Why the coronavirus’s delta variant dominated 2021

2021 was a year of coronavirus variants.

Alpha and beta kicked off the year, and several worrisome variants later, omicron is closing it out. How omicron may come to define the pandemic’s future remains uncertain. But even as omicron comes on strong, one variant, which rose to global dominance midyear in a way variants like alpha and beta never did, continues to largely define the pandemic right now: delta.

Things had actually seemed to be looking up in some parts of the world in the late spring and early summer of 2021, a year and a half into the COVID-19 pandemic. In the United States, for instance, millions of people were vaccinated, cases of the disease were falling, and people were beginning to socialize and resume normal activities.

But then delta hit hard. First spotted in India in October 2020, this variant of SARS-CoV-2, the coronavirus that causes COVID-19, quickly swept around the world, supplanting other versions of the virus in 2021 (SN: 7/2/21). Delta overwhelmed health care systems, tore through unvaccinated populations and showed that even the vaccinated were vulnerable, causing some breakthrough cases.
It soon became clear why delta wreaks so much havoc. People infected with delta make more of the virus and spread it for longer than people infected with other variants, researchers reported in Clinical Infectious Diseases in August. As a result, delta infections are more contagious. Consider two scenarios in a community where no one has immunity to the coronavirus: A person infected with an earlier version of the virus — the one first identified in Wuhan, China, that set off the pandemic — might spread it to two or three others. But a person infected with delta may transmit it to five or six people.

Delta owes its success to mutations in some of its proteins. Take, for instance, a mutation called R203M in the coronavirus’s nucleocapsid, or N protein, located inside the virus. This mutation may increase the amount of viral RNA that can be made or make it easier for the N protein to do its job, packing RNA into newly assembled viral particles, researchers reported in Science in November.
Mutations similar to delta’s have appeared here and there in other variants that proved themselves capable of spreading more easily or better evading the body’s immune defenses than the original virus. That includes alpha, first spotted in the United Kingdom; beta, first characterized in South Africa; and gamma, first noted in Brazil. The recently discovered omicron variant, first described in South Africa and Botswana, also shares some of the same mutations (SN: 12/1/21).

Some of delta’s grab bag of mutations are identical to those found in other variants, while others change the same protein building block, or amino acid, in a different way or pop up in the same part of the virus. For instance, alpha and omicron also have the same mutation of the 203rd amino acid in the N protein, but it is a different amino acid change than seen in delta. And some mutations are entirely new to delta.
Scientists don’t yet know the effect that all those changes have on delta’s ability to replicate or spread to others. What’s more, delta continues to evolve, picking up additional changes over time. But studies have zeroed in on the unique constellation of mutations decorating the virus’ spike protein. It’s the knobby protein studding each coronavirus that helps the virus latch onto and invade human cells. What looks like an individual knob is in fact composed of three identical pieces that fit together, each carrying the same set of mutations.

Some of delta’s spike protein mutations may help the virus more easily break into cells, where it turns cell machinery into virus-making factories. Two of those, dubbed T478K and L452R, are advantageously located on the receptor-binding domain. This is the part of the spike protein that attaches to ACE2, a protein on the surface of host cells.

Other mutations show up in a region of the spike protein called the N-terminal domain, which is a known target of the immune system’s neutralizing antibodies. These mutations may help the virus evade those antibodies, which can stop the virus from infecting cells.

And yet two other mutations, P681R and D614G, may help prep newly made viruses to go out and conquer. Those mutations are nestled near the dividing line for two parts of the spike protein, S1 and S2. Those parts need to be split apart to allow the coronavirus to engage in the gymnastics needed to help it fuse with the membrane of its prospective human host cell.
Human cells actually aid in this process: Inside infected cells a human protein called furin nicks the spike protein between the S1 and S2 segments, opening the receptor-binding domain so it can better grab ACE2. The P681R and D614G mutations may make the spike protein easier for furin to cut. Once snipped, newly-made viruses are primed to infect other cells.

Taken together, these mutations help delta break into cells more quickly and perform several tasks better than other variants do. As a result, in 2021, delta was able to become the dominant variant in the world.

Here’s how specific delta spike protein mutations may aid in a cell take-over:

  1. Some mutations allow the spike protein to get a better grip on cells.
    The coronavirus begins its cellular break-in by latching onto a protein called ACE2 that studs the surface of many types of human cells. Three mutations may make delta grabbier than other variants.

D614G interrupts some molecular interactions in the spike protein near a hinge that controls whether the receptor binding domain is in a closed position where it is protected from antibodies, or in an open position so that it can grab ACE2. With the D614G mutation, it’s more likely that one or more of ACE2-snagging portions of the protein will be open for action.

L452R may strengthen the interaction between ACE2 and the spike protein, making the virus more likely to infect cells. The change switches the charge on a protein building block in a key part of the spike protein from neutral to positive. So, like a magnet attracted to metal, the mutation seems to make the spike protein bind more tightly to a part of ACE2 that has a negative charge.

T478K is unique to the delta variant. It’s so far unclear what it does, but like L452R, it may also help strengthen the spike protein’s hold on ACE2.

  1. Some mutations allow delta to better fuse with the cell’s membrane, paving the way for the coronavirus to dump its genetic material into the cell.
    Once delta latches onto ACE2, a human protein called TMPRSS2 cuts away a part of the spike protein. As a result, the S1 portion of the protein is discarded, freeing up the S2 portion of the protein to twist into shape for the next step in the process: fusing to the cell. Some evidence suggests delta may be better at letting go of S1, making breaking into cells easier.

L452R may help the virus fuse with the membrane on the outside of the cell it’s trying to infect. That allows the virus to release its genetic material and begin hijacking the cell’s machinery to begin making more copies of itself.

P681R may create a stretch of basic amino acids that could help the virus fuse better with the cell membrane, helping more viruses get inside more cells.

As a result of these and other changes, delta can fuse with cells faster and can enter cells that have lower levels of ACE2 studding their surfaces than other variants can, researchers reported in Science in October.

After the virus fuses to the cell, it sets loose its RNA and turns its new lair into a virus factory: Viral RNA is copied, human ribosomes make viral proteins and the cell churns out nearly identical copies of the coronavirus. As the virus makes copies of its RNA, it can make typos. Sometimes, the genetic errors help the virus, which can give rise to variants like delta. But not all changes are good for the virus. Some genetic typos cause damage to viral proteins, meaning the viruses with those mutations can’t infect new cells. Other changes don’t have any effect on the virus at all.

  1. Some delta mutations may better prime newly made viruses to more easily infect cells.
    Before newly made viruses are released from the cell, the human protein furin snips the spike protein between S1 and S2. That lets the spike protein adopt the right shape to snag human cells and sets the protein up to allow for better membrane fusion.

Delta may be snippier than other variants.

Mutations D614G and P681R may increase the number of spike proteins cut by furin on each newly made virus, better prepping the viruses to enter other cells.

D614G makes it easier for furin to make its snips. This preliminary cut happens in a different location than the TMPRSS2 cut. The mutation may also increase the number of spike proteins on each copy of the virus.

Like D614G, P681R may also boost the number of spike proteins cut by the human cell protein furin, priming the newly made viruses to infect new cells.

  1. Some mutations may help newly released viruses evade antibodies as the viruses seek out other cells to infect.
    The immune systems of people who have recovered from an infection or those who got vaccinated make antibodies to the coronavirus. Several of delta’s mutations may help the virus evade these antibodies, which would otherwise block viral entry into other cells.

T19R, G142D, R158G and two spots — called E156del and F157del — where amino acids are missing from the protein may hide parts of the virus from antibodies, helping it slip past those immune system defenses.

T478K, the mutation unique to the delta variant, is close to the same spot as E484K, a mutation that was implicated in the antibody-evasion tactics of the beta variant.

How a warming climate may make winter tornadoes stronger

Though tornadoes can occur in any season, the United States logs the greatest number of powerful twisters in the warmer months from March to July. Devastating winter tornadoes like the one that killed at least 88 people across Kentucky and four other states beginning on December 10 are less common.

But climate change could increase tornado intensity in cooler months by many orders of magnitude beyond what was previously expected, researchers report December 13 in a poster at the American Geophysical Union’s fall meeting.

Tornadoes typically form during thunderstorms when warm, humid airstreams get trapped beneath cooler, drier winds. As the fast-moving air currents move past each other, they create rotating vortices that can transform into vertical, spinning twisters (SN: 12/14/18). Many tornadoes are short-lived, sometimes lasting mere minutes and with a width of only 100 yards, says Jeff Trapp, an atmospheric scientist at the University of Illinois at Urbana-Champaign.
Over the last 20 years, tornado patterns have shifted so that these severe weather events occur later in the season and across a broader range in the United States than before, Trapp says (SN: 10/18/18). But scientists have struggled to pin down a direct link between the twister changes and human-caused climate change.

Unlike hurricanes and other severe storm systems, tornadoes happen at such a small scale that most global climate simulations don’t include the storms, says Kevin Reed, an atmospheric scientist at Stony Brook University in New York who was not involved in the new research.

To see how climate change may affect tornadoes, Trapp and colleagues started with atmospheric measurements of two historical tornadoes and simulated how those storm systems might play out in a warmer future.

The first historical tornado took place in the cool season on February 10, 2013, near Hattiesburg, Miss., and the second occurred in the warm season on May 20, 2013, in Moore, Okla. The researchers used a global warming simulation to predict how the twisters’ wind speeds, width and intensity could change in a series of alternative climate scenarios.

Both twisters would likely become more intense in futures affected by climate change, the team found. But the simulated winter storm was more than eightfold as powerful as its historical counterpart, in part due to a predicted 15 percent increase in wind speeds. Climate change is expected to increase the availability of warm, humid air systems during cooler months, providing an important ingredient for violent tempests.

“This is exactly what we saw on Friday night,” Trapp says. The unseasonably warm weather in the Midwest on the evening of December 10 and in the early morning of December 11 probably contributed to the devastation of the tornado that traveled hundreds of miles from Arkansas to Kentucky, he speculates.

Simulating how historical tornados could intensify in future climate scenarios is a “clever way” to address the knowledge gap around the effects of climate change on these severe weather systems, says Daniel Chavas, an atmospheric scientist at Purdue University in West Lafayette, Ind., who was not involved in the new research.

But Chavas notes that this research is only one piece of a larger puzzle as researchers investigate how tornados might impact communities in the future.

One drawback of this type of simulation is it often requires direct measurements from a historical event, Reed says. That limits its prediction power to re-creating documented tornadoes rather than broadly forecasting shifts in large-scale weather systems.

Though the team based its predictions on only two previous tornados, Trapp says he hopes that adding more historical twisters to the analysis could provide more data for policy makers as well as residents of communities that may have to bear the force of intensifying tornadoes.

Why it matters that health agencies finally said the coronavirus is airborne

This year, health experts around the world revised their views about how the coronavirus spreads. Aerosol scientists, virologists and other researchers had determined in 2020 that the virus spreads through the air, but it took until 2021 for prominent public health agencies to acknowledge the fact. The admission could have wide-ranging consequences for everything from public health recommendations and building codes to marching band practices (SN: 8/14/21, p. 24).

For decades, doctors and many researchers have thought that respiratory viruses such as cold and flu viruses spread mainly by people touching surfaces contaminated by mucus droplets and then touching their faces. That’s why, in the early days of the pandemic, disinfectant wipes flew off store shelves.

Surface-to-face transfer is still a probable route of infection for some cold-causing viruses, such as respiratory syncytial virus, or RSV. But it turns out that the coronavirus spreads mainly through fine aerosol particles that may hang in the air for hours, particularly indoors.

People spread such aerosols when coughing or sneezing, but also when talking, singing, shouting and even quietly breathing, allowing infected people to spread the disease even before they know they’re sick. Some evidence suggests that the coronavirus may be evolving to spread more easily through the air (SN: 9/25/21, p. 6).

It took collecting reams of data and more than 200 scientists pushing the World Health Organization and other public health agencies to acknowledge airborne spread of the coronavirus. In April 2021, both the WHO and U.S. Centers for Disease Control and Prevention updated their recommendations to note that airborne spread is a major route of infection (SN Online: 5/18/21).

That recognition was vital to public understanding of why wearing well-fitting masks is necessary in public indoor places (SN: 3/13/21, p. 14; SN Online: 7/27/21). Masking, social distancing and other measures to guard against the coronavirus are also credited with nearly wiping out flu last winter (SN Online: 2/2/21). Experts fear a resurgence of cold and flu this winter if those measures aren’t continued (SN Online: 8/12/21).

Knowledge that COVID-19 is an airborne disease has led to such measures as rearranging seating in orchestras (SN Online: 6/23/21) and updating recommendations for proper ventilation and filtration in buildings. Some scientists and activists have also suggested that the safety of indoor air should be regulated to reduce the spread of diseases, much like safety standards for food and drinking water.

A custom brain implant lifted a woman’s severe depression

A personalized brain implant eased the crushing symptoms of a woman’s severe depression, allowing her to once again see the beauty of the world. “It’s like my lens on the world changed,” said Sarah, the research volunteer who requested to be identified by her first name only.

The technology, described October 4 in Nature Medicine, brings researchers closer to understanding how to detect and change brain activity in ultraprecise ways (SN: 2/10/19).

The device was bespoke; it was built specifically for Sarah’s brain. The details of the new system may not work as a treatment for many other people, says Alik Widge, a psychiatrist and neural engineer at the University of Minnesota in Minneapolis. Still, the research is “a really significant piece of work,” he says, because it points out a way to study how brain activity goes awry in depression.

Researchers at the University of California, San Francisco implanted temporary thin wire electrodes into Sarah’s brain. The 36-year-old woman had suffered from severe depression for years. These electrodes allowed researchers to monitor the brain activity that corresponded to Sarah’s depression symptoms — a pattern that the researchers could use as a biomarker, a signpost of trouble to come. In Sarah’s case, a particular sign emerged: a fast brain wave called a gamma wave in her amygdala, a brain structure known to be involved in emotions.
With this biomarker in hand, the researchers then figured out where to stimulate the brain to interrupt Sarah’s distressing symptoms. A region called the ventral capsule/ventral striatum, or VC/VS, seemed to be the key. That’s not surprising; previous research suggests the region is involved with feeling good and other emotions. When researchers applied tiny jolts of electrical current to this region, Sarah’s mood improved. “We could learn the road map of Sarah’s brain in a way that we could really improve her depression symptoms,” Katherine Scangos of UCSF said in a Sept. 30 news briefing.

During this mapping phase of the experiment, Sarah felt joy when the right spot was stimulated. “I laughed out loud,” she said in the briefing. “This was the first time I had spontaneously laughed and smiled where it wasn’t faked or forced in five years.”

Surgeons then implanted a more permanent device into Sarah’s brain last June. Scientists programmed the device to detect when gamma signals were high in Sarah’s amygdala, and respond with a tiny jolt to her VC/VS. This happened about 300 times a day. The stimulation was calibrated so Sarah didn’t feel any zaps, but she said they left her feeling a little more energetic.

The research paper describes Sarah’s improvements as the technology did its work in her head over two months; it’s unclear how long the benefits might last, though she’s now had the device implanted for over a year. “As time has gone on, it’s been this virtuous cycle, a spiral upwards,” Sarah said. “Everything has gotten easier and easier and easier.”

The approach used by the UCSF researchers required a lot of sophisticated imaging and machine learning technology. That complexity may prevent it from being a wider treatment, cautions Helen Mayberg, a neurologist at Icahn School of Medicine at Mount Sinai in New York City.

Still, the results — which add to a variety of ways to detect and change problematic brain activity — contain valuable information about how depression takes hold of a brain, and how brain stimulation can change that, says Mayberg, whose research has helped build and refine the field of deep brain stimulation for mood disorders. “What we all want to know is, ‘How does this work?’”

Giant ground sloths may have been meat-eating scavengers

Modern sloths may be dedicated vegetarians, but at least one of their massive Ice Age cousins chowed down on meat when it had the chance. Darwin’s ground sloth — which could grow to over 3 meters long and weigh as much as about 2,000 kilograms — may have been an opportunistic scavenger, chemical analyses of fossil sloth hair suggest.

Paleontologist Julia Tejada of the University of Montpellier in France and colleagues analyzed the chemical makeup of two amino acids, the building blocks of proteins, within the fossil hair of two giant ground sloth species: Darwin’s ground sloth (Mylodon darwinii) of South America and the Shasta ground sloth (Nothrotheriops shastensis) of North America (SN: 4/25/18). The team compared these with samples from living sloths, anteaters and other modern omnivores.
Nitrogen isotopes, different forms of the element, can vary a lot among different food sources as well as between ecosystems. Those isotope values in one amino acid, glutamine, change significantly with diet, increasing the higher the animal is on the food chain. But diet has little impact on the nitrogen values in another amino acid, phenylalamine. By comparing the nitrogen isotopes in the two amino acids found in the sloths’ hair, the researchers were able to eliminate ecosystem effects and zoom in on diets.

The data reveal that while the diet of the Shasta ground slothwas exclusively plant-based, Darwin’s ground sloth was an omnivore, Tejada and colleagues report October 7 in Scientific Reports.

The findings upend what scientists thought they knew about the ancient animals. Scientists have assumed the ancient creatures were herbivores. That’s in part because all six modern species of sloth are confirmed vegetarians, and in part giant ground sloths’ teeth and jaws weren’t adapted for hunting or powerful chewing and tearing (SN: 6/20/16).

But Darwin’s ground sloth could have managed to ingest already-killed meat, Tejada and colleagues say. And that might help solve a long-standing puzzle: the apparent absence of large carnivorous mammals in South America at the time. Darwin’s ground sloth, the researchers add, may have filled a vacant ecological niche: the scavenger who wouldn’t say no to a meaty meal.

Barnacles are famed for not budging. But one species roams its sea turtle hosts

Barnacles aren’t exactly renowned for their athleticism, staying glued in place for much of their lives. But turtle-riding barnacles are fidgety travelers.

As adults, the turtle barnacles (Chelonibia testudinaria) can move about 1.4 millimeters a week across turtle shells, researchers report October 6 in Proceedings of the Royal Society B. Previous observations of barnacles stuck on green sea turtles suggested that the creatures were somehow mobile, propelled by either outside forces or their own actions. But this is the first experimental confirmation that they embark on self-directed treks.

Barnacles start life as free-swimming larvae, eventually settling and adhering to rocks, ship hulls or even the skin of marine mammals (SN: 9/27/16). Some species have been known to rotate on their base or even scooch a smidge when nudged by a too-close neighbor. But once settled in, they live and grow, eating particles of food drifting by what was long considered their permanent address.
Now it turns out some may need forwarding addresses. Benny K.K. Chan, a marine ecologist at Academia Sinica in Taipei, Taiwan, decided to test C. testudinaria’s mobility experimentally when one of his students successfully transferred turtle barnacles from crabs to an acrylic plate. The team followed 15 transferred barnacles with time-series photography over a year.

Chan’s team also collaborated with researchers in Spain to track the movement of barnacles on the shells of five captive loggerhead sea turtles over a few months and with citizen scientist divers who gathered photos of wild green sea turtles in Taiwan. The team logged the positions of the green turtles’ barnacles over 16 weeks.
Turtle-riding barnacles moved as much as 54 millimeters — a little less than the length of an adult human’s thumb — during this time. Laboratory barnacles moved too, leaving trails of pale cement in layered, crescent-shaped patterns. “We were amazed,” says Chan.

How the barnacles move is still a mystery, but researchers think the crustaceans may partially dissolve their own cement and lift their soft base slightly off the surface. “Then the barnacle can secrete a new cement layer and probably surf on the cement,” says Chan.

The barnacles mostly traveled against the flow of any currents, showing that they weren’t just moving from the pressure of flowing water. They also didn’t get closer together, suggesting that the barnacles are seeking better locations to filter food out of the water rather than mating opportunities.
“This is rock-solid proof of something that is otherwise anecdotal,” says marine biologist Henrik Glenner at the University of Bergen in Norway , who was not involved with this study.

Barnacles typically exemplify biological competition for space and resources, because after settling they must compete in that spot for the rest of their lives, Glenner says. But being mobile upends this dynamic.

And it raises new questions. Glenner wonders if any barnacles in crowded, intertidal environments might also be capable of movement. And Tara Essock-Burns, a marine ecologist at the University of Hawaii at Manoa, wants to learn more about the cement itself and its flexible properties. “It is possible that turtle barnacle cement has a very different biochemistry than other barnacles that permanently adhere to [surfaces],” she says. This is precisely what Chan and his team plan on investigating next.

“There is a reason that Darwin was so captivated by barnacles,” says Essock-Burns. “They never cease to amaze us.”

The earliest evidence of tobacco use dates to over 12,000 years ago

Ancient North Americans started using tobacco around 12,500 to 12,000 years ago, roughly 9,000 years before the oldest indications that they smoked the plant in pipes, a new study finds.

This discovery replaces the pipe-smoking report as the oldest direct evidence for the human use of tobacco anywhere in the world.

Excavations at the Wishbone site in Utah’s Great Salt Lake Desert uncovered four charred seeds of wild tobacco plants in a small fireplace, say archaeologist Daron Duke of Far Western Anthropological Research Group in Henderson, Nev., and colleagues.

Those seeds, dated based on radiocarbon dates of burned wood in the fireplace, likely came from plants gathered on foothills or mountains located 13 kilometers or more from the Wishbone area, Duke’s team reports October 11 in Nature Human Behavior.

The site was located in a sprawling marshland at the time of its occupation. Finds in and around the fireplace include bones of ducks and other waterfowl, a long, intact stone point and another point broken in two, a bone implement and seeds of several edible wetland plants.

It’s unclear how ancient North American hunter-gatherers used the tobacco, Duke says. Wads of tobacco leaves, stems and other plant fibers may have been twisted into balls and chewed or sucked, with attached seeds spit out or discarded. Ancestors of Pueblo people in what’s now Arizona chewed wild tobacco between around 1,000 and 2,000 years ago. Tobacco smoking can’t be ruled out at the Wishbone site, Duke adds.

The earliest evidence of domesticated tobacco, which comes from South America, dates to only about 8,000 years ago (SN: 10/29/18). Duke suspects various ancient American populations independently tamed the plant at different times. “Certain groups wound up domesticating particular [tobacco] species, typically alongside food crops,” he suggests.

Methods of getting results from real-world experiments win 2021 economics Nobel

Some of the most insightful — and now most celebrated — studies of such major social issues as minimum wages and immigration have seized on naturally occurring events. Pioneering efforts by three economists to study the effects of real-life economic events that mimic controlled laboratory investigations have won the Nobel Memorial Prize in Economic Sciences.

David Card of the University of California, Berkeley will receive half of the prize of 10 million Swedish kronor (or half of about $1.14 million). The other half will be split by Joshua Angrist of MIT and Guido Imbens of Stanford University. The Royal Swedish Academy of Sciences announced the prize October 11.

Research by the Nobel Prize winners was instrumental in the development during the 1990s of what are known as natural experiments. These investigations rely on naturally occurring differences between groups or populations that either do or don’t experience specific conditions. In this way, social scientists can study, say, how differences in income affect physical health or how immigration influences employment rates.

Natural experiments are especially important because investigators of key social questions, such as whether pollution slows children’s mental development or whether strong public institutions promote economic growth, often can’t assign people at random to treatment and control conditions. It would be unethical, impractical or both.
“The Nobel winners developed techniques that replicate the idea of truly scientific experiments like you would use to test a vaccine, except [the experiments] occurred in the real world,” says economist Phillip Levine of Wellesley College in Massachusetts. These methods “were at the forefront of a ‘credibility revolution’ in economics” that made the field relevant and understandable to the public, he adds. Levine was a Princeton University graduate student with Angrist, and Card was his thesis adviser.

Natural experiments in economics are related to another influential line of research that examines ways to counteract poverty’s harmful effects using field experiments, work that won the 2019 economics Nobel (SN: 10/14/19).

In a key 1994 paper, Card and the late Princeton economist Alan Krueger challenged conventional wisdom in economics that increases in the minimum wage reduce employment. Card and Krueger surveyed fast-food restaurants in New Jersey and a neighboring section of eastern Pennsylvania before and after a minimum wage hike that was instituted only in the Garden State. Full-time employment slightly increased in New Jersey following wage increases, while it declined in Pennsylvania where wages stayed the same.
Further research addressed the complexities of how the minimum wage interacts with employment rates, but it was clear after Card and Krueger’s report that a simple cause-and-effect relationship didn’t exist.

Card also conducted a natural experiment indicating that a huge influx of Cuban refugees to Miami in 1980 did not result in reduced wages and employment for Miami residents with low education levels. That work led Card and others to further explore how new immigration influences the economic standing of native-born citizens and earlier immigrants.

Angrist and Imbens expanded on such work by devising steps to determine under what conditions a natural experiment, such as being given an opportunity to leave school at age 16, affects later outcomes, such as annual income. For instance, the researchers’ method estimated the effect on later income of an additional year of education, which they put at about 9 percent lower for each year lost after age 16, but only for people who chose to leave school early. The estimate excluded earnings histories of individuals who had planned to go to college all along because those people never considered leaving school early.
Card, Angrist and Imbens “have promoted a type of scholarly investigation that is of practical use outside academic journals,” says economist Melissa Kearney of the University of Maryland in College Park, who has studied and worked with both Card and Angrist. The Nobel Prize winners’ research equipped social scientists with “tools to credibly draw causal conclusions about empirical relationships.”

A child’s partial skull adds to the mystery of how Homo naledi treated the dead

A child’s partial skull found in a remote section of a South African cave system has fueled suspicion that an ancient hominid known as Homo naledi deliberately disposed of its dead in caves.

An international team led by paleoanthropologist Lee Berger of University of the Witwatersrand, Johannesburg pieced together 28 skull fragments and six teeth from a child’s skull discovered in a narrow opening located about 12 meters from an underground chamber where cave explorers first found H. naledi fossils (SN: 9/10/15). Features of the child’s skull qualify it as H. naledi, a species with an orange-sized brain and skeletal characteristics of both present-day people and Homo species from around 2 million years ago.

“The case is building for deliberate, ritualized body disposal in caves by Homo naledi,” Berger said at a November 4 news conference held in Johannesburg. While that argument is controversial, there is no evidence that the child’s skull was washed into the tiny space or dragged there by predators or scavengers (SN: 4/19/16).

Berger’s group describes the find in two papers published November 4 in PaleoAnthropology. In one, Juliet Brophy, a paleoanthropologist at Louisiana State University in Baton Rouge and colleagues describe the youngster’s skull. In the other, paleoanthropologist Marina Elliott of Canada’s Simon Fraser University in Burnaby and colleagues detail new explorations in South Africa’s Rising Star cave system.

Researchers nicknamed the new find Leti, short for a word in a local South African language that means “the lost one.” Leti likely dates to the same time as other H. naledi fossils, between 335,000 and 236,000 years ago (SN: 5/9/17). Berger’s team suspects Leti died at about age 4 to 6 years based on the rate at which children grow today. But that’s a rough approximation as the scientists can’t yet say how fast H. naledi kids grew.

Lasers reveal construction inspired by ancient Mexican pyramids in Maya ruins

At Teotihuacan, near Mexico City, three giant pyramids rise above the ancient city’s main street, the Avenue of the Dead. The smallest of these is the Temple of the Feathered Serpent, which sits within La Ciudadela, or the Citadel, a massive sunken plaza with tall walls.

Now, more than a thousand kilometers away at the Maya capital of Tikal in what’s now Guatemala, researchers have found a smaller plaza and pyramid possibly modeled after La Ciudadela and its temple.

Teotihuacan is thought to have conquered Tikal in the year 378 (SN: 9/27/18). The finding adds to evidence of Teotihuacan’s influence over Tikal, the team reports September 28 in Antiquity.

“The architectural layout revealed by this study is stunning,” says anthropological archaeologist Nawa Sugiyama of the University of California, Riverside, who was not involved in the new research. “The very orthogonal city planning with specific orientation of the pyramids gives Teotihuacan a very characteristic architectural style, making it easy to identify any Teotihuacan influence abroad.”、
What’s more, the newfound structures had six construction phases, the researchers say, most dating to a time in Mesoamerica that archaeologists call the Early Classic period, which lasted from about 300 to 550. That means that the Tikal complex possibly predates the Teotihuacan conquest of the Maya city in 378. If true, that would add more evidence to an idea that scientists have worked on for decades — that these civilizations were in contact much earlier than the conquest of Tikal, possibly trading and making political connections with one another.

To uncover the pre-Columbian architecture, archaeologist Stephen Houston of Brown University in Providence, R.I., and colleagues at the Proyecto Arqueológico del Sur de Tikal along with the Pacunam LiDAR Initiative and the University of Texas at Austin used an airborne remote-sensing technique called lidar, or light detection and ranging.
“We knew this area in Guatemala was important to Teotihuacan culture,” says study coauthor David Stuart, director of the Mesoamerica Center of the University of Texas at Austin. But the place where the Citadel-inspired construction is located did not appear on old maps of the Tikal archaeological site because it is covered in vegetation. “As there was no visible stonework there, it was thought to be a natural hill,” Stuart says.

The team decided to look closer because the mound looked unusual for a Maya site. “Since the location was adjacent to an area in Tikal where many Teotihuacan-style artifacts were found in the 1980s, we thought it deserved more attention,” Stuart says. After reviewing the lidar mapping, Houston saw that the general plan of the buildings resembled the Ciudadela and its temple at Teotihuacan.

In her 2004 book The Ancient Maya: New Perspectives, Louisiana State University archaeologist Heather McKillop noted that the abundant presence of Teotihuacan-style architecture and pottery found in Tikal and a number of Maya sites across Guatemala is extensive evidence of the Teotihuacan influence across Mesoamerica from the year 400 to 700. The ancient city in Mexico thrived from about 100 to 750, but much about the people who lived there and why the city was destroyed and abandoned is still a mystery. The Aztecs gave the name Teotihuacanto the city centuries after its collapse.

“It is almost like Teotihuacan had installed their own neighborhood or embassy in Tikal,” says study coauthor and archaeologist Thomas Garrison, also at the University of Texas at Austin. Other research led by Sugiyama shows that “there was also a more permanent Maya presence in Teotihuacan before the conquest of Tikal as well, so influence probably went in both ways.”

Sugiyama studies the Plaza of the Columns Complex at Teotihuacan, where researchers have found Maya ceramics and evidence of Maya-style painted walls. “These murals were destroyed … before the 378 arrival event,” she says. “That makes us wonder whether the conquest [of Tikal] was one of the last chapters” in a long history of contact between the Mayas and the Teotihuacanos.

Eduardo Natalino dos Santos, a Mesoamerica historian at the University of São Paulo who did not take part in the study, agrees with Sugiyama. “The circulation of these ancient architectural styles show that the Mesoamerican Indigenous elites were connected. We used to see traces of one culture in a different region always as a result of a colonizing or domination process. Maybe this is not always the case,” he says.