Fossil DNA may be rewriting the history of elephant evolution.

The first genetic analysis of DNA from fossils of straight-tusked elephants reveals that the extinct animals most closely resembled modern African forest elephants. This suggests that straight-tusked elephants were part of the African, not Asian, elephant lineage, scientists report online June 6 in eLife.

Straight-tusked elephants roamed Europe and Asia until about 30,000 years ago. Much like modern Asian elephants, they sported high foreheads and double-domed skulls. These features convinced scientists for decades that straight-tusked and Asian elephants were sister species, says Adrian Lister, a paleobiologist at the Natural History Museum in London who was not involved in the study.
For the new study, researchers extracted and decoded DNA from the bones of four straight-tusked elephants found in Germany. The fossils ranged from around 120,000 to 240,000 years old. The genetic material in most fossils more than 100,000 years old is too decayed to analyze. But the elephant fossils were unearthed in a lake basin and a quarry, where the bones would have been quickly covered with sediment that preserved them, says study author Michael Hofreiter of the University of Potsdam in Germany.

Hofreiter’s team compared the ancient animals’ DNA with the genomes of the three living elephant species — Asian, African savanna and African forest — and found that straight-tusked genetics were most similar to African forest elephants.

When the researchers told elephant experts what they’d found, “Everybody was like, ‘This can’t possibly be true!’” says study coauthor Beth Shapiro of the University of California, Santa Cruz. “Then it gradually became, ‘Oh yeah, I see.… The way we’ve been thinking about this is wrong.’”

If straight-tusked elephants were closely related to African forest elephants, then the African lineage wasn’t confined to Africa — where all elephant species originated — as paleontologists previously thought. It also raises questions about why straight-tusked elephants bore so little resemblance to today’s African elephants, which have low foreheads and single-domed skulls.
Accounting for this new finding may not be as simple as moving one branch on the elephant family tree, Lister says. It’s possible that straight-tusked elephants really were a sister species of Asian elephants, but they exhibit genetic similarities to African forest elephants from interbreeding before the straight-tusked species left Africa.

It’s also possible that a common ancestor of Asian, African and straight-tusked elephants had particular genetic traits that were, for some reason, only retained by African and straight-tusked elephants, he says.

Lister and colleagues are now reexamining data on straight-tusked skeletons to reconcile the species’ skeletal features with the new information on their DNA. “I will feel most comfortable if we can understand these genetic relationships in terms of the [physical] differences between all these species,” he says. “Then we’ll have a complete story.”

BOSTON — Some aspects of speech are as Southern as pecan pie. Consider the vowel shift that makes the word pie sound more like “pah.” While that pronunciation is found from Florida to Texas, a new study reveals a surprising diversity in Southern vowel pronunciation that’s linked to a speaker’s age, social class, gender, race and geography.

The research, presented June 29 at a meeting of the Acoustical Society of America, could help software developers create better speech recognition tools for smartphones and other devices.
To understand the medley of southern vowel sounds, linguist Margaret Renwick of the University of Georgia in Athens dove into the Digital Archive of Southern Speech. The archive comprises almost 400 hours of interviews with 64 native Southerners representing a mix of ethnicities, social classes, education levels and ages.

Renwick’s analysis of more than 300,000 vowel sounds finds, for example, that Southern upper middle class women are often at the extreme end of variation in pronunciation. While Southern men and women are equally likely to shift the vowel in bet to “bay-ut,” upper middle class Southern women are more likely to stretch the vowel sound in bit to “bee-ut.” They are also most likely to pronounce bait as bite. The finding that women are more inclined to draw a sound out into two syllables — or change it entirely — is in line with other research suggesting that women are linguistic innovators, and less likely to adhere to the norms of standard American English, Renwick said.

For a glue that holds up inside the body, turn to the humble slug, Arion subfuscus. A new super-sticky material mimics slug slime’s ability to stick on slick wet surfaces and could lead to more effective medical adhesives.

The material has two parts: a sticky layer that attaches to a surface, and a shock-absorbing layer that reduces strain. That makes the adhesive less likely to snap off.

Researchers tested the material as a surgical adhesive in a number of different scenarios: It stuck to pig skin and liver. It latched on to a beating pig’s heart, even when the surface was coated in blood. It sealed up a heart defect, preventing liquid from leaking even when the organ was inflated and deflated tens of thousands of times. And it was less toxic in the body than a commonly used commercialized tissue adhesive, researchers report July 28 in Science.

The researchers hope the material could someday be used in surgical procedures in place of invasive sutures and staples.

For the first time in the United States, researchers have used gene editing to repair a mutation in human embryos.

Molecular scissors known as CRISPR/Cas9 corrected a gene defect that can lead to heart failure. The gene editor fixed the mutation in about 72 percent of tested embryos, researchers report August 2 in Nature. That repair rate is much higher than expected. Work with skin cells reprogrammed to mimic embryos had suggested the mutation would be repaired in fewer than 30 percent of cells.
In addition, the researchers discovered a technical advance that may limit the production of patchwork embryos that aren’t fully edited. That’s important if CRISPR/Cas9 will ever be used to prevent genetic diseases, says study coauthor Shoukhrat Mitalipov, a reproductive and developmental biologist at Oregon Health & Science University in Portland. If even one cell in an early embryo is unedited, “that’s going to screw up the whole process,” says Mitalipov. He worked with colleagues in Oregon, California, Korea and China to develop the embryo-editing methods.

Researchers in other countries have edited human embryos to learn more about early human development or to answer other basic research questions (SN: 4/15/17, p. 16). But Mitalipov and colleagues explicitly conducted the experiments to improve the safety and efficiency of gene editing for eventual clinical trials, which would involve implanting edited embryos into women’s uteruses to establish pregnancy.
In the United States, such clinical trials are effectively banned by a rule that prevents the Food and Drug Administration from reviewing applications for any procedure that would introduce heritable changes in human embryos. Such tinkering with embryo DNA, called germline editing, is controversial because of fears that the technology will be used to create so-called designer babies.

“This paper is not announcing the dawn of the designer baby era,” says R. Alta Charo, a lawyer and bioethicist at the University of Wisconsin Law School in Madison. The researchers have not attempted to add any new genes or change traits, only to correct a disease-causing version of a gene.

In the study, sperm from a man who carries a mutation in the MYBPC3 gene was injected into eggs from women with healthy copies of that gene. Carrying just one mutant copy of the gene causes an inherited heart problem called hypertrophic cardiomyopathy (SN: 9/17/16, p. 8). That condition, which strikes about one in every 500 people worldwide, can cause sudden heart failure. Mutations in the MYBPC3 gene are responsible for about 40 percent of cases. Doctors can treat symptoms of the condition, but there is no cure.

Along with the man’s sperm, researchers injected into the egg the DNA-cutting enzyme Cas9 and a piece of RNA to direct the enzyme to snip the mutant copy of the gene. Another piece of DNA was also injected into the egg. That hunk of DNA was supposed to be a template that the fertilized egg could use to repair the breach made by Cas9. Instead, embryos used the mother’s healthy copy of the gene to repair the cut.

Embryos’ self-healing DNA came as a surprise, because gene editing in other types of cells usually requires an external template, Mitalipov says. The discovery could mean that it will be difficult for researchers to fix mutations in embryos if neither parent has a healthy copy of the gene. But the finding could be good news for those concerned about designer babies, because embryos may reject attempts to add new traits.

Timing the addition of CRISPR/Cas9 is important, the researchers also discovered. In their first experiments, the team added the gene editor a day after fertilizing the eggs. Of 54 injected embryos, 13 were patchwork, or mosaic, embryos with some repaired and some unrepaired cells. Such mosaic embryos probably arise when the fertilized egg copies its DNA before researchers add Cas9, Mitalipov says.

Injecting Cas9 along with the sperm — before an egg had a chance to replicate its DNA — produced only one patchwork embryo. That embryo had repaired the mutation in all its cells, but some cells used the mother’s DNA for repair while others used the template supplied by the researchers.

None of the tested embryos showed any signs that Cas9 was cutting where it shouldn’t be. “Off-target” cutting has been a safety concern with the gene editor because of the possibility of creating new DNA errors.

The study makes progress toward using gene editing to prevent genetic diseases, but there’s still has a long way to go before clinical testing can begin, says Janet Rossant, a developmental biologist at the Hospital for Sick Children and the University of Toronto. “We need to be sure this can be done reproducibly and effectively.”

I heard it for the first time a few days ago: “She’s copying me!” my 4-year-old wailed in a righteous complaint about her little sister. And she most certainly was copying, repeating the same nonsense word over and over. While it was distressing to my older kid, I thought it was funny that it took her so long to realize her sister copies almost everything she does.

This egregious violation occurred just after I had read about an experiment that pitted young kids against bonobos in a test to see who might copy other individuals more. I’ll get right to the punch line: Kids won, by a long shot. The results, published online July 24 in Child Development, show that despite imitation annoying older siblings everywhere, it’s actually really important.

“Imitation is one of the most essential skills for being human,” says study coauthor Zanna Clay, a comparative psychologist at the University of Birmingham and Durham University, both in England. Learning how to talk, operating the latest iPhone and figuring out how to buy bulk goods at the local co-op — these skills all rely on imitation. Not only that, but imitation is also important for cementing social relationships. My daughter notwithstanding, “Humans like to be imitated, and we like those who imitate us,” Clay says.
Clay and her colleague Claudio Tennie tested just how strong the urge to imitate is in 77 children ages 3 to 5 and a group of 46 bonobos ages 3 to 29. In one-on-one trials, the researchers sat next to the kids and bonobos with a small wooden box about the size of a hand. Inside was a treat: a sticker for the kids and a bit of apple for the bonobos.

Before opening the box, the researcher performed nonsensical actions over it, either rubbing the box with the back of the hand and doing a wrist twist in the air or tracing a cross into the top of the box and then tracing the edges.

These hand motions were totally irrelevant to the actual opening of the box. Nonetheless, after seeing the gestures, the vast majority of the kids made the same motions before trying to open their own box. Not a single bonobo, though, copied the irrelevant actions.
What the bonobos did — not copying the meaningless gestures — “is the rational thing to do,” says Clay. “Yet the irrational thing that the kids did is part of the reason why human cultures have evolved so rapidly and so diversely.”

Such excessive imitation, called overimitation, is a special form of copying in which people perform actions that clearly serve no purpose. It may be behind rituals, social norms and language that keep our societies running smoothly.

And it may be unique to humans: Other studies have failed to spot overimitation among chimpanzees and orangutans. These findings hint that our powerful urge to imitate even nonsensical gestures may be one of the things that separate humans from other apes.

A growing band of digital characters that converse, read faces and track body language is helping humans to communicate better with one another. While virtual helpers that perform practical tasks, such as dealing with customer service issues, are becoming ubiquitous, computer scientist M. Ehsan Hoque is at the forefront of a more emotionally savvy movement. He and his team at the University of Rochester in New York create software for digital agents that recognize when a person is succeeding or failing in specific types of social interactions. Data from face-to-face conversations and feedback from professional counselors and interviewers with relevant expertise inform this breed of computer advisers.

One of Hoque’s digital helpers grooms people to be better public speakers. With words on a screen, this attentive app notes, for example, how many times in a practice talk a person says “um,” gestures inappropriately or awkwardly shifts vocal tone. With the help of Google Glass, the app even offers useful reminders during actual speeches. Another computerized helper, this one in the form of an avatar, helps people hone their job interviewing skills, flagging long-winded responses or inconsistent eye contact in practice interviews. In the works are computerized conversation coaches that can improve speech and communication skills among people with developmental conditions such as autism and mediate business meetings in ways that encourage everyone to participate in decision making.

“There has been some progress in artificial intelligence, but not much in developing emotional aspects of AI,” Hoque says. “We’re just cracking through the surface at this point.”
The U.S. Department of Defense and the U.S. Army have taken notice. With their financial support, Hoque is developing avatars that collaborate with humans to solve complex problems, and digital observers that monitor body language to detect when people are lying.
This is heady stuff for a 35-year-old who earned a doctoral degree just four years ago. Hoque, who was born in Bangladesh and immigrated to the United States as a teenager, did his graduate work with the MIT Media Lab’s Affective Computing research group. The group’s director, Rosalind Picard, helped launch the field of “affective computing” in the 1990s, which focuses on the study and development of computers and robots that recognize, interpret and simulate human emotions.

Hoque’s approach puts a service spin on affective computing. As a grad student, he developed software he dubbed MACH, short for My Automated Conversation coacH. This system simulates face-to-face conversations with a computer-generated, 3-D man or woman that sees, hears and makes decisions while conversing with a real-life partner. Digital analyses of a human partner’s speech and nonverbal behavior inform the avatar’s responses during a session. A simulated coach may, for instance, let a user know if smiles during an interview look forced or are mistimed. After a session, users see a video of the interaction accompanied by displays of how well or poorly they did on various interaction skills, such as keeping eye contact and nodding at appropriate times.

MACH got its start in trials that trained MIT undergraduates how to conduct themselves during interviews with career counselors. First, Hoque analyzed smiles and other behaviors that either helped or hurt the impressions job candidates left on experienced counselors in mock interviews. In a series of follow-up studies, his team developed an automated system that recognized impression-enhancing behaviors during simulated interviews. That pilot version of MACH was then put to the test. Women, but not men, who received MACH training and got feedback from their digital coach while watching videos of their initial interviews with a counselor displayed substantial improvement in follow-up interviews. MACH trainees who watched interview videos but got no feedback showed minimal improvement. Testing with larger groups of men and women is under way.
As he developed MACH, Hoque consulted MIT sociologist and clinical psychologist Sherry Turkle. That was a bold move, since Turkle has warned for 30 years that, despite its pluses, digital culture discourages person-to-person connections. Social robots, in particular, represent a way for people to escape the challenges of forging authentic relationships, Turkle contends.

But she came away impressed with Hoque, whose goals she calls refreshingly modest and transparent. “His avatars will be helpers and facilitators,” she says, “not companions, friends, therapists and pretend people.”

Hoque’s approach grew out of personal experience. He is the primary caregiver for his 16-year-old brother, Eshteher, who has Down syndrome and does not speak. Eshteher can make sounds to refer to certain things, such as food, and has limited use of sign language. “I’ve spent a lot of time with him and can read what he’s experiencing, like when he’s frustrated or repentant,” Hoque says.
So it’s not surprising that Hoque’s next-generation MACH, dubbed LISSA for Live Interactive Social Skill Assistance, is an avatar that conducts flexible, “getting acquainted” conversations while providing feedback on users’ eye contact, speaking volume, smiling and body movements via flashing icons.

LISSA has shown promise in preliminary tests aimed at improving the conversational chops of college students attending speed-dating sessions and individuals with autism spectrum disorders. Hoque plans to expand this technology for use with people suffering from social phobia and post-traumatic stress disorder. He’s also working on an avatar that trains doctors to communicate clearly and compassionately with patients being treated for life-threatening cancers.

Hoque’s work on emotionally perceptive avatars may eventually transform the young industry of digital assistants, currently limited to voices-in-a-box such as Apple’s Siri and Microsoft’s Cortana, says cognitive scientist Mary Czerwinski, a principal researcher at Microsoft Research Lab in Redmond, Wash. Avatar research “could lead to more natural, personable digital assistants,” Czerwinski predicts. Hoque agrees.

“In the future, we’ll all have digital, personalized assistants,” he says. If he gets his way, emotionally attuned helpers will make us more social and less isolated. That’s something to applaud — if we can manage to put down our smartphones.

One of the planet’s deadliest viruses makes an annual pass through the United States with little fanfare. It rarely generates flashy headlines or news footage of health workers in hazmat suits. There’s no sudden panic when a sick person shows up coughing and feverish in an emergency room. Yet before next spring, this season’s lethal germ will probably have infected millions of Americans, killing tens of thousands. Still, it’s often referred to as just the flu.

The influenza virus seems so normal to most Americans that only about half of us will heed those “time for your flu shot” banners that pop up at pharmacies and worksites every autumn. Those annual shots remain the best means of protection, but they must be manufactured months before flu season starts, based on a best educated guess of what strains of the virus will be circulating. That means even in a successful year, vaccine performance may not be impressive. During the 2015–2016 season, only about half of those immunized were protected, according to a study in the Aug. 10 New England Journal of Medicine. Some years’ vaccines are duds: For the 2014–2015 season, the vaccine protected only 19 percent of people who received it, based on U.S. Centers for Disease Control and Prevention data.
Scientists have long worked to develop a flu shot that works better and lasts longer. But, unlike the very stable measles virus, influenza is a moving target. While only a few strains of flu virus circulate worldwide in a typical year, dozens more may exist. Each one is highly likely to mutate from year to year, with just enough shape-shifting to be unrecognizable to the body’s defenses.

Now, after years of searching, scientists believe they have better strategies to attack the parts of the virus that stay the same from year to year, offering the hope of protection across multiple seasons. The vaccines being developed in laboratories around the world “offer more promise than we’ve ever had,” says Walter Orenstein, associate director of the Emory Vaccine Center in Atlanta. And there are new creative approaches: One research group is trying to make a kind of super shot by anticipating every possible mutation a circulating virus might undergo.

“I’m optimistic we are going to get to a vaccine,” says Anthony Fauci, head of the National Institute of Allergy and Infectious Diseases, or NIAID, in Bethesda, Md. Then, you may need to heed those “time for your flu shot” messages only once.
Researchers often describe the flu virus as looking like a ball with lollipops sticking out. Tucked inside the ball is RNA, which the virus needs to make copies of itself. The lollipops on the outside are proteins: hemagglutinin and neuraminidase. There are 18 different kinds of hemagglutinin and 11 kinds of neuraminidase. Each kind of flu virus is named for its particular combination of these proteins; the current forms circulating around the world are H1N1 and H3N2. Hemagglutinin attaches to human cells to launch an infection; neuraminidase is more important for spreading the virus once infection has occurred.

Flu viruses involved in human epidemics are divided into types A and B, and A viruses are sliced even further into group 1 and group 2. Influenza A, the most troublesome for vaccine scientists, travels the world among birds, pigs and humans. The bird and pig versions don’t easily infect people, but the virus is constantly mutating and even swapping genes with other influenza viruses it meets along the way. Sometimes these genetic changes create a version that allows a bird or pig flu to move directly into humans. In 2013, one called H7N9 moved into people in China (SN Online: 3/11/15). The virus has since infected more than 1,500 people. Mostly, though, the genetic changes are more subtle, with just enough alterations to evade the human immune system.
Like kids with a sweet tooth, the immune system gets most excited about the top part of the hemagglutinin lollipop, and makes antibodies against it. The top is, after all, the first thing the immune system notices once the virus slips inside the nose, mouth and lungs. Every year, genetic mutations in the virus slightly change the chemical flavor of the lollipop, making it more sweet or sour than last season’s — just different enough so the immune system doesn’t recognize it. That’s why most years there’s a new flu shot.

Sometimes, in the gene shuffling with viruses in birds and pigs, the changes are so great that the flavor changes completely. Those are pandemic years, when there is so little residual immunity that a large portion of the global population falls ill from the new virus. The devastating 1918 flu, which killed an estimated 50 million people globally, was caused by such a drastic genetic shift (SN Online: 4/29/14). The most recent pandemic occurred in 2009, with the appearance of the “swine flu,” so named because the virus was first found in pigs. By one analysis, it caused between 148,000 and 249,000 deaths around the world.

Attack the stem
The 2009 disaster helped provide a blueprint for some of the latest experimental vaccines. Researchers noticed that when people with swine flu developed antibodies to the virus, those antibodies did something odd: They favored the hemagglutinin stem — the stick of the lollipop. And, more important, they appeared to react broadly against two kinds of flu virus. Scientists had known that the hemagglutinin stem, or stalk, isn’t as apt to change as the lollipop top, which theoretically makes the stem a good target for a universal vaccine. But in a usual flu season, the human body isn’t inclined to make infection-fighting antibodies against the stem.

“Unfortunately, the immune system preferentially recognizes the head, and we don’t know why it does that,” says Adrian McDermott, an immunologist at NIAID. So after infection, the biggest share of antibodies flocks to the hemagglutinin head. (Neuraminidase, the bigger player in disease after infection, is a target for influenza treatments but not a major focus for vaccine development.)

But in a study reported in the Journal of Experimental Medicine in 2011, a team of scientists from Emory and elsewhere found that antibodies to the so-called swine flu behaved unexpectedly. “If you have a head that the immune system hasn’t seen, you potentially redirect to a stalk response,” McDermott says. “That was an aha! moment.”
Researchers investigated further. For one study in 2012 in Frontiers in Immunology, scientists from Canada injected these stem-recognizing antibodies into mice to see if the mice were shielded from a different strain of flu. Not only were the mice protected from lethal doses of flu virus, but the protection was also in large part due to the absence of familiar antibodies against the head, the researchers found. Without the distraction of a head it recognized, the immune system seemed to rally against the stem.

Then came the what ifs: What if a vaccine produced just antibodies to the stem? Would that be enough protection? For the last few years, McDermott and others have been trying to develop vaccines made of “headless stalks” — just the sticks of the lollipops. With no head in place to hoard the immune response, the vaccine might coax the body to make enough stem-focused antibodies to protect against flu, the researchers hoped, regardless of the seasonal mutations occurring at the top.

Several groups soon found that headless stalks are difficult to make. Without the top to stabilize it, the molecular assembly tended to break apart. Two teams working independently reported in 2015 their success in keeping the stalk in one piece. NIAID scientists and their partners held the stalks together by anchoring them to the protein ferritin, which can assemble itself into nanoparticles. In a study in Nature Medicine, the team reported that vaccinated mice and ferrets appeared to be protected from dying of the H5N1 bird flu after receiving the vaccine, even when they developed symptoms. Unvaccinated mice and ferrets died.

The second team, from the Janssen Center of Excellence for Immunoprophylaxis in Leiden, the Netherlands, and the Scripps Research Institute in La Jolla, Calif., glued the stalk together by creating a series of genetic mutations at its top. In Science, the researchers reported that the vaccine reduced the symptoms of flu in vaccinated monkeys.

“We realized that the stem has much less variability than the head, and then we developed the capability to use it for a possible vaccine,” says Fauci, commenting on both efforts. “These were two important things that came together.”

Despite progress, these stalk-focused vaccines haven’t yet been put to human tests that would show whether they could protect broadly against many mutations of flu circulating annually, which is the ultimate test. And some stalk-directed antibodies might be better than others. In July in Science Immunology, McDermott and colleagues reported that the stalk antibodies against group 2 of the A viruses appear to be more broadly effective than those against group 1 viruses.

Other researchers have stabilized the stalk by attaching a new hemagglutinin head — a lollipop flavor that the human immune system has never tasted. In this case, researchers from the Icahn School of Medicine at Mount Sinai in New York City took tops from two flu strains that circulate only in birds, and connected each one to a human hemagglutinin stalk. This experimental vaccine consists of two doses. The first dose prompts the immune system to make antibodies against the stalk with the first top, and a second dose produces a second round of antibodies against the stalk with the second top. The idea is that the abundance of stem-focused antibodies — amplified from the two shots of vaccine — will come to the rescue during a natural infection from a virus that possesses a third, totally different head.
“The human immune system will try to find something it has seen before,” says Peter Palese, chairman of microbiology at Mount Sinai. In theory, the only antibodies in play will be the ones responding to the parts of the stalk that the immune system recognizes, known as the “conserved domains.”

“The $64,000 question,” according to Palese: “Will the immune response to these conserved domains be enough to elicit a broad immune system reaction?”

In 2016, Palese and colleagues described a test of the vaccine in the Journal of Virology. Six ferrets given the two doses were housed with six ferrets infected with H1N1 flu. Within 10 days, the vaccinated animals had become infected but had no symptoms or signs of being able to easily spread virus to others. A report in June in the same journal described tests of the vaccine in mice against influenza B viruses; the animals were protected from normally lethal doses of flu.

What’s not known is whether the stem-focused antibodies are enough to protect people from all virus variants. The vaccine from the Mount Sinai researchers is entering the first human safety trials with drugmaker GlaxoSmithKline.

Unhide and seek
Another approach incorporates proteins that don’t tend to mutate like the hemagglutinin head but are hidden from the immune system under normal circumstances. When these proteins are made visible to types of white blood cells called T cells, the immune system wakes up. T cells don’t make antibodies, but certain T cells hold on to a memory of foreign molecules seen before. When these pre-programmed T cells recognize an infection, they destroy the invader.

This work began in the 1990s, when researchers at the Weizmann Institute of Science in Rehovot, Israel, set out to find parts of the virus that remain unchanged from year to year. The team identified stable regions in three proteins — hemagglutinin, plus one from the virus membrane and one from the virus core. In 2003, a company called BiondVax Pharmaceuticals formed to develop and test, in humans, an experimental vaccine that takes these proteins and packages them in a way that the immune system can recognize them.

So far, almost 700 volunteers have participated in six small trials, all of which showed signs of a lasting immune response among most volunteers. Writing in February in Vaccine, the researchers reported that the stored serum of elderly volunteers who received the vaccine in 2011 showed an immune response to new strains of flu that were circulating three years later. The company is starting larger trials to see if the vaccine can actually protect people from getting sick.
Out of many, one
Other experimental vaccines take a different approach. Rather than relying on precision to hit a narrow target, microbiologist Ted Ross and colleagues at the University of Georgia in Athens are attempting to cast a wide net. The researchers are taking hemagglutinin mutations from every flu strain that has ever circulated, dumping them into a kind of scientific blender and attaching them to particles that can form the basis of a vaccine.

“The question we asked is, how can we make a vaccine against a strain we don’t even know exists?” Ross says. The technique he uses is called COBRA for computationally optimized broadly reactive antigen. A computer compiles all seemingly possible genetic iterations of a particular flu type — in this case H1N1 — and then bundles them into one molecule. It’s kind of like taking every novel in your local library and combining them into one giant book.

Last year in the Journal of Virology, Ross and colleagues described a COBRA-derived vaccine that represented almost all forms of H1N1 that have been around for the last 100 years. The vaccine protected mice against infection from strains of H1N1 that the mice had never been exposed to. “We took a bunch of different hemagglutinins and mixed them into one hemagglutinin molecule,” Ross says. “It protected against any strain of H1N1 we could throw at it.”

The study caught the attention of vaccine maker Sanofi Pasteur, which plans to test the vaccine in clinical trials. Ross’ lab is now using the same strategy to develop a vaccine against H3N2 strains, the other dominant kind of flu circulating around the world. Same approach, different library.

Meanwhile, the virus isn’t waiting around. Based on the heavy flu season in the Southern Hemisphere, some experts are predicting this year’s epidemic could be severe. It’s still too early to know whether the current vaccine will provide good protection, but someday, a super shot may remove the guesswork altogether.

To craft a new color-switching material, scientists have again taken inspiration from one of nature’s masters of disguise: the chameleon.

Thin films made of heart cells and hydrogel change hues when the films shrink or stretch, much like chameleon skin. This material, described online March 28 in Science Robotics, could be used to test new medications or possibly to build camouflaging robots.

The material is made of a paper-thin hydrogel sheet engraved with nanocrystal patterns, topped with a layer of living heart muscle cells from rats. These cells contract and expand — just as they would inside an actual rat heart to make it beat — causing the underlying hydrogel to shrink and stretch too. That movement changes the way light bounces off the etched crystal, making the material reflect more blue light when it contracts and more red light when it’s relaxed.
This design is modeled after nanocrystals embedded in chameleon skin, which also reflect different colors of light when stretched (SN Online: 3/13/15).

When researchers treated the material with a drug normally used to boost heart rate, the films changed color more quickly — indicating the heart cells were pulsating more rapidly. That finding suggests the material could help drug developers monitor how heart cells react to new medications, says study coauthor Luoran Shang, a physicist at Southeast University in Nanjing, China. Or these kinds of films could also be used to make color-changing skins for soft robots, Shang says.

The center of the Milky Way may be abuzz with black holes. For the first time, a dozen small black holes have been spotted within the inner region of the galaxy in an area spanning just a few light-years — and there could be thousands more.

Astrophysicist Charles Hailey of Columbia University and his colleagues spotted the black holes thanks to the holes’ interactions with stars slowly spiraling inward, the team reports in Nature on April 4. Isolated black holes emit no light, but black holes stealing material from orbiting stars will heat that material until it emits X-rays.
In 12 years of telescope data from NASA’s orbiting Chandra X-ray Observatory, Hailey and colleagues found 12 objects emitting the right X-ray energy to be black holes with stellar companions. Based on theoretical predictions of how many black holes are paired with stars, there should be up to 20,000 invisible solo black holes just in that small part of the galaxy.
The discovery follows decades of astronomers searching for small black holes in the galactic center, where a supermassive black hole lives (SN: 3/4/17, p. 8). Theory predicted that the galaxy should contain millions or even 100 million black holes overall, with a glut of black holes piled up near the center (SN: 9/16/17, p. 7). But none had been found.
“It was always kind of a mystery,” Hailey says. “If there’s so many that are supposed to be jammed into the central parsec [about 3.26 light-years], why haven’t we seen any evidence?” Finding the 12 was “really hard,” he admits.

It’s unclear how the black holes got to the galaxy’s center. Gravity could have tugged them toward the supermassive black hole. Or a new theory from Columbia astronomer Aleksey Generozov suggests black holes could be born in a disk around the supermassive black hole.

The researchers ruled out other objects emitting X-rays, such as neutron stars and white dwarfs, but acknowledged that up to half of the sources they found could be fast-spinning stellar corpses called millisecond pulsars rather than black holes. That could add to the debate over whether a mysterious excess in gamma rays at the galactic center is from pulsars or dark matter (SN: 12/23/17, p. 12).

“The theorists are going to have to slug it out and figure out what’s going on,” Hailey says.

Every few years, a buzz fills the air in the southeastern United States as adolescent cicadas crawl out from the soil to molt and make babies. After a childhood spent sipping tree sap underground, some species emerge every 13 years, others every 17 years, rarely overlapping. Yet somehow in this giant cicada orgy, hybridization happens between species that should be out of sync.

Researchers have sought to explain how the two life cycle lengths developed. A new study published online April 19 in Communications Biology fails to pin the difference on genetics, but finds some interesting things along the way.
Cicadas fall into three species groups that diverged from one another about 3.9 million to 2.5 million years ago. Within each of those groups, species on a 13-year schedule diverged from 17-year-cycle cicadas about 200,000 to 100,000 years ago, the researchers from the United States and Japan report.

But the researchers also found that the 17-year and 13-year broods within each group share genetic code — evidence of hybridization. It’s possible that neighboring broods swapped DNA when their emergence overlapped — something that happens every 221 years — or if stragglers emerged early or late.