In the fall of 2020, the world was staggering under the attack of the SARS-CoV-2 virus. In the United States, more than 4 million cases were reported in November, more than double the number in October. Hospitals were overwhelmed. On the Thursday before Thanksgiving, 1,962 people died.
Now, despite more than 1 million deaths in the United States and more than 6 million worldwide, it’s almost easy to forget that the pandemic’s assault continues. That is, until you hear Belinda Hankins’ story.
Hankins has been diagnosed with long COVID, a collection of symptoms that can include crushing fatigue, brain fog, pain and dizziness and that may affect 1 in 5 people infected with SARS-CoV-2, according to one conservative estimate. She talked with Science News staff writer Meghan Rosen during her appointment at the long COVID clinic at the Johns Hopkins Bayview Medical Center.
“For months we’ve heard estimates about how many people have long COVID,” Rosen told me. “I was interested in going beyond the stats to find out what it’s like for the patients and doctors living with this.”
That effort involved talking with doctors who are trying to figure out how to treat the symptoms of long COVID when the cause is still unknown. And talking with Hankins. “I thought it was extraordinary that [she] let me into her appointment,” Rosen said. “It’s just so generous and so brave.”
I share Rosen’s gratitude. Asking someone in the midst of a life-altering illness to talk with a journalist is a big request. I always worry that people might feel pressure to participate, and I want to be sure that they’ve had time to think through the implications of going public with personal information. Hankins was clear about why she said yes. “She wanted to share her story because a lot of people in her life don’t know what long COVID is and why she’s still so sick,” Rosen said.
In reporting, Rosen brings both her empathy and her serious science chops. She has a Ph.D. in biochemistry and molecular biology and is a graduate of the science journalism program at the University of California, Santa Cruz. She explored careers in biotech but decided that wasn’t the right fit. She wanted to write about health and medicine.
This is actually Rosen’s third stint at Science News: first as an intern, then as a reporter, and now back on the beat after five years of doing communications work for the Howard Hughes Medical Institute. We’re glad she’s back. Not only is she tackling complex issues surrounding COVID-19, including how U.S. public health guidelines affect kids in school (SN Online: 8/19/22), she’s also been sharing her delight in science. That includes stories on genetic variants linked to uncombable hair in children (SN: 10/8/22 & 10/22/22, p. 5); an unusual “snough” call that zoo gorillas appear to have invented to get zookeepers’ attention (SN Online: 8/10/22); and a new robotic pill designed to deliver drugs by scrubbing away mucus in the intestines.
Yes, science is serious and important, but it’s also crazy fun. I don’t think I’m ready to sign up for the robotic intestinal scrub brush, but I sure do enjoy finding out about it.
Across the United States, kids are prepping for back-to-school, or are already in classrooms, and parents are buckling up for another pandemic school year. Like me, many are trying to get a handle on what COVID-19 precautions to take. Updated guidance released last week by the U.S. Centers for Disease Control and Prevention hasn’t exactly helped. It may have made dealing with back-to-school more confusing — and could even spur new outbreaks.
Last November, my fifth grader had to quarantine at home for 10 days after a close contact tested positive. Now, the CDC has nixed the quarantine recommendation for people exposed to COVID-19. Today, our situation could look something like this: My COVID-exposed daughter would mask for 10 days, test on day five, and remain in school the whole time — only the infected child would isolate. That child would stay home for at least five days after a positive test. Then, if the child is fever-free and symptoms are improving, according to the new guidance, they could pop on a mask and hightail it back to class — no testing needed. That advice could mean more COVID-19 in classrooms. Scientists have shown that people can remain infectious after day five. So without testing for COVID-19, students and teachers won’t know if they’re bringing the disease back to school.
On the same day the CDC’s guidance came out, the U.S. Food and Drug Administration added yet another wrinkle. If you think you’ve been exposed to COVID-19 but test negative with an at-home COVID-19 antigen test, the FDA now recommends testing again … and again. Repeat testing over time cuts the chances you’ll miss an infection and unknowingly spread the virus, the FDA advised on August 11.
It’s hard to say how that advice jibes with the CDC’s new, more-relaxed guidelines. Even the agency has said its public guidance during the pandemic has been “confusing and overwhelming,” the New York Times reports. CDC director Rochelle Walensky is now planning a shake-up that could include restructuring the communications office as well as relying more on preliminary studies rather tha The CDC’s new guidance has sparked a range of reactions, many negative, among scientists, doctors, parents and teachers. In an informal Twitter poll of Science News followers, roughly 80 percent of the 353 respondents reported that the new CDC guidance made them feel confused, worried or angry and/or exasperated.
Now, it’s up to local school districts to decide what COVID-19 measures to take. “Just because guidance has changed does not mean COVID is gone,” Becky Pringle, president of the National Education Association labor union, said in a statement. Not by a long shot. The United States is currently averaging nearly 500 daily coronavirus deaths and more than 100,000 new cases a day, an almost certain undercount.
As my own children gear up for school, I wonder about COVID-19’s constantly shifting landscape. Like other families with school-aged children, we’ve bounced from virtual school to in-person mask mandates to mask-optional recommendations. And we still don’t know our district’s plans for the upcoming year. School starts in about a week.
There is reason for hope, though: We know what measures can slow COVID-19’s spread in schools. Masking is a big one. A preliminary study posted August 9 linked lifting school mask mandates in Boston-area K–12 schools with a rise in cases among students and staff. At Boston University, mandatory masking plus a vaccine mandate seemed to keep the virus in check in classrooms, scientists reported August 5 in JAMA Network Open. Testing can help, too. A computer analysis from England suggests that regularly rapid testing students can curb classroom transmission, scientists report August 10 in the Royal Society Open Science. But knowing what works is not the same as actually employing evidence-based measures in the classroom, says Anne Sosin, a public health researcher at Dartmouth College whose research focuses on COVID-19 and rural health equity. She has studied how pandemic policies have impacted schools in northern New England. “I worry that we simply have not seen the political leadership to ensure that all children and educators can safely participate in school.”
I spoke with Sosin about the CDC’s new guidance, and what kids and parents might expect heading into the new school year. Our conversation has been edited for length and clarity.
SN: What do you think of the updated guidance?
Sosin: I was very disappointed that the CDC did not adopt a test-to-exit-isolation recommendation.
What we’re going to see in schools are infected students and educators returning after five days still positive for COVID-19. Multiple studies have demonstrated that most people are infectious beyond five days. Not only is it highly likely that they’ll be seeding outbreaks. They’ll also be putting high-risk members of school communities in danger.
SN: What could the guidance mean for vulnerable kids?
Sosin: I think that vulnerable people are going to be in a very precarious situation. The guidance mentions the need to ensure protections for immunocompromised and other high-risk people but there’s a problem of implementation. Will schools actually implement those protections?
SN: Do scientists have a good handle on what protections can help?
Sosin: Definitely. We have really strong evidence showing that when layered mitigation strategies are in place, we can almost eliminate transmission in school settings. That means that we should have upgraded ventilation, lunchroom strategies [like taking kids outside to eat] and testing. And I continue to think that data-driven mask policies have a role to play. Not masking forever, but masking at times when we see an uptick in transmission.
SN: How could the new guidance affect different communities across the United States?
Sosin: Different communities have not only been impacted in dramatically different ways, but they’re also on unequal footing at this stage of the pandemic.
[If we compare white communities with communities of color], we see disparities in vaccination coverage and caregiver loss. Some communities have suffered enormous losses while others have really been untouched. Black children have lost caregivers at more than two times the rate of white children. For Indigenous children, the rate is 4.5 times as high. Those are sharp disparities.
Communities of color also have less access to testing, treatment and health care. I worry that if we don’t have a renewed focus on equity, then we’re just going to see an exacerbation of disparities that have existed throughout the pandemic.
SN: What advice do you have for parents as they head into the new school year?
Sosin: We all want as normal a school year as possible. Masking should be one of the tools we’re ready to employ to keep our kids in the classroom. In addition, we should be advocating that our schools invest in ventilation. Vaccination also represents a critical piece of the strategy.
We see such abysmal vaccination coverage among children. Less than 1 in 3 kids ages 5 to 11 are fully vaccinated. I think many parents no longer see it as important — there’s been this narrative that the pandemic is over. We need clear messaging that vaccination remains an important tool.
Now is a great time to plan back-to-school campaigns to vaccinate kids and to begin to prepare for the arrival of omicron-specific boosters in the fall.
Archaeologist Peter Bellwood’s academic odyssey wended from England to teaching posts halfway around the world, first in New Zealand and then in Australia. For more than 50 years, he has studied how humans settled islands from Southeast Asia to Polynesia.
So it’s fitting that his new book, a plain-English summary of what’s known and what’s not about the evolution of humans and our ancestors, emphasizes movement. In The Five-Million-Year Odyssey, Bellwood examines a parade of species in the human evolutionary family — he collectively refers to them as hominins, whereas some others (including Science News) use the term hominids (SN: 9/15/21) — and tracks their migrations across land and sea. He marshals evidence indicating that hominids in motion continually shifted the direction of biological and cultural evolution. Throughout his tour, Bellwood presents his own take on contested topics. But when available evidence leaves a debate unresolved, he says so. Consider the earliest hominids. Species from at least 4.4 million years ago or more whose hominid status is controversial, such as Ardipithecus ramidus, get a brief mention. Bellwood renders no verdict on whether those finds come from early hominids or ancient apes. He focuses instead on African australopithecines, a set of upright but partly apelike species thought to have included populations that evolved into members of our own genus, Homo, around 2.5 million to 3 million years ago. Bellwood hammers home the point that stone-tool making by the last australopithecines, the first Homo groups or both contributed to the evolution of bigger brains in our ancestors.
The action speeds up when Homo erectus becomes the first known hominid to leave Africa, roughly 2 million years ago. Questions remain, Bellwood writes, about how many such migrations occurred and whether this humanlike species reached distant islands such as Flores in Indonesia, perhaps giving rise to small hominids called hobbits, or Homo floresiensis (SN: 3/30/16). What’s clear is that H. erectus groups journeyed across mainland Asia and at least as far as the Indonesian island of Java.
Intercontinental migrations flourished after Homo sapiens debuted, around 300,000 years ago in Africa. Bellwood regards H. sapiens, Neandertals and Denisovans as distinct species that interbred in certain parts of Asia and Europe. He suggests that Neandertals disappeared around 40,000 years ago as they mated with members of more numerous H. sapiens populations, leaving a genetic legacy in people today. But he does not address an opposing argument that different Homo populations at this time, including Neandertals, were too closely related to have been separate species and that it was intermittent mating among these mobile groups that drove the evolution of present-day humans (SN: 6/5/21).
Bellwood gives considerable attention to the rise of food production and domestication in Europe and Asia after around 9,000 years ago. He builds on an argument, derived from his 2004 book First Farmers, that expanding populations of early cultivators migrated to new lands in such great numbers that they spread major language families with them. For instance, farmers in what’s now Turkey spread Indo-European languages into much of Europe sometime after roughly 8,000 years ago, Bellwood contends.
He rejects a recent alternative proposal, based on ancient DNA evidence, that horse-riding herders of Central Asia’s Yamnaya culture brought their traditions and Indo-European tongues to Europe around 5,000 years ago (SN: 11/15/17). Too few Yamnaya immigrated to impose a new language on European communities, Bellwood says. Similarly, he argues, ancient Eurasian conquerors, from Alexander the Great to Roman emperors, couldn’t get speakers of regional languages to adopt new ones spoken by their outnumbered military masters.
Bellwood rounds out his evolutionary odyssey with a reconstruction of how early agricultural populations expanded through East Asia and beyond, to Australia, a string of Pacific islands and the Americas. Between about 4,000 and 750 years ago, for instance, sea-faring farmers spread Austronesian languages from southern China and Taiwan to Madagascar in the west and Polynesia in the east. Precisely how they accomplished that remarkable feat remains a puzzle.
Disappointingly, Bellwood doesn’t weigh in on a recent archaeological argument that ancient societies were more flexible and complex than long assumed (SN: 11/9/21). On the plus side, his evolutionary odyssey moves along at a brisk pace and, like our ancestors, covers a lot of ground.
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.
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.”
As Tanina Agosto went through her normal morning routine in July 2007, she realized something was wrong. The 29-year-old couldn’t control her left side, even her face. “Literally the top of my head to the bottom of my foot on the left side of my body could not feel anything.”
The next day, Agosto spoke with a doctor at the New York City hospital where she works as a medical secretary. He told her that she probably had a pinched nerve and to see a chiropractor.
But chiropractic care didn’t help. Months later, Agosto needed a cane to get around, and moving her left leg and arm required lots of concentration. She couldn’t work. Numbness and tingling made cooking and cleaning difficult. It felt a bit like looping a rubber band tightly around a finger until it loses sensation, Agosto says. Once the rubber band comes off, the finger tingles for a bit. But for her, the tingling wouldn’t stop.
Finally, she recalls, one chiropractor told her, “I’m not too big of a person to say there’s something very wrong with you, and I don’t know what it is. You need to see a neurologist.” In November 2008, tests confirmed that Agosto had multiple sclerosis. Her immune system was attacking her brain and spinal cord.
Agosto knew nothing about MS except that a friend of her mother’s had it. “At the time, I was like, there’s no way I’ve got this old lady’s condition,” she says. “To be hit with that and know that there’s no cure — that was just devastating.”
Why people develop the autoimmune disorder has been a long-standing question. Studies have pointed to certain gene variations and environmental factors. For decades, a common virus called Epstein-Barr virus has also been high on the list of culprits.
Now recent studies paint a clearer picture that Epstein-Barr virus instigates MS when the central nervous system gets caught in the cross hairs of an immune response to the virus’s attack. This recognition opens new options for treatment, or even vaccines. Perhaps therapies that target Epstein-Barr itself — or remove the cells in the body where the virus camps out — could jettison the virus before damage is done. Vaccines might one day “make multiple sclerosis become a historical disease like polio,” says Lawrence Steinman, a neurologist at Stanford University. “The trials will be arduous,” Steinman says. Still, “I think we might be able to put MS in the rearview mirror.”
For now, there’s a lot to learn, including how exactly the virus triggers MS, says Francesca Aloisi, a neuroscientist at the Italian National Institute of Health in Rome.
For many people with MS, even with current therapies, the disease can progress. Right now, Agosto’s symptoms are largely under control. Thanks to physical therapy, an anti-inflammatory diet and medication, she has about 90 percent function on the left side of her body. “Things like long-distance running are out of the question,” she says. Carrying grocery bags with her left arm is a challenge.
Studying the virus’s role in MS “will be an amazing game changer,” says Agosto, who is a patient advocate with the National Multiple Sclerosis Society’s New York City chapter. If Epstein-Barr virus is driving her disease, she wants to know: “How do we get this virus out of the driver’s seat?”
A familiar virus Multiple sclerosis is an uncommon disease, affecting nearly 3 million people globally. Yet Epstein-Barr virus is almost everywhere.
The virus, discovered in 1964, infects an estimated 90 percent of people around the world. People infected as young children might have a mild cold or show no symptoms. Teenagers or young adults may experience a bout of debilitating fatigue called infectious mononucleosis, or mono, that can last weeks or months.
These symptoms eventually fade. But Epstein-Barr infections hang on. The virus belongs to the herpesvirus family — a group known for instigating lifelong infections. The herpesviruses behind cold sores, genital herpes and chicken pox also stick around for life, usually staying quiet for long stretches. For example, varicella-zoster virus, which causes chicken pox, goes latent inside nerve cells but can resurface to cause the painful disease shingles (SN: 3/2/19, p. 22).
In the body, Epstein-Barr virus slips into the epithelial cells that line the surface of the throat, allowing the virus to spread to other people via saliva — hence mono’s nickname, “the kissing disease.” The virus also infects a type of immune cell called B cells, where it enters viral hibernation.
Epstein-Barr virus can cause problems long after the initial infection. People who had mono are more likely to develop cancers such as Hodgkin’s lymphoma than people who didn’t. And they are more likely to be diagnosed with MS. A teenage case of mono doesn’t mean long-term problems are inevitable. But avoiding mono-related fatigue doesn’t guarantee an escape from risk either. Agosto, for instance, doesn’t recall ever having mono. Establishing the link In March 2000, epidemiologist Alberto Ascherio of the Harvard T.H. Chan School of Public Health published research exploring the link between Epstein-Barr virus and MS. With colleague Mette Munch of the University of Aarhus in Denmark, Ascherio analyzed data from eight studies suggesting that MS patients are more likely to have had an Epstein-Barr infection than those without MS. Studies over the next 20 years continued to hint that the virus plays a role, but “the problem is to go from a suggestion or suspicion to proof,” says Ascherio. Getting that proof is difficult, because nearly everyone has been infected with Epstein-Barr virus, or EBV, yet very few have MS.
“If it’s true that EBV causes MS, then you would expect to find that those individuals who are not infected with EBV, they will not get MS,” Ascherio says. “It’s very simple.” He and colleagues needed to follow a large group of young adults who had never been infected.
The researchers found such a group in the U.S. military. Through the Department of Defense Serum Repository, the team had access to repeated blood samples from more than 10 million individuals, taken when active-duty members were screened for diseases such as HIV at the start of their service and then every two years. Using blood samples taken between 1993 and 2013, Ascherio and colleagues could identify people who had never been infected with Epstein-Barr virus, track new infections and learn when people who developed MS started showing symptoms.
Over that 20-year span, 801 people whose blood was tested were diagnosed with MS. Thirty-five of those people had no signs of Epstein-Barr virus infection in their first blood sample. But all but one became infected before their MS diagnosis. People infected with the virus were 32 times as likely to develop MS as uninfected people. What’s more, the researchers found that blood concentrations of a nervous system protein that is a signal of nerve damage rose after Epstein-Barr virus infection, before an MS diagnosis. The results prompted Ascherio and his team to make a bold claim in Science in January: “These findings cannot be explained by any known risk factor for MS and suggest EBV as the leading cause of MS.”
It is still possible that infection with Epstein-Barr virus is a time stamp for something else, perhaps not yet identified, that’s also relevant for MS, says Mark Allegretta, vice president of research at the National Multiple Sclerosis Society. “The way we talk about it now is that it’s very strong evidence that it’s necessary for development of MS, but it’s insufficient on its own.”
Ascherio isn’t deterred. “After 20 years of talking about EBV and MS, it’s quite exciting that we’ve finally nailed it down,” he says. “There was a lot of skepticism until now and that is fading away.” A skeptic convinced The fact that Epstein-Barr virus is implicated in so many diseases had many researchers skeptical of its link to MS, says Tobias Lanz, a neurologist at Stanford University. “It’s involved in tumors, it’s involved in MS, it’s involved in lupus, it’s in chronic fatigue syndrome. Somehow, people link it to everything and that makes us reasonably suspicious.”
Lanz’s mentor, Stanford rheumatologist William Robinson, was one of those skeptics. Once Lanz, Robinson and their colleagues found hints of how Epstein-Barr virus could spark nerve damage, however, Robinson became a believer.
The team discovered that immune proteins called antibodies from some MS patients attach to a key Epstein-Barr virus protein, as well as to a protein from the central nervous system. This finding, described in the March 10 Nature, suggests that as the immune system learns how to recognize the virus, it may also learn to attack nerve cells.
The viral protein, called EBNA1, helps Epstein-Barr virus persist in the body for life, hidden away inside B cells. Its molecular twin in the central nervous system, a portion of a protein called GlialCAM, is so similar that antibodies for the virus recognize and bind tightly to it too, the team found in lab experiments.
“That really changed everything,” Robinson says, calling it “an in-your-face result that you can’t dismiss as not being real.” In addition to adding to the evidence that Epstein-Barr virus causes MS, the finding also provides a hint of a possible mechanism: GlialCAM is found in glial cells, which support nerve cells and form the insulating layer myelin that helps nerve cells send signals (SN: 8/22/15, p. 18). Myelin is the very thing that is destroyed in MS.
About a quarter of patients in the study had antibodies that recognize both EBNA1 and GlialCAM. The similarities between the two proteins, called molecular mimicry, means that EBNA1 may not be a good viral protein to include in vaccines to curb diseases related to Epstein-Barr virus, says Steinman, the Stanford neurologist, who was also involved with the research. If the virus indeed sparks an autoimmune reaction, vaccines that target this viral protein or other mimics could harm myelin and spur MS. Viral damage Several studies support the idea that molecular mimicry causes MS damage. But other hypotheses are on the table.
Those B cells, for instance, where Epstein-Barr viruses hide out, produce antibodies. One possibility is that B cells infected with Epstein-Barr virus transform in ways that encourage the immune system to attack the body’s own tissues.
Aloisi, the neuroscientist in Rome, backs a different hypothesis: Perhaps the immune system’s attack on the virus itself is behind the damage.
“The biology of the virus is so similar to the biology of the disease,” Aloisi says. For some people, MS can go through phases of silence where the disease is stable, no better, no worse. The disease then reactivates, producing new brain lesions and worsening symptoms. Epstein-Barr virus can similarly come out of latency, perhaps causing a surge of problems before returning to hibernation inside host cells.
In 2007, Aloisi and colleagues discovered unexpected clusters of B cells within the membranes that cover and protect the brain. In all but one of 22 patients studied, some of those B cells were infected with Epstein-Barr virus.
The finding “was like a bomb in the field,” Aloisi says, “because nobody ever thought about this possibility.” Other researchers initially failed to replicate the results. But “little by little other work came out [in support],” she says. “It’s difficult to find these [clusters of B cells] in the brain because people with MS don’t have large, inflamed brains. It’s small spots here and there.”
It’s possible that the central nervous system becomes a stronghold for the virus, Aloisi says. Immune cells called T cells, which can either coordinate an attack or kill infected cells, rush in. Some virus-infected B cells die, but the immune system can’t eliminate the virus. Myelin gets caught in the cross fire. “This creates a situation that is extremely detrimental to the tissue,” she says. Treatment tactics Regardless of whether Epstein-Barr virus drives MS symptoms directly or causes the body’s immune response to go haywire, the big question is what to do about it.
One obvious path is to develop MS drugs that go after the virus, Aloisi says. Some drugs that block hepatitis B virus and HIV have shown potential against Epstein-Barr virus in lab-grown cells, says Ascherio, the Harvard epidemiologist. But those results are very preliminary.
Another option is to go after the infected cells. A few MS therapies may do that already. The existing MS therapy natalizumab already prevents B and T cells from crossing into the central nervous system. Fingolimod may do that as well. Another drug called ocrelizumab, approved for patients with MS in 2017, is an antibody that attaches to a protein on B cells and triggers cell death. The drug helps patients, like Agosto, who have relapsing-remitting MS, but it’s less effective for people with a progressive form of the disease, who have fewer treatment options (SN: 12/9/17, p. 20).
Researchers thought the drug dampened faulty immune responses by depleting B cells, Lanz says. “But it could also well be that we’re hitting those particular pathogenic B cells that are infected with Epstein-Barr virus. So the B cell depletion might actually be an anti-EBV drug and nobody appreciated that.”
Aloisi agrees. “Now we need something that targets the EBV-infected cells, not all of the B cells,” she says. Indiscriminately killing B cells puts patients at risk for other infections. One way to get around that could come in the form of T cell therapies that go after only infected cells. Such therapies are already in clinical trials in MS patients.
Some researchers suspect that antiviral treatments would probably make the most sense when used early on, before the immune system eats away at the myelin around the nerve cells. Once the virus has kick-started an immune response to attack the nervous system, “the train may already be out of the station,” says neuroimmunologist Emily Harrington of Ohio State University’s Wexner Medical Center in Columbus.
A vaccine Even better than stopping the infection once it starts would be to build defenses before the virus invades, or to stop it from reawakening. Enter vaccines.
The widespread impact of mono and Epstein-Barr virus’s links to cancer and autoimmune disease had already spurred vaccine research, so a few potential shots are already in the pipeline. But Epstein-Barr virus has a complex way of invading the body, says vaccinologist Javier Gordon Ogembo of City of Hope, a cancer care center in Duarte, Calif. The virus uses at least five viral proteins to invade both epithelial cells and B cells. A vaccine would need to drive an immune response that blocks the virus’s entry into both cell types to prevent infection. “This is the reason, I think, why there has not been a vaccine so far,” Ogembo says. Pharmaceutical company GlaxoSmithKline took one vaccine candidate to clinical trials in the early 2000s. It seemed to stop people from developing mono, but it didn’t meet the original goal of preventing infection overall. So the company abandoned the vaccine.
Moderna, the biotechnology company made famous for its effective COVID-19 vaccine, recently launched a clinical trial of an mRNA vaccine for Epstein-Barr virus. The shot teaches the body to recognize four of the five viral proteins that help the virus invade both cell types, says viral immunologist Katherine Luzuriaga of the University of Massachusetts Chan Medical School in Worcester, who is involved in the trial. For now, the team is testing whether the vaccine sparks a strong immune response and getting a sense for whether it might curb cases of mono.
In March, the U.S National Institutes of Health launched a clinical trial to test a vaccine that uses nanoparticles to teach the body to recognize the virus and get rid of it. Ogembo and colleagues at City of Hope are developing another vaccine that uses a modified virus as the immune system’s instructor.
Although clinical trials could reveal within the next few years whether the vaccines can control mono, it will be decades before researchers learn anything about the potential impact on cancer or MS, Luzuriaga and Ogembo say. The hope is to see an outcome like the vaccines for human papillomaviruses, Luzuriaga says, which reduce the number of HPV infections and led to a dramatic reduction in cervical cancers.
Developing therapeutic vaccines for people who already have MS may also be possible, Ascherio says. The aim would be to stop the virus from emerging from its slumber inside B cells. It would be akin to the shingles vaccine, which prevents the painful reactivation of varicella-zoster virus in nerve cells.
That is Steinman’s aim as well, but he envisions a shot that would put a check on the undesirable immune response. Steinman and colleagues have tested such a vaccine to try and teach MS patients’ immune systems to ignore and not harm a protein called myelin basic protein, which helps add myelin to nerves. There were hints the vaccine might have been effective, but the team ultimately stopped the project.
“If it weren’t for other very powerful therapies becoming approved in that same time frame, we may have continued,” Steinman says. Now, he wants to make a vaccine that helps MS patients tolerate, rather than attack, the central nervous system protein GlialCAM.
Researchers at BioNTech, also famous for developing a COVID-19 vaccine, are working on something similar. In mice with a disease close to MS, the company showed that an mRNA vaccine could keep the immune system from attacking myelin proteins, the team reported in January 2021 in Science.
Time will tell how effective any of these shots might be. But with studies providing more and more evidence that Epstein-Barr virus is linked to many diseases, Ogembo says, “it’s time to make a vaccine and get rid of it.”
The Arctic is heating up at a breakneck speed compared with the rest of Earth. And new analyses show that the region is warming even faster than scientists thought. Over the last four decades, the average Arctic temperature increased nearly four times as fast as the global average, researchers report August 11 in Communications Earth & Environment.
And that’s just on average. Some parts of the Arctic Ocean, such as the Barents Sea between Russia and Norway’s Svalbard archipelago, are warming as much as seven times as fast, meteorologist Mika Rantanen of the Finnish Meteorological Institute in Helsinki and colleagues found. Previous studies have tended to say that the Arctic’s average temperature is increasing two to three times as fast as elsewhere, as humans continue causing the climate to change. To calculate the true pace of the accelerated warming, a phenomenon called Arctic amplification, the researchers analyzed observational data from 1979 to 2021 (SN: 7/1/20). Globally, the average temperature increase over that time was about 0.2 degrees Celsius per decade. But the Arctic was warming by about 0.75 degrees C per decade. Even the best climate models are not doing a great job of reproducing that warming, Rantanen and colleagues say. The inability of the models to realistically simulate past Arctic amplification calls into question how well the models can project future changes there.
It’s not clear where the problem lies. One issue may be that the models are struggling with correctly simulating the sensitivity of Arctic temperatures to the loss of sea ice. Vanishing snow and ice, particularly sea ice, are one big reason why Arctic warming is on hyperspeed. The bright white snow and ice create a reflective shield that bounces incoming radiation from the sun back into space. But open ocean waters or bare rocks absorb that heat, raising the temperature.
