Sometimes a photo is literally a matter of life, death — and zombies.

This haunting image, winner of the 2022 BMC Ecology and Evolution photography competition, certainly fits that description. It captures the fruiting bodies of a parasitic fungus, emerging from the lifeless body of an infected fly in the Peruvian rainforest.

The fungus-infested fly was one of many images submitted to the contest from all over the world, aiming to showcase the beauty of the natural world and the challenges it faces. The journal revealed the winners August 18.
Roberto García-Roa, a conservation photographer and evolutionary biologist at the University of Valencia in Spain, took the winning photo while visiting the Tambopata National Reserve, a protected habitat in the Amazon.

The fungus erupting from the fly belongs to the genus Ophiocordyceps, a diverse collection of parasitic fungi known as “zombie fungi,” due to their ability to infect insects and control their minds (SN: 7/17/19).

“There is still much to unravel about the diversity of these fungi as it is likely that each insect species infected succumbs to its own, specialized fungus,” says Charissa de Bekker, an expert in parasitic fungi at Utrecht University in the Netherlands.

First, spores of the fungus land on the ill-fated fly. So begins the manipulative endgame. The spores infiltrate the fly’s exoskeleton before infecting its body and eventually hijacking its mind. Once in control, the fungus uses its new powers of locomotion to relocate to a microclimate more suitable to its own growth — somewhere with the right temperature, light and moisture.

Fungus and fly then bide their time until the fly dies, becoming a food source for the fungus to consume. Fruiting bodies work their way out of the fly, filled with spores that are released into the air to continue the macabre cycle in a new, unsuspecting host. It is a “conquest shaped by thousands of years of evolution,” García-Roa said in a statement announcing the winners.

Research into the molecular aspects of fungal mind control is under way, De Bekker says, including in her own lab. “These fungi harbor all sorts of bioactive chemicals that we have yet to characterize and that could have novel medicinal and pest control applications.”

This is the first picture of an exoplanet from the James Webb Space Telescope.

“We’re actually measuring photons from the atmosphere of the planet itself,” says astronomer Sasha Hinkley of the University of Exeter in England. Seeing those particles of light, “to me, that’s very exciting.”

The planet is about seven times the mass of Jupiter and lies more than 100 times farther from its star than Earth sits from the sun, direct observations of exoplanet HIP 65426 b show. It’s also young, about 10 million or 20 million years old, compared with the more than 4-billion-year-old Earth, Hinkley and colleagues report in a study submitted August 31 at arXiv.org.
Those three features — size, distance and youth — made HIP 65426 b relatively easy to see, and so a good planet to test JWST’s observing abilities. And the telescope has once again surpassed astronomers’ expectations (SN: 7/11/22).

“We’ve demonstrated really how powerful JWST is as an instrument for the direct imaging of exoplanets,” says exoplanet astronomer and coauthor Aarynn Carter of the University of California, Santa Cruz.

Astronomers have found more than 5,000 planets orbiting other stars (SN: 3/22/22). But almost all of those planets were detected indirectly, either by the planets tugging on the stars with their gravity or blocking starlight as they cross between the star and a telescope’s view.

To see a planet directly, astronomers have to block out the light from its star and let the planet’s own light shine, a tricky process. It’s been done before, but for only about 20 planets total (SN: 11/13/08; SN: 3/14/13; SN: 7/22/20).

“In every area of exoplanet discovery, nature has been very generous,” says MIT astrophysicist Sara Seager, who was not involved in the JWST discovery. “This is the one area where nature didn’t really come through.”

In 2017, astronomers discovered HIP 65426 b and took a direct image of it using an instrument on the Very Large Telescope in Chile. But because that telescope is on the ground, it can’t see all the light coming from the exoplanet. Earth’s atmosphere absorbs a lot of the planet’s infrared wavelengths — exactly the wavelengths JWST excels at observing. The space telescope observed the planet on July 17 and July 30, capturing its glow in four different infrared wavelengths.

“These are wavelengths of light that we’ve never ever seen exoplanets in before,” Hinkley says. “I’ve literally been waiting for this day for six years. It feels amazing.”

Pictures in these wavelengths will help reveal how planets formed and what their atmospheres are made of.

“Direct imaging is our future,” Seager says. “It’s amazing to see the Webb performing so well.”

While the team has not yet studied the atmosphere of HIP 65426 b in detail, it did report the first spectrum — a measurement of light in a range of wavelengths — of an object orbiting a different star. The spectrum allows a deeper look into the object’s chemistry and atmosphere, astronomer Brittany Miles of UC Santa Cruz and colleagues reported September 1 at arXiv.org.

That object is called VHS 1256 b. It’s as heavy as 20 Jupiters, so it may be more like a transition object between a planet and a star, called a brown dwarf, than a giant planet. JWST found evidence that the amounts of carbon monoxide and methane in the atmosphere of the orb are out of equilibrium. That means the atmosphere is getting mixed up, with winds or currents pulling molecules from lower depths to its top and vice versa. The telescope also saw signs of sand clouds, a common feature in brown dwarf atmospheres (SN: 7/8/22).

“This is probably a violent and turbulent atmosphere that is filled with clouds,” Hinkley says.

HIP 65426 b and VHS 1256 b are unlike anything we see in our solar system. They’re more than three times the distance of Uranus from their stars, which suggests they formed in a totally different way from more familiar planets. In future work, astronomers hope to use JWST to image smaller planets that sit closer to their stars.

“What we’d like to do is get down to study Earths, wouldn’t we? We’d really like to get that first image of an Earth orbiting another star,” Hinkley says. That’s probably out of JWST’s reach — Earth-sized planets are still too small see. But a Saturn? That may be something JWST could focus its sights on. Those three features — size, distance and youth — made HIP 65426 b relatively easy to see, and so a good planet to test JWST’s observing abilities. And the telescope has once again surpassed astronomers’ expectations (SN: 7/11/22).

“We’ve demonstrated really how powerful JWST is as an instrument for the direct imaging of exoplanets,” says exoplanet astronomer and coauthor Aarynn Carter of the University of California, Santa Cruz.

Astronomers have found more than 5,000 planets orbiting other stars (SN: 3/22/22). But almost all of those planets were detected indirectly, either by the planets tugging on the stars with their gravity or blocking starlight as they cross between the star and a telescope’s view.

To see a planet directly, astronomers have to block out the light from its star and let the planet’s own light shine, a tricky process. It’s been done before, but for only about 20 planets total (SN: 11/13/08; SN: 3/14/13; SN: 7/22/20).

“In every area of exoplanet discovery, nature has been very generous,” says MIT astrophysicist Sara Seager, who was not involved in the JWST discovery. “This is the one area where nature didn’t really come through.”

In 2017, astronomers discovered HIP 65426 b and took a direct image of it using an instrument on the Very Large Telescope in Chile. But because that telescope is on the ground, it can’t see all the light coming from the exoplanet. Earth’s atmosphere absorbs a lot of the planet’s infrared wavelengths — exactly the wavelengths JWST excels at observing. The space telescope observed the planet on July 17 and July 30, capturing its glow in four different infrared wavelengths.

“These are wavelengths of light that we’ve never ever seen exoplanets in before,” Hinkley says. “I’ve literally been waiting for this day for six years. It feels amazing.”

Pictures in these wavelengths will help reveal how planets formed and what their atmospheres are made of.

“Direct imaging is our future,” Seager says. “It’s amazing to see the Webb performing so well.”

While the team has not yet studied the atmosphere of HIP 65426 b in detail, it did report the first spectrum — a measurement of light in a range of wavelengths — of an object orbiting a different star. The spectrum allows a deeper look into the object’s chemistry and atmosphere, astronomer Brittany Miles of UC Santa Cruz and colleagues reported September 1 at arXiv.org.

That object is called VHS 1256 b. It’s as heavy as 20 Jupiters, so it may be more like a transition object between a planet and a star, called a brown dwarf, than a giant planet. JWST found evidence that the amounts of carbon monoxide and methane in the atmosphere of the orb are out of equilibrium. That means the atmosphere is getting mixed up, with winds or currents pulling molecules from lower depths to its top and vice versa. The telescope also saw signs of sand clouds, a common feature in brown dwarf atmospheres (SN: 7/8/22).

“This is probably a violent and turbulent atmosphere that is filled with clouds,” Hinkley says.

HIP 65426 b and VHS 1256 b are unlike anything we see in our solar system. They’re more than three times the distance of Uranus from their stars, which suggests they formed in a totally different way from more familiar planets. In future work, astronomers hope to use JWST to image smaller planets that sit closer to their stars.

“What we’d like to do is get down to study Earths, wouldn’t we? We’d really like to get that first image of an Earth orbiting another star,” Hinkley says. That’s probably out of JWST’s reach — Earth-sized planets are still too small see. But a Saturn? That may be something JWST could focus its sights on.

For some ant queens, the secret to long life might be a self-produced insulin blocker.

Ant queens are famously long-lived, even though they shouldn’t be. Generally, animals that put lots of energy into reproduction sacrifice some time off their life. But ant queens produce millions of eggs and live an extraordinarily long time compared with worker ants that don’t reproduce.

Now, researchers have shown how one ant species pulls off this anti-aging feat. When queens and wannabe queens of the species Harpegnathos saltator gear up to reproduce, a part of what’s called the insulin signaling pathway gets blocked, slowing aging, the researchers report in the Sept. 2 Science. That molecular pathway has long been implicated in aging in mammals, including humans.
“There’s been a need to understand why queens, or reproductives, in social insects can live for so amazingly long,” says Marc Tatar, a biologist at Brown University in Providence, R.I., who was not involved with the study. Some ant species have queens that survive 30 times as long as their workers. Other social insects such as bees and termites also have long-lived queens.

In a rare behavior for ants, when a queen H. saltator dies, some female workers begin competing in duels for the chance to replace her (SN: 1/17/14). These hopeful royals develop ovaries, start laying eggs and transition into queenlike forms called gamergates. When a worker transitions to a gamergate, her life span becomes five times as long as it was. But if she doesn’t end up becoming queen and reverts back to a worker, her life span shortens again.

The researchers exploited this behavior to investigate the molecular underpinnings of anti-aging in these ants. H. saltator gamergates, it turns out, extend their life spans by taking advantage of a split in the insulin signaling pathway, the chain of chemical reactions that drive insulin’s effects on the body. One branch of this pathway is involved with reproduction, while the other is implicated in aging.

“Insulin comes with our life — [after] we eat, we have high insulin,” says Hua Yan, a biologist at the University of Florida in Gainesville. “But a constant high level of insulin is bad for longevity.”

Examining patterns of gene activity, Yan and colleagues found that gamergates have more active insulin genes than regular worker ants and, as a result, have increased metabolic activity and ovary development. But the secret sauce protecting the ants from the insulin’s aging effects appears to be a molecule called Imp-L2, which blocks the branch of the insulin pathway linked to aging, experiments showed. The branch involved in reproduction, however, remains active.

“What we don’t understand is how Imp-L2 can act on one aspect of the pathway and not on the other,” says study coauthor Claude Desplan, a developmental biologist at New York University.

These results represent a leap forward in our understanding of extreme social insect longevity, the researchers say, while also showcasing an anti-aging evolutionary adaptation that hasn’t been seen in the wild before.

For some ant queens, the secret to long life might be a self-produced insulin blocker.

Ant queens are famously long-lived, even though they shouldn’t be. Generally, animals that put lots of energy into reproduction sacrifice some time off their life. But ant queens produce millions of eggs and live an extraordinarily long time compared with worker ants that don’t reproduce.

Now, researchers have shown how one ant species pulls off this anti-aging feat. When queens and wannabe queens of the species Harpegnathos saltator gear up to reproduce, a part of what’s called the insulin signaling pathway gets blocked, slowing aging, the researchers report in the Sept. 2 Science. That molecular pathway has long been implicated in aging in mammals, including humans.
“There’s been a need to understand why queens, or reproductives, in social insects can live for so amazingly long,” says Marc Tatar, a biologist at Brown University in Providence, R.I., who was not involved with the study. Some ant species have queens that survive 30 times as long as their workers. Other social insects such as bees and termites also have long-lived queens.

In a rare behavior for ants, when a queen H. saltator dies, some female workers begin competing in duels for the chance to replace her (SN: 1/17/14). These hopeful royals develop ovaries, start laying eggs and transition into queenlike forms called gamergates. When a worker transitions to a gamergate, her life span becomes five times as long as it was. But if she doesn’t end up becoming queen and reverts back to a worker, her life span shortens again.

The researchers exploited this behavior to investigate the molecular underpinnings of anti-aging in these ants. H. saltator gamergates, it turns out, extend their life spans by taking advantage of a split in the insulin signaling pathway, the chain of chemical reactions that drive insulin’s effects on the body. One branch of this pathway is involved with reproduction, while the other is implicated in aging.

“Insulin comes with our life — [after] we eat, we have high insulin,” says Hua Yan, a biologist at the University of Florida in Gainesville. “But a constant high level of insulin is bad for longevity.”

Examining patterns of gene activity, Yan and colleagues found that gamergates have more active insulin genes than regular worker ants and, as a result, have increased metabolic activity and ovary development. But the secret sauce protecting the ants from the insulin’s aging effects appears to be a molecule called Imp-L2, which blocks the branch of the insulin pathway linked to aging, experiments showed. The branch involved in reproduction, however, remains active.

“What we don’t understand is how Imp-L2 can act on one aspect of the pathway and not on the other,” says study coauthor Claude Desplan, a developmental biologist at New York University.

These results represent a leap forward in our understanding of extreme social insect longevity, the researchers say, while also showcasing an anti-aging evolutionary adaptation that hasn’t been seen in the wild before.

Meet the Milky Way in its own words.

The Milky Way: An Autobiography of Our Galaxy takes a tour of our home in the cosmos from an unexpected perspective. Astrophysicist and folklorist Moiya McTier presents herself not as the author, but as the lucky human vessel through which the Milky Way has chosen to tell its story. Then she lets the galaxy take it away, with humor, heart and a huge dose of snark.

The book alternates chapters between science and mythology, reflecting McTier’s dual specialties (her bio says she was the first student in Harvard University’s history to study both). “Many of you don’t realize this, but myths were some of your species’ first attempt at scientific inquiry,” the Milky Way tells us.

The Milky Way is telling its story now because it’s sick of being ignored. Once upon a time, humans looked to the glittering smudge of stars in the sky for insight into when to plant crops or avoid floods. We told stories about the Milky Way’s importance in the origin and fate of the world.

Our galaxy ate it up: For an entity that spends most of its time ripping up smaller galaxies and watching its own stars die, “your stories made me feel loved and needed and, perhaps for the first time in my long existence, more helpful than I was ruinous.” But in the last few centuries, technology and light pollution have pulled humankind away. “At first, I thought it was just a phase,” the Milky Way says. “Then I remembered … that several hundred years is actually a long time for humans.”
So the Milky Way decided to remind us why it’s so important. Its autobiography covers big-picture scientific questions about galaxies, like where they come from (“When a gas cloud loves itself very much,” the Milky Way explains, “it hugs itself extra tight, and after a few hundred million years, a baby galaxy is born. Leave the storks out of it, please.”). It also gets into what galaxies are made of, how they interact with other galaxies, and how they live and die. The book then zooms out to cover the origins and possible ends of the universe, mysteries like dark matter and dark energy, and even humankind’s search for other intelligent life (SN: 8/4/20).

The author takes pains to explain scientific jargon and the technical tools that astronomers use to study the sky. A lot of popular astronomy writing glosses over how astronomers think about cosmic distance or exactly what a spectrum is, but not this book. If you’ve ever been curious about these insider details, The Milky Way has you covered.

McTier’s version of our home galaxy is heavily anthropomorphized. The Milky Way is brash, vain and arrogant in a way that may hide a secret insecurity. Its central black hole is characterized as the physical embodiment of the galaxy’s shame and regrets, a source of deep existential angst. And its relationship with the Andromeda galaxy is like a long-term, long-distance romance, with each galaxy sending stars back and forth as love notes until the two can eventually merge (SN: 3/05/21).

This could have felt gimmicky. But McTier’s efforts to make the metaphors work while keeping the science accurate and up-to-date made the premise endearing and entertaining.

I laughed twice on Page 1. I learned a new word on Page 2. I dog-eared the endnotes early on because it became instantly clear I would want to read every one. I read this book while traveling in rural upstate New York, where the sky is much clearer than at my home outside of Boston. The Milky Way reminded me to look up and appreciate my home in the universe, just like its narrator wanted.

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 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

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.