease characterized by extreme fatigue. Other studies have found signs of the virus itself. And in 2021, Davis and colleagues found that 40 out of 580 people with symptoms of long COVID who responded to an online survey reported having a current or recent Epstein-Barr virus infection.

With ME/CFS, it’s possible that another illness caused by a different virus triggers the Epstein-Barr virus, which then causes the fatigue syndrome. Given the parallels between that condition and long COVID, some scientists are wondering if the two are actually the same disease, with the coronavirus now known as one trigger.

Examining health conditions that raise the chances of long COVID could provide answers for both diseases, says Nancy Klimas, an immunologist at Nova Southeastern University in Fort Lauderdale, Fla. That’s in part because researchers can more easily identify people who developed lingering symptoms after a bout of COVID-19 compared with unknown infections that may precede ME/CFS.

Also, “there’s a huge difference in these two fields and it’s money,” Klimas says. She now has funding from the CDC to compare long COVID patients with people who have ME/CFS. The team hopes that physical exams and specialized tests will reveal whether the two diseases are indeed the same and be a step toward understanding the mechanisms behind the lingering symptoms.

Still, since long COVID as a whole encompasses such a wide range of symptoms, it will take time to uncover who is at risk of what.

If COVID-19 were just one disease impacting the lungs, heart or brain, the research might be easier, Horwitz says. “But we have to test everything.”

A crying baby, a screaming adult, a teenager whose voice cracks — people could have sounded this shrill all the time, a new study suggests, if not for a crucial step in human evolution.

It’s what we’re missing that makes the difference. Humans have vocal cords, muscles in our larynx, or voice box, that vibrate to produce sound (SN: 11/18/15). But unlike all other studied primates, humans don’t have small bits of tissue above the vocal cords called vocal membranes. That uniquely human trait helps people control their voices well enough to produce the sounds that are the building blocks of spoken language, researchers report in the Aug. 12 Science.

Vocal membranes act like a reed in a clarinet, making it easier for some animals to shout loud and shrill. Think of the piercing calls of howler monkeys (SN: 10/22/15). When researchers used MRI and CT scans to look for vocal membranes in 43 different primate species, the scientists were surprised by what they saw: All primates except humans had the tissue.

That loss of vocal membranes would have been a “very major, very revolutionary event in human evolution,” says Takeshi Nishimura, a paleontologist at Kyoto University in Japan.

Primates mostly make sound in the same basic way: They push air out from their lungs while vibrating muscles in the larynx to create sound waves. To understand the role that vocal membranes play, Nishimura’s team studied videos of primate voice boxes in action in chimpanzees, rhesus macaques and squirrel monkeys. The researchers also took larynges from macaques and chimpanzees that had died of natural causes and — in what’s common practice for the field — mounted the parts on tubes, pushing air through the larynges to see how the vocal cords and membranes would react.

In both experiments, the larynges made sounds that would often fluctuate wildly in pitch. Nishimura’s team found that happens only when an animal has both vocal membranes and vocal cords.
In humans, that sort of screeching can happen when we put extreme amounts of pressure on our voice, like when we scream — or when teens struggle with controlling their growing vocal cords and their voices crack. But those are rare cases. Since humans don’t have vocal membranes, we usually make more stable sounds than other primates, the team concludes. Our mouths and tongues, the idea goes, can then manipulate those stable tones into the complex sounds that language is based on.

“That’s a really elegant explanation,” says Sue Anne Zollinger, an animal physiologist at Manchester Metropolitan University in England who was not involved in the study. It’s almost counterintuitive, she says: “You lose complexity to be able to produce more complex sounds.”

The loss of vocal membranes isn’t the only thing that makes humans more eloquent than other primates. Beyond anatomical differences, humans have specific genes that may have helped drive language evolution (SN: 8/3/18). And perhaps most importantly, human brains are structured differently from other primates in ways that also give us more control over our speech (SN: 12/19/16).

Mother’s Day is on my mind, and I’ve been thinking about the ways I’m connected to my mom and my two little daughters. Every so often I see flickers of my mom in my girls — they share the lines around their smiles and a mutual adoration of wildflowers. Of course, I’m biased. I know that I’m seeing what I’m looking for. But biologically speaking, mothers and their children are connected in a way that may surprise you.

Way back when you and your mom shared a body, your cells mingled. Her cells slipped into your body and your cells circled back into her. This process, called fetal-maternal microchimerism, turns both mother and child into chimeras harboring little pieces of each other.

Cells from my daughters are knitted into my body and bones and brain. I also carry cells from my mom, and quite possibly from my grandma. I may even harbor cells from my older brother, who may have given some cells to my mom, who then gave them to me. It means my younger brother just might have cells from all of us, poor guy. This boundary blurring invites some serious existential wonder, not least of which might involve you wondering if this means your family members really are in your head.

These cellular threads tie families together in ways that scientists are just starting to discover. Here are a few of my favorite instances of how cells from a child have woven themselves into a mother’s body:
Fetal cells are probably sprinkled throughout a mother’s brain. A study of women who had died in their 70s found that over half of the women had male DNA (a snippet from the Y chromosome) in their brains, presumably from when their sons were in the womb. Scientists often look for male DNA in women because it’s easier than distinguishing a daughter’s DNA from her mother’s. If DNA from daughters were included, the number of women with children’s cells in their brains would probably be even higher.

When the heart is injured, fetal cells seem to flock to the site of injury and turn into several different types of specialized heart cells. Some of these cells may even start beating, a mouse study found. So technically, those icky-sweet Mother’s Day cards may be right: A mother really does hold her children in her heart.

Fetal cells circulate in a mother’s blood. Male DNA turned up in blood samples from women who were potential stem cell donors. That result may have implications for stem cell transplants. This cell swapping may make parents better donor candidates for their children than strangers, for instance.
Other studies have found fetal cells in a mother’s bones, liver, lungs and other organs, suggesting that these cells have made homes for themselves throughout a mother’s body. Maybe this is a way for a child to give back to the mother, in a sense. Growing fetuses slurp nutrients and energy out of a mother’s body during pregnancy (not to mention the morning sickness, heartburn and body aches). In return, fetuses offer up these young, potentially helpful cells. Perhaps these fetal cells, which may possess the ability to turn into lots of different kinds of cells, can help repair a damaged heart, liver or thyroid, as some studies have hinted.

Before I get carried away, a caveat: these cells may also make mischief. They may have a role in autoimmune disorders, for instance.

Microchimerism also has implications here for women who have lost pregnancies, an extremely common situation hidden by the taboo of talking about miscarriages. Fetal cells seem to migrate early in pregnancy, meaning that even brief pregnancies may leave a cellular mark on a woman.

Scientists are just starting to discover how this cellular heritage works, and how it might influence health. The scientist in me can’t wait to see how this story unfolds. But for now, I’m content to marvel at the mother and daughters in me.

A zap to the head can stretch the time between intention and action, a new study finds. The results help illuminate how intentions arise in the brain.

The study, published in the May 6 Journal of Neuroscience, “provides fascinating new clues” about the process of internal decision making, says neuroscientist Gabriel Kreiman of Harvard University. These sorts of studies are bringing scientists closer to “probing some of the fundamental questions about who we are and why we do what we do,” he says.
Figuring out how the brain generates a sense of control may also have implications for people who lack those feelings. People with alien hand syndrome, psychogenic movement disorders and schizophrenia can experience a troubling disconnect between intention and action, says study coauthor Biyu Jade He of the National Institutes of Health in Bethesda, Md.

In the study, the researchers manipulated people’s intentions without changing their actions. The researchers told participants to click a mouse whenever the urge struck. Participants estimated when their intention to click first arose by monitoring a dot’s position on a clockface.

Intention to click usually preceded the action by 188 milliseconds on average, the team found. But a session of transcranial direct current stimulation, or tDCS, moved the realization of intention even earlier, stretching time out between awareness of intention and the action. tDCS electrodes delivered a mild electrical zap to participants’ heads, dialing up the activity of carefully targeted nerve cells. After stimulation, intentions arrived about 60 to 70 milliseconds sooner than usual. tDCS seemed to change certain kinds of brain activity that may have influenced the time shift, EEG recordings suggested.

The results highlight how thoughts and intentions can be separated from the action itself, a situation that appears to raise thorny questions about free will. But these tDCS zaps didn’t change the action outcome or participants’ feelings of control, only the reported timing of a person’s conscious intention.

MONTREAL — For the first time, scientists have precisely captured a map of the boisterous bang radiating from a lightning strike. The work could reveal the energies involved in powering some of nature’s flashiest light shows.

As electric current rapidly flows from a negatively charged cloud to the ground below, the lightning rapidly heats and expands the surrounding air, generating sonic shock waves. While scientists have a basic understanding of thunder’s origins, they lack a detailed picture of the physics powering the crashes and rumbles.
Heliophysicist Maher Dayeh of the Southwest Research Institute in San Antonio and colleagues sparked their own lightning by firing a long, Kevlar-coated copper wire into an electrically charged cloud using a small rocket. The resulting lightning followed the conductive wire to the ground. Using 15 sensitive microphones laid out 95 meters from the strike zone, Dayeh said he and his colleagues precisely recorded the incoming sound waves. Because sound waves from higher elevations took longer to reach the microphones, the scientists could create an acoustic map of the lightning strike with “surprising detail,” Dayeh said. He presented the results May 5 at a meeting of the American Geophysical Union and other organizations.

The loudness of a thunderclap depends on the peak electric current flowing through the lightning, the researchers found. This discovery could one day allow scientists to use thunder to sound out the amount of energy powering a lightning strike, Dayeh said.
SHOCK AND AWE Scientists shot a long copper wire into a lightning-prone cloud using a small rocket. The generated lightning followed the wire down to the ground, allowing the researchers to record the sound waves of the resulting thunder. The green flashes are caused by the intense heating of the copper wire. Credit: Univ. of Florida, Florida Institute of Technology, SRI

Pocket gophers certainly don’t qualify as card-carrying 4-H members, but the rodents might be farming roots in the open air of their moist, nutrient-rich tunnels.

The gophers subsist mostly on roots encountered in the tunnels that the rodents excavate. But the local terrain doesn’t always provide enough roots to sustain gophers, two researchers report in the July 11 Current Biology. To make up the deficit, the gophers practice a simple type of agriculture by creating conditions that promote more root growth, suggest ecologist Jack Putz of the University of Florida in Gainesville and his former zoology undergraduate student Veronica Selden.
But some scientists think it’s a stretch to call the rodents’ activity farming. Gophers aren’t actively working the soil, these researchers say, but inadvertently altering the environment as the rodents eat and poop their way around — much like all animals do.

Tunnel digging takes a lot of energy — up to 3,400 times as much as walking along the surface for gophers. To see how the critters were getting all this energy, Selden and Putz in 2021 began investigating the tunnels of southeastern pocket gophers (Geomys pinetis) in an area being restored to longleaf pine savanna in Florida that Putz partially owns.

The pair took root samples from soil adjacent to 12 gopher tunnels and extrapolated how much root mass a gopher would encounter as it excavated a meter of tunnel. Then the researchers calculated the amount of energy that those roots would provide.

“We were able to compare energy cost versus gain, and found that on average there is a deficit, with about half the cost of digging being unaccounted for,” Selden says.

Upon examining some tunnels, Selden and Putz saw gopher feces spread through the interior along with signs of little bites taken out of roots and churning of the soil.

The gophers, the researchers conclude, provide conditions that favor root growth by spreading their own waste as fertilizer, aerating the soil and repeatedly nibbling on roots to encourage new sprouting.

“All of these activities encourage root growth, and once the roots grow into the tunnels, the gophers crop the roots,” Selden says. She and Putz say that this amounts to a rudimentary form of farming. If so, gophers would be the first nonhuman mammals to be recognized as farmers, Putz says. Other organisms, such as some insects, also farm food and started doing so much earlier than humans (SN: 4/23/20).

But the study has its skeptics. “I don’t really think you can call it farming per the human definition. All herbivores eat plants, and everybody poops,” says J.T. Pynne, a wildlife biologist at the Georgia Wildlife Federation in Covington who studies southeastern pocket gophers. So the root nibbling and tunnel feces might not be signs of agriculture, just gophers doing what all animals do.

Evolutionary biologist Ulrich Mueller agrees. “If we accept the tenuous evidence presented in the Selden article as evidence for farming … then most mammals and most birds are farmers because each of them accidentally have also some beneficial effects on some plants that these mammals or birds also feed on,” he says.

Not only that, but the study is also dangerous, says Mueller, of the University of Texas at Austin. The public will see through “the shallowness of the data,” he says, and will conclude that science is “just a bunch of storytelling, eroding general trust in science.”

For her part, Selden says she understands that because gophers don’t plant their crops, not everyone is comfortable calling them farmers. Still, she argues that “what qualifies the gophers as farmers and sets them apart from, say, cattle, which incidentally fertilize the grass they eat with their wastes, is that gophers cultivate and maintain this ideal environment for roots to grow into.”

At the very least, Putz says, he hopes their research makes people kinder toward the rodents. “If you go to the web and put in ‘pocket gopher,’ you’ll see more ways to kill them than you can count.”

Widespread volcanic eruptions around 202 million years ago had a profound effect on Earth’s climate, triggering a mass extinction event that killed off three-fourths of the planet’s species, including many large reptiles. Yet dinosaurs, somehow, survived and went on to thrive.

Dinosaurs are often thought of as heat-loving, well suited to the steamy greenhouse environment of the Triassic Period. But the secret to their survival may have been how well adapted they were to the cold, unlike other reptiles of the time. The dinosaurs’ warm coats of feathers could have helped the creatures weather relatively brief but intense bouts of volcanic winter associated with the massive eruptions, researchers report July 1 in Science Advances.
“We’ve known for a while that there were probably volcanic winters” associated with the massive eruptions, says paleontologist Paul Olsen of the Lamont-Doherty Earth Observatory at Columbia University. Along with carbon dioxide, volcanoes spew sulfur particles into the atmosphere that can darken skies for years and lower global temperatures — as the Philippines’ Mount Pinatubo did after its powerful 1991 eruption (SN: 8/8/18). “But how [such winters] fit into the picture of the end-Triassic mass extinction has been very unclear.”

In the new study, Olsen and his colleagues present the first physical evidence that not only did such winters occur at the end of the Triassic, but also that dinosaurs were there to weather them. At a site called the Junggar Basin, which at the close of the Triassic was found high in the Arctic Circle, the team identified rock fragments that could only have been deposited by ancient ice alongside the footprints of dinosaurs.

“There is a stereotype that dinosaurs always lived in lush tropical jungles,” says Stephen Brusatte, a paleontologist at the University of Edinburgh who was not involved in the new study. “But this new research shows convincingly that the higher latitudes would have been freezing and even covered in ice during parts of the year” at the beginning of the rise of the dinosaurs, he says.

The Triassic Period ended with a bang beginning around 202 million years ago, as the supercontinent Pangea began to break apart. Massive volcanic eruptions burst forth as the crust split, opening up a basin that became the Atlantic Ocean. The hardened lava from those eruptions now spans 7 million square kilometers across Africa, Europe and North and South America, forming a rock sequence collectively known as the Central Atlantic Magmatic Province, or CAMP.

Carbon dioxide levels were extremely high during the late Triassic and early Jurassic, much of it now thought to have been pumped into the atmosphere by those eruptions. Earth has been assumed to have been in a steamy greenhouse state as a result. Supporting this hypothesis is the fact that there’s no evidence of any polar ice sheets at the time; instead, thick forests extended all the way to the poles.

The Junggar Basin, in what’s now northwestern China, was one such region, covered with forests of conifers and deciduous trees growing alongside a massive ancient lake. Dinosaurs certainly lived there: No bones have yet been discovered at the site, but many footprints of the creatures are preserved in the shallow-water siltstones and sandstones that formed at the bottom of the lake.
The new data suggest that — despite the extremely high CO2 levels — this region also experienced harsh, frigid winters, with the lake at least partially freezing over. The evidence comes from the same rocks that bear the footprints. Analyzing the distribution of grain sizes in the rocks, the researchers determined that a large portion of the grains weren’t part of the original lake mud, but had been carried there from elsewhere.

The most likely explanation, Olsen says, is that these grains are “ice-rafted debris” — a well-known phenomenon in which bits of rock freeze to the base of ice along a shoreline, and then hitch a ride with the ice as it eventually drifts into open water. As the floating ice melts, the bits of rock sink, deposited in new territory.

Volcanic winters might last for tens or even hundreds of years, Olsen says, depending on how long volcanoes continue to erupt. In this case, the huge sheets of lava linked to the CAMP eruptions point to at least tens of thousands of years of eruption pulses, maybe even a million years. That could have kept the winters going for a good long time — long enough to drive many less-well-insulated reptiles off the face of the Earth, he adds. Episodes of those freezing conditions may have even extended all the way to the tropics, the team says.

Evidence of feathers has been found in the fossils of many types of dinosaurs, from carnivorous theropods to herbivorous ornithischians. Recent reports that flying reptiles called pterosaurs had feathers too now suggests that the insulating fuzz has been around for even longer than once thought — possibly appearing as early as 250 million years ago, in a common ancestor of dinosaurs and pterosaurs (SN: 4/29/22).

Thanks to those insulating feathers, dinosaurs were able to survive the lengthy winters that ensued during the end-Triassic mass extinction, Olsen and colleagues say. Dinosaurs might then have been able to spread rapidly during the Jurassic, occupying niches left vacant by less hardy reptiles.

This study “shows the complexity of disentangling not only the success of certain groups, but also the causes and effects of mass extinction events,” says paleontologist Randall Irmis of the University of Utah in Salt Lake City, who was not connected with the study. “There’s a pretty good consensus that [the CAMP eruptions are] the cause of the mass extinction — but there are a lot of subtleties we haven’t appreciated.”

That dinosaurs living in the far north at the time were able to survive due to their feathery insulation makes sense, Irmis says. But whether a volcanic winter caused by dimming could have extended far enough south to freeze the tropics too — giving dinosaurs a similar advantage there — isn’t yet clear. “Dimming is a global effect, but how that plays out is a lot more severe at the poles compared to low latitudes.”

Feathers are probably just one of many reasons why dinosaurs diversified and spread rapidly across the globe at the start of the Jurassic, Irmis says. “There’s a lot that plays into why they became such a successful group.”

Monkeypox is not yet a global public health emergency, the World Health Organization said June 25.

The decision comes as the outbreak of the disease related to smallpox continues to spread, affecting at least 4,100 people in 46 countries as of June 24. That includes at least 201 cases in the United States. Those cases have been found in 25 states and the District of Columbia, according to the U.S. Centers for Disease Control and Prevention.
“Controlling the further spread of outbreak requires intense response efforts,” and the situation should be reevaluated in a few weeks, the WHO committee evaluating the outbreak said in an announcement.

The declaration of a public health emergency would have potentially made it easier to get treatments and vaccines to people infected with or exposed to the virus. Some medications and vaccines that could help fend off monkeypox are approved for use against smallpox, and can be used against monkeypox only with special authorization.

The virus that causes monkeypox, named for its discovery in monkeys in 1958 though it is probably a virus that mainly infects rodents, is not a new threat. Countries in central Africa, where monkeypox is endemic, have had sporadic outbreaks since researchers found the first human case in 1970. Places in western Africa had few cases until 2017. But most cases outside the continent were travel-related, with limited spread to others (SN: 5/26/22).

“Monkeypox has been circulating in a number of African countries for decades and has been neglected in terms of research, attention and funding,” WHO director-general Tedros Ghebreyesus said in a statement announcing the decision. “This must change not just for monkeypox but for other neglected diseases in low-income countries as the world is reminded yet again that health is an interconnected proposition.”

Monkeypox typically kills fewer than 10 percent of people who contract it. At least one person has died in the global outbreak.

As case numbers climb, researchers are working to decipher the genetic blueprint of the virus, in hopes of uncovering whether some viral mutations might explain why the virus has quickly gained a foothold in new places.

Tracing the mutations
The closest known relative of the versions of the virus behind the global outbreak comes from Nigeria, hinting that the outbreak may have got its start there.

In the newest surge in cases, scientists have uncovered more viral changes than anticipated — a sign that the virus may have been circulating undetected among people for a while, perhaps since Nigeria’s 2017–2018 monkeypox outbreak, new research suggests. What’s more, a group of enzymes known for their virus-fighting abilities in the body may be to blame for many of those mutations.

A genetic analysis of monkeypox viruses involved in the global outbreak from 15 people across seven countries shows that these viruses have an average of 50 more genetic tweaks than versions circulating in 2018 and 2019, researchers report June 24 in Nature Medicine. That’s roughly six to 12 times as many mutations as scientists would have expected the virus to develop over that time. Unlike some other types of viruses, poxviruses, which include smallpox and monkeypox viruses, typically mutate fairly slowly.

The changes have a pattern that is a hallmark of an enzyme family called APOBEC3, the researchers say. These enzymes edit DNA’s building blocks — represented by the letters G, C, A and T — in a specific way: Gs change to As and Cs to Ts. The analysis found that particular pattern in the viral sequences, suggesting that APOBEC3s are responsible for the mutations.

Ideally, so many DNA building blocks are swapped for another that a virus is effectively destroyed and can’t infect more cells. But, sometimes, APOBEC3 enzymes don’t make enough changes to knock out the virus. Such mutated, though still functional, viruses can go on to infect additional cells, and possibly another person.

A big question, though, is whether the genetic tweaks seen in the monkeypox virus are helpful, harmful or have no effect at all on the virus.

While it’s still unknown whether the enzymes are directly responsible for the changes in the monkeypox virus, similar mutations are still popping up, the team found. So, APOBEC3s may still be helping the virus change as it continues to spread. One member of the enzyme family is found in skin cells, where people with monkeypox can develop infectious pox lesions.
Different symptoms
Symptoms reported in the global outbreak have been generally milder than those reported in previous outbreaks, perhaps allowing the disease to spread before a person knows they’re infected.

It is not clear whether those differences in symptoms are related to changes in the virus, Inger Damon, director of the CDC’s Division of High-Consequence Pathogens and Pathology, said June 21 in a news briefing hosted by SciLine, a service for journalists and scientists sponsored by the American Association for the Advancement of Science.

Typically, in previous outbreaks, people would develop flu-like symptoms, including fever, headaches, muscle aches and exhaustion about a week or two after exposure to the virus. Then, one to three days after those symptoms start, a rash including large pus-filled lesions pops up generally starting on the face and limbs, particularly the hands, and spreads over the body. Though generally milder, those symptoms are similar to smallpox, but people with monkeypox also tend to develop swollen lymph nodes.

All patients in the U.S. outbreak have gotten rashes, Damon said, “but the lesions have been scattered or localized to a specific body site, rather than diffuse, and have not generally involved the face or the … palms of the hand or the soles of the feet.” Instead, rashes may start in the genital or anal area where they can be mistaken for sexually transmitted diseases, such as syphilis or herpes, she said.

In many cases, the rashes have not spread to other parts of the body. And the classical early symptoms such as fever have been “mild and sometimes nonexistent before a rash appears,” Damon said.

Monkeypox is transmitted from person to person through close skin-to-skin contact or by contact with contaminated towels, clothes or bedding. It may also be spread by droplets of saliva exchanged during kissing or other intimate contact. The CDC is investigating whether the virus might be spread by semen as well as skin-to-skin contact during sex, Agam Rao, a captain in the U.S. Public Health Service, said June 23 at a meeting of the CDC’s Advisory Committee on Immunization Practices.

“We don’t have any reason to suspect it is spread any other way,” such as through the air, Rao said.

In Nigeria, more monkeypox cases have been recorded among women, while the global outbreak has affected mainly men, particularly men who have sex with men. Experts warn that anyone can be infected with monkeypox, and some people face an increased risk of severe disease. Those at increased risk include children, people who are immunocompromised, pregnant people and people with eczema.

The risk of catching monkeypox through casual contact is still low in the United States, Rao said. But data she presented show that while people in the country have contracted monkeypox while traveling abroad, cases have also spread locally.

At the time, Conover was a Ph.D. student in particle physics (she’s now physics senior writer for Science News). She was part of a team building a detector in the cavern to observe elusive particles called neutrinos. It was the Fourth of July 2012. A few hundred kilometers away, scientists were announcing the discovery of another elusive subatomic particle, the Higgs boson, which physicists had been hunting for decades. As hundreds of researchers cheered in the main auditorium at the CERN particle physics lab near Geneva, Conover and the small group of physicists in the chilly French cavern cheered too, as did scientists worldwide. The Higgs boson filled in a missing piece in the standard model of particle physics, which explains just about everything known about the particles that make up atoms and transmit the forces of nature. No Higgs boson, no life as we know it.

In this issue’s cover story, “The Higgs boson at 10,” Conover looks back at the excitement around the discovery of the Higgs boson and looks ahead to the many things that researchers hope to find out with its help. She also reviews a new biography of Peter Higgs, a modest man who made clear that he was just one of many scientists who contributed to the breakthrough.

The discovery is part of Science News history too. Journalists around the world were eagerly awaiting the big announcement, which was being kept under wraps. But when Kate Travis, a Science News editor at the time, uncovered an announcement video accidentally posted early on CERN’s website, we published the big news the day before the official announcement.

“Even though its discovery is 10 years old now, that’s still new in the grand scheme of particle physics, so we’re still learning lots about it,” Conover told me. “It’s very cool that I get the opportunity to write about this particle that is still so new to science.” And it’s very cool that we get to explore it with her.

In the 1920s, laborers and amateur archaeologists at gravel quarry pits in southeastern England uncovered more than 300 ancient, sharp-edged oval tools. Researchers have long suspected that these hand axes were made 500,000 to 700,000 years ago. A new study confirms that suspicion in the first systematic excavation of the site, known as Fordwich.

Dating those tools and more recent finds suggests that humanlike folk inhabited the area between about 560,000 and 620,000 years ago, researchers report in the June Royal Society Open Science. Relatively warm conditions at that time drew hominids to what’s now northern Europe before the evolutionary rise of Neandertals and Homo sapiens.
The results confirm that Fordwich is one of the oldest hominid sites in England. Previous discoveries place hominids in what’s now southeastern England at least 840,000 years ago (SN: 7/7/10) and perhaps as far back as nearly 1 million years ago (SN: 2/11/14). No hominid fossils have been found at Fordwich. It’s unclear which species of the human genus made the tools.

In 2020, archaeologist Alastair Key of the University of Cambridge and colleagues unearthed 238 stone artifacts at Fordwich that display grooves created by striking the surface with another stone. Other finds include three stones with resharpened edges, presumably used to scrape objects like animal hides.

A method for determining when sediment layers were last exposed to sunlight indicated that the newly discovered artifacts date to roughly 542,000 years ago. The previously unearthed hand axes probably came from the same sediment.

Hominids must have fashioned tools at Fordwich a bit earlier than 542,000 years ago because ancient climate data suggest that an ice age at that time made it hard to survive in northern Europe, the team concludes. Warmer conditions between 560,000 and 620,000 years ago would have enabled the hominid toolmakers to live so far north.