The oldest known fossils of pollen-laden insects are of earwig-like ground-dwellers that lived in what is now Russia about 280 million years ago, researchers report. Their finding pushes back the fossil record of insects transporting pollen from one plant to another, a key aspect of modern-day pollination, by about 120 million years.

The insects — from a pollen-eating genus named Tillyardembia first described in 1937 — were typically about 1.5 centimeters long, says Alexander Khramov, a paleoentomologist at the Borissiak Paleontological Institute in Moscow. Flimsy wings probably kept the creatures mostly on the forest floor, he says, leaving them to climb trees to find and consume their pollen.

Recently, Khramov and his colleagues scrutinized 425 fossils of Tillyardembia in the institute’s collection. Six had clumps of pollen grains trapped on their heads, legs, thoraxes or abdomens, the team reports February 28 in Biology Letters. A proportion that small isn’t surprising, Khramov says, because the fossils were preserved in what started out as fine-grained sediments. The early stages of fossilization in such material would tend to wash away pollen from the insects’ remains.
The pollen-laden insects had only a couple of types of pollen trapped on them, the team found, suggesting that the critters were very selective in the tree species they visited. “That sort of specialization is in line with potential pollinators,” says Michael Engel, a paleoentomologist at the University of Kansas in Lawrence who was not involved in the study. “There’s probably vast amounts of such specialization that occurred even before Tillyardembia, we just don’t have evidence of it yet.”

Further study of these fossils might reveal if Tillyardembia had evolved special pollen-trapping hairs or other such structures on their bodies or heads, says Conrad Labandeira, a paleoecologist at the National Museum of Natural History in Washington, D.C., also not part of the study. It would also be interesting, he says, to see if something about the pollen helped it stick to the insects. If the pollen grains had structures that enabled them to clump more readily, for example, then those same features may have helped them grab Velcro-like onto any hairlike structures on the insects’ bodies.

Fungi may help some tree-killer beetles turn a tree’s natural defense system against itself.

The Eurasian spruce bark beetle (Ips typographus) has massacred millions of conifers in forests across Europe. Now, research suggests that fungi associated with these bark beetles are key players in the insect’s hostile takeovers. These fungi warp the chemical defenses of host trees to create an aroma that attracts beetles to burrow, researchers report February 21 in PLOS Biology.

This fungi-made perfume might explain why bark beetles tend to swarm the same tree. As climate change makes Europe’s forests more vulnerable to insect invasions, understanding this relationship could help scientists develop new countermeasures to ward off beetle attacks.
Bark beetles are a type of insect found around the world that feed and breed inside trees (SN: 12/17/10). In recent years, several bark beetle species have aggressively attacked forests from North America to Australia, leaving ominous strands of dead trees in their wake.

But trees aren’t defenseless. Conifers — which include pine and fir trees — are veritable chemical weapons factories. The evergreen smell of Christmas trees and alpine forests comes from airborne varieties of these chemicals. But while they may smell delightful, these chemicals’ main purpose is to trap and poison invaders.

Or at least, that’s what they’re meant to do.

“Conifers are full of resin and other stuff that should do horrible things to insects,” says Jonathan Gershenzon, a chemical ecologist at the Max Planck Institute for Chemical Ecology in Jena, Germany. “But bark beetles don’t seem to mind at all.”

This ability of bark beetles to overcome the powerful defense system of conifers has led some scientists to wonder if fungi might be helping. Fungi break down compounds in their environment for food and protection (SN: 11/30/21). And some type of fungi — including some species in the genus Grosmannia — are always found in association with Eurasian spruce bark beetles.
Gershenzon and his colleagues compared the chemicals released by spruce bark infested with Grosmannia and other fungi to the chemical profile of uninfected trees. The presence of the fungi fundamentally changed the chemical profile of spruce trees, the team found. More than half the airborne chemicals — made by fungi breaking down monoterpenes and other chemicals that are likely part of the tree defense system — were unique to infected trees after 12 days.

This is surprising because researchers had previously assumed that invading fungi hardly changed the chemical profile of trees, says Jonathan Cale, a fungal ecologist at the University of Northern British Columbia in Prince George, Canada, who was not involved with the research.
Later experiments revealed that bark beetles can detect many of these fungi-made chemicals. The team tested this by attaching tiny electrodes on bark beetles’ heads and detecting electrical activity when the chemicals wafted passed their antennae. What’s more, the smell of these chemicals combined with beetle pheromones led the insects to burrow at higher rates than the smell of pheromones alone.

The study suggests that these fungi-made chemicals can help beetles tell where to feed and breed, possibly by advertising that the fungi has taken down some of the tree’s defenses. The attractive nature of the chemicals could also explain the beetle’s swarming behavior, which drives the death of healthy adult trees.

But while the fungi aroma might doom trees, it could also lead to the beetles’ demise. Beetle traps in Europe currently use only beetle pheromones to attract their victims. Combining pheromones with fungi-derived chemicals might be the secret to entice more beetles into traps, making them more effective.

The results present “an exciting direction for developing new tools to manage destructive bark beetle outbreaks” for other beetle species as well, Cale says. In North America, mild winters and drought have put conifer forests at greater risk from mountain pine beetle (Dendroctonus pendersoae) attacks. Finding and using fungi-derived chemicals might be one way to fend off the worst of the bark beetle invasions in years to come.

In August 2021 on a lonely crater floor, the newest Mars rover dug into one of its first rocks.

The percussive drill attached to the arm of the Perseverance rover scraped the dust and top several millimeters off a rocky outcrop in a 5-centimeter-wide circle. From just above, one of the rover’s cameras captured what looked like broken shards wedged against one another. The presence of interlocking crystal textures became obvious. Those textures were not what most of the scientists who had spent years preparing for the mission expected.
Then the scientists watched on a video conference as the rover’s two spectrometers revealed the chemistry of those meshed textures. The visible shapes along with the chemical compositions showed that this rock, dubbed Rochette, was volcanic in origin. It was not made up of the layers of clay and silt that would be found at a former lake bed.

Nicknamed Percy, the rover arrived at the Jezero crater two years ago, on February 18, 2021, with its sidekick helicopter, Ingenuity. The most complex spacecraft to explore the Martian surface, Percy builds on the work of the Curiosity rover, which has been on Mars since 2012, the twin Spirit and Opportunity rovers, the Sojourner rover and other landers.

But Perseverance’s main purpose is different. While the earlier rovers focused on Martian geology and understanding the planet’s environment, Percy is looking for signs of past life. Jezero was picked for the Mars 2020 mission because it appears from orbit to be a former lake environment where microbes could have thrived, and its large delta would likely preserve any signs of them. Drilling, scraping and collecting pieces of the Red Planet, the rover is using its seven science instruments to analyze the bits for any hint of ancient life. It’s also collecting samples to return to Earth.
Since landing, “we’ve been able to start putting together the story of what has happened in Jezero, and it’s pretty complex,” says Briony Horgan, a planetary scientist at Purdue University in West Lafayette, Ind., who helps plan Percy’s day-to-day and long-term operations.

Volcanic rock is just one of the surprises the rover has uncovered. Hundreds of researchers scouring the data Perseverance has sent back so far now have some clues to how the crater has evolved over time. This basin has witnessed flowing lava, at least one lake that lasted perhaps tens of thousands of years, running rivers that created a mud-and-sand delta and heavy flooding that brought rocks from faraway locales.

Jezero has a more dynamic past than scientists had anticipated. That volatility has slowed the search for sedimentary rocks, but it has also pointed to new alcoves where ancient life could have taken hold.

Perseverance has turned up carbon-bearing materials — the basis of life on Earth — in every sample it has abraded, Horgan says. “We’re seeing that everywhere.” And the rover still has much more to explore.
Perseverance finds unexpected rocks
Jezero is a shallow impact crater about 45 kilo­meters in diameter just north of the planet’s equator. The crater formed sometime between 3.7 billion and 4.1 billion years ago, in the solar system’s first billion years. It sits in an older and much larger impact basin known as Isidis. At Jezero’s western curve, an etched ancient riverbed gives way to a dried-out, fan-shaped delta on the crater floor.

That delta “is like this flashing signpost beautifully visible from orbit that tells us there was a standing body of water here,” says astrobiologist Ken Williford of Blue Marble Space Institute of Science in Seattle.

Perseverance landed on the crater floor about two kilometers from the front of the delta. Scientists thought they’d find compacted layers of soil and sand there, at the base of what they dubbed Lake Jezero. But the landscape immediately looked different than expected, says planetary geologist Kathryn Stack Morgan of NASA’s Jet Propulsion Laboratory in Pasadena, Calif. Stack Morgan is deputy project scientist for Perseverance.
For the first several months after the landing, the Mars 2020 mission team tested the rover’s movements and instruments, slowly, carefully. But from the first real science drilling near the landing location, researchers back on Earth realized what they had found. The texture of the rock, Stack Morgan says, was “a textbook igneous volcanic rock texture.” It looked like volcanic lava flows.

Over the next six months, several more rocks on the crater floor revealed igneous texture. Some of the most exciting rocks, including Rochette, showed olivine crystals throughout. “The crystal fabric was obviously cooled from a melt, not transported grains,” as would be the case if it were a sedimentary sample, says Abigail Allwood of the Jet Propulsion Lab. She leads the rover’s PIXL instrument, which uses an X-ray beam to identify each sample’s composition.

Mission scientists now think the crater floor is filled with igneous rocks from two separate events — both after the crater was created, so more recently than the 3.7 billion to 4.1 billion years ago time frame. In one, magma from deep within the planet pushed toward the surface, cooled and solidified, and was later exposed by erosion. In the other, smaller lava flows streamed at the surface.
Sometime after these events, water flowed from the nearby highlands into the crater to form a lake tens of meters deep and lasting tens of thousands of years at least, according to some team members. Percy’s instruments have revealed the ways that water altered the igneous rocks: For example, scientists have found sulfates and other minerals that require water to form, and they’ve seen empty pits within the rocks’ cracks, where water would have washed away material. As that water flowed down the rivers into the lake, it deposited silt and mud, forming the delta. Flooding delivered 1.5-meter-wide boulders from that distant terrain. All of these events preceded the drying of the lake, which might have happened about 3 billion years ago.

Core samples, which Perseverance is collecting and storing on board for eventual return to Earth, could provide dates for when the igneous rocks formed, as well as when the Martian surface became parched. During the time between, Lake Jezero and other wet environments may have been stable enough for microbial life to start and survive.

“Nailing down the geologic time scale is of critical importance for us understanding Mars as a habitable world,” Stack Morgan says. “And we can’t do that without samples to date.”

About a year after landing on Mars, Perseverance rolled several kilometers across the crater floor to the delta front — where it encountered a very different geology.

The delta might hold signs of ancient life
Deltas mark standing, lasting bodies of water — stable locales that could support life. Plus, as a delta grows over time, it traps and preserves organic matter.

Sand and silt deposited where a river hits a lake get layered into sedimentary material, building up a fan-shaped delta. “If you have any biological material that is trapped between that sediment, it gets buried very quickly,” says Mars geologist Eva Scheller of MIT, a researcher with the Percy team. “It creates this environment that is very, very good for preserving the organic matter.”

While exploring the delta front between April 2022 and December 2022, Perseverance found some of the sedimentary rocks it was after.
Several of the rover’s instruments zoomed in on the textures and shapes of the rocks, while other instruments collected detailed spectral information, revealing the elements present in those rocks. By combining the data, researchers can piece together what the rocks are made of and what processes might have changed them over the eons. It’s this chemistry that could reveal signs of ancient Martian life — biosignatures. Scientists are still in the early stages of these analyses.

There won’t be one clear-cut sign of life, Allwood says. Instead, the rover would more likely reveal “an assemblage of characteristics,” with evidence slowly building that life once existed there.

Chemical characteristics suggestive of life are most likely to hide in sedimentary rocks, like those Perseverance has studied at the delta front. Especially interesting are rocks with extremely fine-grained mud. Such mud sediments, Horgan says, are where — in deltas on Earth, at least — organic matter is concentrated. So far, though, the rover hasn’t found those muddy materials.

But the sedimentary rocks studied have revealed carbonates, sulfates and unexpected salts — all materials indicating interaction with water and important for life as we know it. Percy has found carbon-based matter in every rock it has abraded, Horgan says.

“We’ve had some really interesting results that we’re pretty excited to share with the community,” Horgan says about the exploration of the delta front. Some of those details may be revealed in March at the Lunar and Planetary Science Conference.

Perseverance leaves samples for a future mission
As of early February, Perseverance has collected 18 samples, including bits of Mars debris and cores from rocks, and stored them on board in sealed capsules for eventual return to Earth. The samples come from the crater floor, delta front rocks and even the thin Martian atmosphere.

In the final weeks of 2022 and the first weeks of 2023, the rover dropped — or rather, carefully set down — half of the collected samples, as well as a tube that would reveal whether samples contained any earthly contaminants. These captured pieces of Mars are now sitting at the front of the delta, at a predetermined spot called the Three Forks region.
If Perseverance isn’t functioning well enough to hand over its onboard samples when a future sample-return spacecraft arrives, that mission will collect these samples from the drop site to bring back to Earth.

Researchers are currently working on designs for a joint Mars mission between NASA and the European Space Agency that could retrieve the samples. Launching in the late 2020s, it would land near the Perseverance rover. Percy would transfer the samples to a small rocket to be launched from Mars and returned to Earth in the 2030s. Lab tests could then confirm what Perseverance is already uncovering and discover much more.

Meanwhile, Percy is climbing up the delta to explore its top, where muddy sedimentary rocks may still be found. The next target is the edge of the once-lake, where shallow water long ago stood. This is the site Williford is most excited about. Much of what we know about the history of how life has evolved on Earth comes from environments with shallow water, he says. “That’s where really rich, underwater ecosystems start to form,” he says. “There’s so much going on there chemically.”

Scientists have finally figured out how those arches, loops and whorls formed on your fingertips.

While in the womb, fingerprint-defining ridges expand outward in waves starting from three different points on each fingertip. The raised skin arises in a striped pattern thanks to interactions between three molecules that follow what’s known as a Turing pattern, researchers report February 9 in Cell. How those ridges spread from their starting sites — and merge — determines the overarching fingerprint shape.
Fingerprints are unique and last for a lifetime. They’ve been used to identify individuals since the 1800s. Several theories have been put forth to explain how fingerprints form, including spontaneous skin folding, molecular signaling and the idea that ridge pattern may follow blood vessel arrangements.

Scientists knew that the ridges that characterize fingerprints begin to form as downward growths into the skin, like trenches. Over the few weeks that follow, the quickly multiplying cells in the trenches start growing upward, resulting in thickened bands of skin.

Since budding fingerprint ridges and developing hair follicles have similar downward structures, researchers in the new study compared cells from the two locations. The team found that both sites share some types of signaling molecules — messengers that transfer information between cells — including three known as WNT, EDAR and BMP. Further experiments revealed that WNT tells cells to multiply, forming ridges in the skin, and to produce EDAR, which in turn further boosts WNT activity. BMP thwarts these actions.

To examine how these signaling molecules might interact to form patterns, the team adjusted the molecules’ levels in mice. Mice don’t have fingerprints, but their toes have striped ridges in the skin comparable to human prints. “We turn a dial — or molecule — up and down, and we see the way the pattern changes,” says developmental biologist Denis Headon of the University of Edinburgh.

Increasing EDAR resulted in thicker, more spaced-out ridges, while decreasing it led to spots rather than stripes. The opposite occurred with BMP, since it hinders EDAR production.

That switch between stripes and spots is a signature change seen in systems governed by Turing reaction-diffusion, Headon says. This mathematical theory, proposed in the 1950s by British mathematician Alan Turing, describes how chemicals interact and spread to create patterns seen in nature (SN: 7/2/10). Though, when tested, it explains only some patterns (SN: 1/21/14).

Mouse digits, however, are too tiny to give rise to the elaborate shapes seen in human fingerprints. So, the researchers used computer models to simulate a Turing pattern spreading from the three previously known ridge initiation sites on the fingertip: the center of the finger pad, under the nail and at the joint’s crease nearest the fingertip.
By altering the relative timing, location and angle of these starting points, the team could create each of the three most common fingerprint patterns — arches, loops and whorls — and even rarer ones. Arches, for instance, can form when finger pad ridges get a slow start, allowing ridges originating from the crease and under the nail to occupy more space.

“It’s a very well-done study,” says developmental and stem cell biologist Sarah Millar, director of the Black Family Stem Cell Institute at the Icahn School of Medicine at Mount Sinai in New York City.

Controlled competition between molecules also determines hair follicle distribution, says Millar, who was not involved in the work. The new study, she says, “shows that the formation of fingerprints follows along some basic themes that have already been worked out for other types of patterns that we see in the skin.”

Millar notes that people with gene mutations that affect WNT and EDAR have skin abnormalities. “The idea that those molecules might be involved in fingerprint formation was floating around,” she says.

Overall, Headon says, the team aims to aid formation of skin structures, like sweat glands, when they’re not developing properly in the womb, and maybe even after birth.

“What we want to do, in broader terms, is understand how the skin matures.”

A mysterious new disease may be to blame for severe, unexplained inflammation in older men. Now, researchers have their first good look at who the disease strikes, and how often.

VEXAS syndrome, an illness discovered just two years ago, affects nearly 1 in 4,000 men over 50 years old, scientists estimate January 24 in JAMA. The disease also occurs in older women, though less frequently. Altogether, more than 15,000 people in the United States may be suffering from the syndrome, says study coauthor David Beck, a clinical geneticist at NYU Langone Health in New York City. Those numbers indicate that physicians should be on the lookout for VEXAS, Beck says. “It’s underrecognized and underdiagnosed. A lot of physicians aren’t yet aware of it.”
Beck’s team reported discovering VEXAS syndrome in 2020, linking mutations in a gene called UBA1 to a suite of symptoms including fever, low blood cell count and inflammation. His team’s new study is the first to estimate how often VEXAS occurs in the general population — and the results are surprising. “It’s more prevalent than we suspected,” says Emma Groarke, a hematologist at the National Institutes of Health in Bethesda, Md., who was not involved with the study.
VEXAS tends to show up later in life ­­— after people somehow acquire UBA1 mutations in their blood cells. Patients may feel overwhelming fatigue, lethargy and have skin rashes, Beck says. “The disease is progressive, and it’s severe.” VEXAS can also be deadly. Once a person’s symptoms begin, the median survival time is about 10 years, his team has found.

Until late 2020, no one knew that there was a genetic thread connecting VEXAS syndrome’s otherwise unexplained symptoms. In fact, individuals may be diagnosed with other conditions, including polyarteritis nodosa, an inflammatory blood disease, and relapsing polychondritis, a connective tissue disorder, before being diagnosed with VEXAS.

To ballpark the number of VEXAS-affected individuals, Beck’s team combed through electronic health records of more than 160,000 people in Pennsylvania, in a collaboration with the NIH and Geisinger Health. In people over 50, the disease-causing UBA1 mutations showed up in roughly 1 in 4,000 men. Among women in that age bracket, about 1 in 26,000 had the mutations.

A genetic test of the blood can help doctors diagnose VEXAS, and treatments like steroids and other immunosuppressive drugs, which tamp down inflammation, can ease symptoms. Groarke and her NIH colleagues have also started a small phase II clinical trial testing bone marrow transplants as a way to swap patients’ diseased blood cells for healthy ones.

Beck says he hopes to raise awareness about the disease, though he recognizes that there’s much more work to do. In his team’s study, for instance, the vast majority of participants were white Pennsylvanians, so scientists don’t know how the disease affects other populations. Researchers also don’t know what spurs the blood cell mutations, nor how they spark an inflammatory frenzy in the body.

“The more patients that are diagnosed, the more we’ll learn about the disease,” Beck says. “This is just one step in the process of finding more effective therapies.”

A type of bacteria that’s overabundant in the nasal passages of people with hay fever may worsen symptoms. Targeting that bacteria may provide a way to rein in ever-running noses.

Hay fever occurs when allergens, such as pollen or mold, trigger an inflammatory reaction in the nasal passages, leading to itchiness, sneezing and overflowing mucus. Researchers analyzed the composition of the microbial population in the noses of 55 people who have hay fever and those of 105 people who don’t. There was less diversity in the nasal microbiome of people who have hay fever and a whole lot more of a bacterial species called Streptococcus salivarius, the team reports online January 12 in Nature Microbiology.
S. salivarius was 17 times more abundant in the noses of allergy sufferers than the noses of those without allergies, says Michael Otto, a molecular microbiologist at the National Institute of Allergy and Infectious Diseases in Bethesda, Md. That imbalance appears to play a part in further provoking allergy symptoms. In laboratory experiments with allergen-exposed cells that line the airways, S. salivarius boosted the cells’ production of proteins that promote inflammation.

And it turns out that S. salivarius really likes runny noses. One prominent, unpleasant symptom of hay fever is the overproduction of nasal discharge. The researchers found that S. salivarius binds very well to airway-lining cells exposed to an allergen and slathered in mucus — better than a comparison bacteria that also resides in the nose.

The close contact appears to be what makes the difference. It means that substances on S. salivarius’ surface that can drive inflammation — common among many bacteria — are close enough to exert their effect on cells, Otto says.

Hay fever, which disrupts daily activities and disturbs sleep, is estimated to affect as many as 30 percent of adults in the United States. The new research opens the door “to future studies targeting this bacteria” as a potential treatment for hay fever, says Mahboobeh Mahdavinia, a physician scientist who studies immunology and allergies at Rush University Medical Center in Chicago.

But any treatment would need to avoid harming the “good” bacteria that live in the nose, says Mahdavinia, who was not involved in the research.

The proteins on S. salivarius’ surface that are important to its ability to attach to mucus-covered cells might provide a target, says Otto. The bacteria bind to proteins called mucins found in the slimy, runny mucus. By learning more about S. salivarius’ surface proteins, Otto says, it may be possible to come up with “specific methods to block that adhesion.”

SEATTLE — Luke Skywalker’s home planet in Star Wars is the stuff of science fiction. But Tatooine-like planets in orbit around pairs of stars might be our best bet in the search for habitable planets beyond our solar system.

Many stars in the universe come in pairs. And lots of those should have planets orbiting them (SN: 10/25/21). That means there could be many more planets orbiting around binaries than around solitary stars like ours. But until now, no one had a clear idea about whether those planets’ environments could be conducive to life. New computer simulations suggest that, in many cases, life could imitate art.
Earthlike planets orbiting some configurations of binary stars can stay in stable orbits for at least a billion years, researchers reported January 11 at the American Astronomical Society meeting. That sort of stability, the researchers propose, would be enough to potentially allow life to develop, provided the planets aren’t too hot or cold.

Of the planets that stuck around, about 15 percent stayed in their habitable zone — a temperate region around their stars where water could stay liquid — most or even all of the time.

The researchers ran simulations of 4,000 configurations of binary stars, each with an Earthlike planet in orbit around them. The team varied things like the relative masses of the stars, the sizes and shapes of the stars’ orbits around each other, and the size of the planet’s orbit around the binary pair.

The scientists then tracked the motion of the planets for up to a billion years of simulated time to see if the planets would stay in orbit over the sorts of timescales that might allow life to emerge.

A planet orbiting binary stars can get kicked out of the star system due to complicated interactions between the planet and stars. In the new study, the researchers found that, for planets with large orbits around star pairs, only about 1 out of 8 were kicked out of the system. The rest were stable enough to continue to orbit for the full billion years. About 1 in 10 settled in their habitable zones and stayed there.

Of the 4,000 planets that the team simulated, roughly 500 maintained stable orbits that kept them in their habitable zones at least 80 percent of the time.

“The habitable zone . . . as I’ve characterized it so far, spans from freezing to boiling,” said Michael Pedowitz, an undergraduate student at the College of New Jersey in Ewing who presented the research. Their definition is overly strict, he said, because they chose to model Earthlike planets without atmospheres or oceans. That’s simpler to simulate, but it also allows temperatures to fluctuate wildly on a planet as it orbits.
“An atmosphere and oceans would smooth over temperature variations fairly well,” says study coauthor Mariah MacDonald, an astrobiologist also at the College of New Jersey. An abundance of air and water would potentially allow a planet to maintain habitable conditions, even if it spent more of its time outside of the nominal habitable zone around a binary star system.

The number of potentially habitable planets “will increase once we add atmospheres,” MacDonald says, “but I can’t yet say by how much.”

She and Pedowitz hope to build more sophisticated models in the coming months, as well as extend their simulations beyond a billion years and include changes in the stars that can affect conditions in a solar system as it ages.

The possibility of stable and habitable planets in binary star systems is a timely issue says Penn State astrophysicist Jason Wright, who was not involved in the study.

“At the time Star Wars came out,” he says, “we didn’t know of any planets outside the solar system, and wouldn’t for 15 years. Now we know that there are many and that they orbit these binary stars.”

These simulations of planets orbiting binaries could serve as a guide for future experiments, Wright says. “This is an under-explored population of planets. There’s no reason we can’t go after them, and studies like this are presumably showing us that it’s worthwhile to try.”

When some bacteria manage to escape being killed by a virus, the microbes end up hamstringing themselves. And that could be useful in the fight to treat infections.

The bacterium Shigella flexneri — one cause of the infectious disease shigellosis — can spread within cells that line the gut by propelling itself through the cells’ barriers. That causes tissue damage that can lead to symptoms like bloody diarrhea. But when S. flexneri in lab dishes evolved to elude a type of bacteria-killing virus, the bacteria couldn’t spread cell to cell anymore, making it less virulent, researchers report November 17 in Applied and Environmental Microbiology.

The research is a hopeful sign for what’s known as phage therapy (SN: 11/20/02). With antibiotic-resistant microbes on the rise, some researchers see viruses that infect and kill only bacteria, known as bacteriophages or just phages, as a potential option to treat antibiotic-resistant infections (SN: 11/13/19). With phage therapy, infected people are given doses of a particular phage, which kill off the problematic bacteria. The problem, though, is that over time those bacteria can evolve to be resistant against the phage, too.

“We’re kind of expecting phage therapy to fail, in a sense,” says Paul Turner, an evolutionary biologist and virologist at Yale University. “Bacteria are very good at evolving resistance to phages.”
But that doesn’t mean the bacteria emerge unscathed. Some phages attack and enter bacteria by latching onto bacterial proteins crucial for a microbe’s function. If phage therapy treatments relied on such a virus, that could push the bacteria to evolve in such a way that not only helps them escape the virus but also impairs their abilities and makes them less deadly. People infected with these altered bacteria might have less severe symptoms or may not show symptoms at all.

Previous studies with the bacteria Pseudomonas aeruginosa, for instance, have found that phage and bacteria can engage in evolutionary battles that drive the bacteria to be more sensitive to antibiotics. The new study hints that researchers could leverage the arms race between S. flexneri and the newly identified phage, which was dubbed A1-1 after being found in Mexican wastewater, to treat shigellosis.

S. flexneri in contaminated water is a huge problem in parts of the world where clean water isn’t always available, such as sub-Saharan Africa and southern Asia, says Kaitlyn Kortright, a microbiologist also at Yale University. Every year, approximately 1.3 million people die from shigellosis, which is caused by four Shigella species. More than half of those deaths are in children younger than 5 years old. What’s more, antibiotics to treat shigellosis can be expensive and hard to access in those places. And S. flexneri is becoming resistant to many antibiotics. Phage therapy could be a cheaper, more accessible option to treat the infection.

The blow to S. flexneri’s cellular spread comes because to enter cells, A1-1 targets a protein called OmpA, which is crucial for the bacteria to rupture host cell membranes. The researchers found two types of mutations that made S. flexneri resistant to A1-1. Some bacteria had mutations in the gene that produces OmpA, damaging the protein’s ability to help the microbes spread from cell to cell. Others had changes to a structural component of bacterial cells called lipopolysaccharide.

The mutations in lipopolysaccharide were surprising, Kortright says, because the relationship between that structural component and OmpA isn’t fully worked out. One possibility is that those mutations distort OmpA’s structure in a way that the phage no longer recognizes it and can’t enter bacterial cells.

One lingering question is whether S. flexneri evolves in the same way outside a lab dish, says Saima Aslam, an infectious diseases physician at the University of California, San Diego who was not involved in the work. Still, the findings show that it’s “not always a bad thing” when bacteria become phage-resistant, she says.

The twilight time between fully awake and sound asleep may be packed with creative potential.

People who recently drifted off into a light sleep later had problem-solving power, scientists report December 8 in Science Advances. The results help demystify the fleeting early moments of sleep and may even point out ways to boost creativity.

Prolific inventor and catnapper Thomas Edison was rumored to chase those twilight moments. He was said to fall asleep in a chair holding two steel ball bearings over metal pans. As he drifted off, the balls would fall. The ensuing clatter would wake him, and he could rescue his inventive ideas before they were lost to the depths of sleep.

Delphine Oudiette, a cognitive neuroscientist at the Paris Brain Institute, and colleagues took inspiration from Edison’s method of cultivating creativity. She and her colleagues brought 103 healthy people to their lab to solve a tricky number problem. The volunteers were asked to convert a string of numbers into a shorter sequence, following two simple rules. What the volunteers weren’t told was that there was an easy trick: The second number in the sequence would always be the correct final number, too. Once discovered, this cheat code dramatically cut the solving time.
After doing 60 of these trials on a computer, the volunteers earned a 20-minute break in a quiet, dark room. Reclined and holding an equivalent of Edison’s “alarm clock” (a light drinking bottle in one dangling hand), participants were asked to close their eyes and rest or sleep if they desired. All the while, electrodes monitored their brain waves.

About half of the participants stayed awake. Twenty-four fell asleep and stayed in the shallow, fleeting stage of sleep called N1. Fourteen people progressed to a deeper stage of sleep called N2.

After their rest, participants returned to their number problem. The researchers saw a stark difference between the groups: People who had fallen into a shallow, early sleep were 2.7 times as likely to spot the hidden trick as people who didn’t fall asleep, and 5.8 times as likely to spot it as people who had reached the deeper N2 stage.

Such drastic differences in these types of experiments are rare, Oudiette says. “We were quite astonished by the extent of the results.” The researchers also identified a “creative cocktail of brain waves,” as Oudiette puts it, that seemed to accompany this twilight stage — a mixture of alpha brain waves that usually mark relaxation mingled with the delta waves of deeper sleep.

The study doesn’t show that the time spent in N1 actually triggered the later realization, cautions John Kounios, a cognitive neuroscientist at Drexel University in Philadelphia who cowrote the 2015 book The Eureka Factor: Aha Moments, Creative Insight, and the Brain. “It could have been possible that grappling with the problem and initiating an incubation process caused both N1 and the subsequent insight,” he says, making N1 a “by-product of the processes that caused insight rather than the cause.”

More work is needed to untangle the connection between N1 and creativity, Oudiette says. But the results raise a tantalizing possibility, one that harkens to Edison’s self-optimizations: People might be able to learn to reach that twilight stage of sleep, or to produce the cocktail of brain waves associated with creativity on demand.

It seems Edison was onto something about the creative powers of nodding off. But don’t put too much stock in his habits. He is also said to have considered sleep “a criminal waste of time.”

2021 was the year the COVID-19 vaccines had to prove their mettle. We started the year full of hope: With vaccines in hand in record-breaking time and their rollout ramping up, we’d get shots in arms, curb this pandemic and get life back to normal. That was too optimistic.

Roughly 200 million people in the United States — and billions globally — have now been fully vaccinated. Three vaccines — one from Pfizer and its partner BioNTech, and the other two from Moderna and Johnson & Johnson — are available in the United States. Pfizer’s is even available for children as young as 5. About two dozen other vaccines have also been deployed in other parts of the world. In some higher-income countries, the United States included, people have already queued up for booster shots.

But 2021 has also been the year of learning the limits of the vaccines’ superpowers. With the vaccines pitted against aggressive coronavirus variants, inequitable distribution, some people’s hesitancy and the natural course of waning effectiveness, there’s still a lot of work to do to bring this pandemic to an end. As if to hammer home that point, the detection of the omicron variant in late November brought new uncertainty to the pandemic’s trajectory. Here are some of the top lessons we’ve learned in the first year of the COVID-19 vaccine. — Macon Morehouse
The shots work, even against emerging variants
Many COVID-19 vaccines proved effective over the last year, particularly at preventing severe disease and death (SN: 10/9/21 & 10/23/21, p. 4). That’s true even with the emergence of more transmissible coronavirus variants.

In January, in the midst of a bleak winter surge that saw average daily cases in the United States peaking at nearly 250,000, the vaccination rollout here began in earnest. Soon after, case numbers began a steep decline.

Over the summer, though, more reports of coronavirus infections in vaccinated people began to pop up. Protection against infection becomes less robust in the months following vaccination in people who received Pfizer’s or Moderna’s mRNA vaccines, multiple studies have shown (SN Online: 9/21/21). Yet the shots’ original target — preventing hospitalization — has held steady, with an efficacy of about 80 percent to 95 percent.
A single dose of Johnson & Johnson’s vaccine is less effective at preventing symptoms or keeping people out of the hospital than the mRNA jabs. The company claims there’s not yet evidence that the protection wanes. But even if that protection is not waning, some real-world data hint that the shot may not be as effective as clinical trials suggested (SN Online: 10/19/21).

Evidence of waning or lower protection ultimately pushed the United States and some other countries to green-light COVID-19 booster shots for adults (SN: 12/4/21, p. 6).

Much of the worry over waning immunity came amid the spread of highly contagious variants, including alpha, first identified in the United Kingdom in September 2020, and delta, first detected in India in October 2020 (SN Online: 7/30/21). Today, delta is the predominant variant globally.

The good news is that vaccinated people aren’t unarmed against these mutated foes. The immune system launches a multipronged attack against invaders, so the response can handle small molecular tweaks to viruses, says Nina Luning Prak, an immunologist at the University of Pennsylvania. Dealing with variants “is what the immune system does.”
Vaccine-prompted antibodies still attack alpha and delta, though slightly less well than they tackle the original virus that emerged in Wuhan, China, two years ago. Antibodies also still recognize more immune-evasive variants such as beta, first identified in South Africa in May 2020, and gamma, identified in Brazil in November 2020. Although protection against infection dips against many of these variants, vaccinated people remain much less likely to be hospitalized compared with unvaccinated people.
Experts will continue to track how well the vaccines are doing, especially as new variants, like omicron, emerge. In late November, the World Health Organization designated the omicron variant as the latest variant of concern after researchers in South Africa and Botswana warned that it carries several worrisome mutations. Preliminary studies suggest that, so far, omicron is spreading fast in places including South Africa and the United Kingdom, and can reinfect people who have already recovered from an infection. The variant might be at least as transmissible as delta, though that’s still far from certain, according to a December 9 report from researchers with Public Health England, a U.K. health agency. How omicron may affect vaccine effectiveness is also unclear. Pfizer’s two-dose shot, for instance, may be about 30 percent effective at preventing symptoms from omicron infections while a booster could bring effectiveness back up to more than 70 percent, according to estimates from Public Health England. But those estimates are based on low case numbers and could change as omicron spreads.

“This is the first time in history that we’re basically monitoring virus mutations in real time,” says Müge Çevik, an infectious diseases physician and virologist at the University of St. Andrews in Scotland. “This is what the viruses do. It’s just that we’re seeing it because we’re looking for it.”

But it’s unlikely that any new variant will take us back to square one, Çevik says. Because of the immune system’s varied defenses, it will be difficult for a coronavirus variant to become completely resistant to vaccine-induced protection. The vaccines are giving our immune systems the tools to fight back. — Erin Garcia de Jesús

The shots are safe, with few serious side effects
With billions of doses distributed around the world, the shots have proved not only effective, but also remarkably safe, with few serious side effects.

“We have so much safety data on these vaccines,” says Kawsar Talaat, an infectious diseases physician at the Johns Hopkins Bloomberg School of Public Health. “I don’t know of any vaccines that have been scrutinized to the same extent.”

Commonly reported side effects include pain, redness or swelling at the spot of the shot, muscle aches, fatigue, fever, chills or a headache. These symptoms usually last only a day or two.
More rare and serious side effects have been noted. But none are unique to these shots; other vaccines — plus infectious diseases, including COVID-19 — also cause these complications.

One example is inflammation of the heart muscle, known as myocarditis, or of the sac around the heart, pericarditis. Current estimates are a bit squishy since existing studies have different populations and other variables (SN Online: 10/19/21). Two large studies in Israel estimated that the risk of myocarditis after an mRNA vaccine is about 4 of every 100,000 males and 0.23 to 0.46 of every 100,000 females, researchers reported in October in the New England Journal of Medicine. Yet members of Kaiser Permanente Southern California who had gotten mRNA vaccines developed myocarditis at a much lower rate: 5.8 cases for every 1 million second doses given, researchers reported, also in October, in JAMA Internal Medicine.

What all the studies have in common is that young males in their teens and 20s are at highest risk of developing the side effect, and that risk is highest after the second vaccine dose (SN Online: 6/23/21). But it’s still fairly rare, topping out at about 15 cases for every 100,000 vaccinated males ages 16 to 19, according to the larger of the two Israeli studies. Males in that age group are also at the highest risk of getting myocarditis and pericarditis from any cause, including from COVID-19.
Components of the mRNA vaccines may also cause allergic reactions, including potentially life-threatening anaphylaxis. The U.S. Centers for Disease Control and Prevention calculated that anaphylaxis happens at a rate of about 0.025 to 0.047 cases for every 10,000 vaccine doses given.

But a study of almost 65,000 health care system employees in Massachusetts suggests the rate may be as high as 2.47 per 10,000 vaccinations, researchers reported in March in JAMA. Still, that rate is low, and people with previous histories of anaphylaxis have gotten the shots without problem. Even people who developed anaphylaxis after a first shot were able to get fully vaccinated if the second dose was broken down into smaller doses (SN Online: 6/1/21).

The only side effect of the COVID-19 vaccines not seen with other vaccines is a rare combination of blood clots accompanied by low numbers of blood-clotting platelets. Called thrombosis with thrombocytopenia syndrome, or TTS, it’s most common among women younger than 50 who got the Johnson & Johnson vaccine or a similar vaccine made by AstraZeneca that’s used around the world (SN Online: 4/23/21).
About 5 to 6 TTS cases were reported for every 1 million doses of the J&J vaccine, the company reported to the U.S. Food and Drug Administration. The clots may result from antibodies triggering a person’s platelets to form clots (SN Online: 4/16/21). Such antibodies also cause blood clots in COVID-19 patients, and the risk of developing strokes or clots from the disease is much higher than with the vaccine, Talaat says. In one study, 42.8 of every 1 million COVID-19 patients developed one type of blood clot in the brain, and 392.3 per 1 million developed a type of abdominal blood clot, researchers reported in EClinicalMedicine in September.

“Your chances of getting any of these side effects, except for the sore arm, from an illness with COVID are much higher” than from the vaccines, Talaat says. — Tina Hesman Saey

Getting everyone vaccinated is … complicated
The quest to vaccinate as many people as quickly as possible this year faced two main challenges: getting the vaccine to people and convincing them to take it. Strategies employed so far — incentives, mandates and making shots accessible — have had varying levels of success.

“It’s an incredibly ambitious goal to try to get the large majority of the country and the globe vaccinated in a very short time period with a brand-new vaccine,” says psychologist Gretchen Chapman of Carnegie Mellon University in Pittsburgh, who researches vaccine acceptance. Usually “it takes a number of years before you get that kind of coverage.”
Globally, that’s sure to be the case due to a lack of access to vaccines, particularly in middle- and lower-income countries. The World Health Organization set a goal to have 40 percent of people in all countries vaccinated by year’s end. But dozens of countries, mostly in Africa and parts of Asia, are likely to fall far short of that goal.

In contrast, the United States and other wealthy countries got their hands on more than enough doses. Here, the push to vaccinate started out with a scramble to reserve scarce appointments for a free shot at limited vaccination sites. But by late spring, eligible people could pop into their pharmacy or grocery store. Some workplaces offered vaccines on-site. For underserved communities that may have a harder time accessing such vaccines, more targeted approaches where shots are delivered by trusted sources at community events proved they could boost vaccination numbers (SN Online: 6/18/21).

Simply making the shot easy to get has driven much of the progress made so far, Chapman says. But getting people who are less enthusiastic has proved more challenging. Many governments and companies have tried to prod people, initially with incentives, later with mandates.
Free doughnuts, direct cash payments and entry into million-dollar lottery jackpots were among the many perks rolled out. Before the pandemic, such incentives had been shown to prompt some people to get vaccines, says Harsha Thirumurthy, a behavioral economist at the University of Pennsylvania. This time, those incentives made little difference nationwide, Thirumurthy and his colleagues reported in September in a preliminary study posted to SSRN, a social sciences preprint website. “It’s possible they moved the needle 1 or 2 percentage points, but we’ve ruled out that they had a large effect,” he says. Some studies of incentives offered by individual states have found a marginal benefit.

“People who are worried about side effects or safety are going to be more difficult to reach,” says Melanie Kornides, an epidemiologist at the University of Pennsylvania. And with vaccination status tangled up in personal identity, “you’re just not going to influence lots of people with a mass communication campaign right now; it’s really about individual conversations,” she says, preferably with someone trusted.
“Or,” she adds, “they’re going to respond to mandates.” Historically, sticks such as being fired from a job or barred from school are the most effective way of boosting vaccination rates, Kornides says. For example, hospitals that require flu shots for workers tend to have higher vaccination rates than those that don’t. For decades, mandates in schools have helped push vaccination rates up for diseases like measles and chickenpox, she says.

As COVID-19 mandates went into effect in the fall, news headlines often focused on protests and refusals. Yet early anecdotal evidence suggests some mandates have helped. For instance, after New York City public schools announced a vaccine requirement in late August for its roughly 150,000 employees, nearly 96 percent had received at least one shot by early November. Still, about 8,000 employees opted not to get vaccinated and were placed on unpaid leave, the New York Times reported.

Many people remain vehemently opposed to the vaccines, in part because of rampant misinformation that can spread quickly online. Whether more mandates, from the government or private companies, and targeted outreach will convince them remains to be seen. — Jonathan Lambert

Vaccines can’t single-handedly end the pandemic
One year in, it’s clear that vaccination is one of the best tools we have to control COVID-19. But it’s also clear vaccines alone can’t end the pandemic.

While the jabs do a pretty good job preventing infections, that protection wanes over time (SN Online: 3/30/21). Still, the vaccines have “worked spectacularly well” at protecting most people from severe disease, says Luning Prak, the University of Pennsylvania immunologist. And as more people around the world get vaccinated, fewer people will die, even if they do fall ill with COVID-19.

“We have to make a distinction between the superficial infections you can get — [like a] runny nose — versus the lower respiratory tract stuff that can kill you,” such as inflammation in the lungs that causes low oxygen levels, Luning Prak says. Preventing severe disease is the fundamental target that most vaccines, including the flu shot, hit, she notes. Stopping infection entirely “was never a realistic goal.”
Because vaccines aren’t an impenetrable barrier against the virus, we’ll still need to rely on other tactics to help control spread amid the pandemic. “Vaccines are not the sole tool in our toolbox,” says Saad Omer, an epidemiologist at Yale University. “They should be used with other things,” such as masks to help block exposure and COVID-19 tests to help people know when they should stay home.

For now, it’s crucial to have such layered protection, Omer says. “But in the long run, I think vaccines provide a way to get back to at least a new normal.” With vaccines, people can gather at school, concerts or weddings with less fear of a large outbreak.

Eventually the pandemic will end, though when is still anyone’s guess. But the end certainly won’t mean that COVID-19 has disappeared.

Many experts agree that the coronavirus will most likely remain with us for the foreseeable future, sparking outbreaks in places where there are pockets of susceptible people. Susceptibility can come in many forms: Young children who have never encountered the virus before and can’t yet get vaccinated, people who choose not to get the vaccine and people whose immunity has waned after an infection or vaccination. Or the virus may evolve in ways that help it evade the immune system.

The pandemic’s end may still feel out of reach, with the high hopes from the beginning of 2021 a distant memory. Still, hints of normalcy have returned: Kids are back in school, restaurants and stores are open and people are traveling more.

Vaccines have proved to be an invaluable tool to reduce the death and destruction that the coronavirus can leave in its wake. — Erin Garcia de Jesús