A doctor explains to a young couple that he has screened the pair’s in vitro fertilized embryos and selected those that had no major inheritable diseases. The couple had specified they want a son with hazel eyes, dark hair and fair skin. Then the doctor announces that he has also taken the liberty of eliminating the “burden” of genetic propensities for baldness, nearsightedness, alcoholism, obesity and domestic violence.

The prospective mother replies that they didn’t want those revisions. “I mean diseases, yes, but …” Her husband jumps in to say, “We were just wondering if it’s good to leave a few things to chance.”
But the doctor reminds the would-be parents why they came to him in the first place. They want to give their child “the best possible start.”

That’s a scene from the movie Gattaca, which premiered 20 years ago in October. But thanks to recent advances in gene-editing tools such as CRISPR/Cas9, genetic manipulation of human embryos is becoming reality.

Soon, designer babies like those described in the film may even become morally mandatory, some ethicists say.

Gattaca’s narrator tells us that such genetic manipulation of in vitro fertilized embryos has become “the natural way of giving birth” in the near future portrayed in the film. It has also created an underclass of people whose parents didn’t buy those genetic advantages for their children.
Until recently, that sort of fiddling with human DNA was only science fiction and allegory, a warning against a new kind of eugenics that could pit the genetic haves and have-nots against each other. At a symposium sponsored by the Hastings Center on October 26 before the World Conference of Science Journalists in San Francisco, ethicists and journalists explored the flip side of that discussion: whether parents have a moral obligation to make “better” babies through genetic engineering. Technology that can precisely change a baby’s genes is quickly becoming reality. This year, scientists reported using CRISPR/Cas9 in viable human embryos to fix mutations that cause heart and blood disorders. CRISPR/Cas9 acts as a molecular scissors that relatively easily and precisely manipulates DNA. Scientists have honed and developed the tool in the roughly five years it has been around, creating myriad “CRISPR” mice, fish, pigs, cows, plants and other creatures. Its use in human embryos has been hotly debated. Should we or shouldn’t we?

For many people, the fear of a class of genetically enhanced people is reason enough not to tinker with the DNA of the human germline — eggs, sperm, embryos and the cells that give rise to eggs and sperm. By all means, correct diseases, these folks say, but don’t add extras or meddle with characteristics that don’t have anything to do with health. A panel of ethicists convened by the U.S. National Academies of Medicine and Science also staked out that position in February, ruling that human germline engineering might someday be permissible for correcting diseases, but only if there are no alternatives and not for enhancements.

But the question “should we?” may not matter much longer, predicted the Hastings Center’s Josephine Johnston at the symposium. As science advances and people become more comfortable with gene editing, laws prohibiting tinkering with embryos will fall, she said, and it will be up to prospective moms and dads to decide for themselves. “Will editing a baby’s genes be mandatory, the kind of thing you’re supposed to do?”

For Julian Savulescu, an ethicist at the University of Oxford, the answer is yes. Parents are morally obligated to take steps to keep their children healthy, he says. That includes vaccinating them and giving them medicine when they’re ill. Genetic technologies are no different, he argues. If these techniques could make children resistant to infections, cancer or diabetes, then parents have an obligation to use them, he says.

For now, he cautions, CRISPR’s safety and efficacy haven’t been established, so parents shouldn’t subject their children to the risks. He also points out that this sort of editing would also require in vitro fertilization, which is prohibitively costly for many people. (And couples could pretty much forget about having the perfect baby through sexual intercourse. Designer darlings would have to be created in the lab.)

But someday, possibly soon, gene editing could become a viable medical intervention. “If CRISPR were safe and not excessively costly, we have a moral obligation to use it to prevent and treat disease,” Savulescu says.

Using gene editing to cure genetic diseases is something retired bioethicist Ronald Green of Dartmouth College can get behind. “I fully support the reproductive use of gene-editing technology for the prevention and elimination of serious genetic diseases,” Green said at the symposium. “If we could use gene editing to remove the sequences in an embryo that cause sickle cell disease or cystic fibrosis, I would say not only that we may do so, but in the case of such severe diseases, we have a moral obligation to do so.”

But that’s where a parent’s obligation stops, Green said. Parents and medical professionals aren’t required to enhance health “to make people who are better than well,” he said.

Savulescu, however, would extend the obligation to other nondisease conditions that could prevent a kid from having a full set of opportunities in life. For instance, children with poor impulse control may have difficulty succeeding in school and life. The drug Ritalin is sometimes prescribed to such kids. “If CRISPR could do what Ritalin does and improve impulse control and give a child a greater range of opportunities,” he says, “then I’d have to say we have the same moral obligation to use CRISPR as we do to provide education, to provide an adequate diet or to provide Ritalin.”

Green rejected the idea that parents should, or even could, secure a better life for their kids through genetic manipulation. Scientists haven’t identified all the genes that contribute to good lives — and there are plenty of factors beyond genetics that go into making someone happy and successful. Already, Green said, “the healthy natural human genome has enough variety in it to let any child successfully navigate the world and fulfill his or her own vision of happiness.” (A version of his remarks was posted on the Hastings Center’s Bioethics Forum.)

Many traits that would help a person make more money or have an easier life are associated with social prejudices and discrimination, says Marcy Darnovsky, the executive director of the Center for Genetics and Society in Berkeley, Calif. People who are taller and fair-skinned tend to make more money. If parents were to engineer their children to have such traits, “I think we would be inscribing those kinds of social prejudices in biology,” she says. “We get to very troubled waters very quickly as a society once we start down that road.”

Creating a class of “genobility,” as Green calls genetically enhanced people, would increase already staggering levels of inequality, Darnovsky says. That, says Savulescu, “is the Gattaca objection I often get.”

Yes, he acknowledges, “it could create even greater inequalities, there’s no doubt about that.” Whenever money is involved, people who have more of it can afford better treatments, diets and healthier lifestyles — and disparities will exist. “However, this is not inevitable,” Savulescu says. Countries with national health care systems could provide such services for free. Such measures could even correct natural inequalities, he argues.

Johnston worries that genetic manipulation could change family dynamics. Parents might be disappointed if their designer baby doesn’t turn out as desired. That’s a variation of the old problem of unfulfilled parental expectations, Savulescu says. “It’s a problem that deserves attention, but it’s not a problem that deserves banning CRISPR,” he says.

A misfit gang of superconducting materials may be losing their outsider status.

Certain copper-based compounds superconduct, or transmit electricity without resistance, at unusually high temperatures. It was thought that the standard theory of superconductivity, known as Bardeen-Cooper-Schrieffer theory, couldn’t explain these oddballs. But new evidence suggests that the standard theory applies despite the materials’ quirks, researchers report in the Dec. 8 Physical Review Letters.

All known superconductors must be chilled to work. Most must be cooled to temperatures that hover above absolute zero (–273.15° Celsius). But some copper-based superconductors work at temperatures above the boiling point of liquid nitrogen (around –196° C). Finding a superconductor that functions at even higher temperatures — above room temperature — could provide massive energy savings and new technologies (SN: 12/26/15, p. 25). So scientists are intent upon understanding the physics behind known high-temperature superconductors.
When placed in a magnetic field, many superconductors display swirling vortices of electric current — a hallmark of the standard superconductivity theory. But for the copper-based superconductors, known as cuprates, scientists couldn’t find whirls that matched the theory’s predictions, suggesting that a different theory was needed to explain how the materials superconduct. “This was one of the remaining mysteries,” says physicist Christoph Renner of the University of Geneva. Now, Renner and colleagues have found vortices that agree with the theory in a high-temperature copper-based superconductor, studying a compound of yttrium, barium, copper and oxygen.

Vortices in superconductors can be probed with a scanning tunneling microscope. As the microscope tip moves over a vortex, the instrument records a change in the electrical current. Renner and colleagues realized that, in their copper compound, there were two contributions to the current that the probe was measuring, one from superconducting electrons and one from nonsuperconducting ones. The nonsuperconducting contribution was present across the entire surface of the material and masked the signature of the vortices.

Subtracting the nonsuperconducting portion revealed the vortices, which behaved in agreement with the standard superconductivity theory. “That, I think, is quite astonishing; it’s quite a feat,” says Mikael Fogelström of Chalmers University of Technology in Gothenburg, Sweden, who was not involved with the research.
The result lifts some of the fog surrounding cuprates, which have so far resisted theoretical explanation. But plenty of questions still surround the materials, Fogelström says. “It leaves many things still open, but it sort of gives a new picture.”

One person infected with strep bacteria might get a painful sore throat; another might face a life-threatening blood infection. Now, scientists are trying to pin down why.

Variation between individuals’ immune systems may not be entirely to blame. Instead, extra genes picked up by some pathogens can cause different strains to have wildly different effects on the immune system, even in the same person, researchers report January 11 in PLOS Pathogens.

The idea that different strains of bacteria can behave differently in the body isn’t new. Take E. coli: Some strains of the bacteria that can cause foodborne illness make people far sicker than other strains­. But bacteria have exceptionally large amounts of genetic variation, even between members of the same species. Scientists are still trying to figure out how that genetic diversity affects the way microbes interact with the immune system.
Any species of bacteria has a core set of genes that all its members share. Then there’s a whole pot of genes that different strains of the species pick and choose to create what’s known as an accessory genome. These genes are custom add-ons that specific strains have acquired over time, from their environment or from other microbes — something like an expansion pack for a card game. Sometimes, that extra genetic material gives bacteria new traits.

Uri Sela and his colleagues at the Rockefeller University in New York City tested the way these extra genes influenced the way two common species of bacteria, Staphylococcus aureus and Streptococcus pyogenes, interacted with the immune system. Staphylococcus bacteria can cause everything from rashes to food poisoning to blood infections. Streptococcus bacteria can cause strep throat, as well as a host of more serious illnesses (SN: 10/4/14, p. 22).

Different strains of the same species provoked wildly different immune responses in blood samples collected from the same patient, the researchers first showed. But the strain-specific responses were consistent across patients. Some strains triggered lots of T cells to be made in every sample, for example; others increased B cell activity. (T cells and B cells are the two main weapons of the adaptive immune response, which enables the body to build long-lasting immunity against a particular pathogen.) In tests of strains missing some of their extra genes, though, the T cells didn’t respond as strongly as they did to a matching strain that contained the extra genes. This finding suggests that the variation in immune response across strains was coming, at least in part, from differences in these supplementary genes.
“Currently when a patient comes to the hospital with an infection, we don’t define the strain of the species” for common infections like strep and staph, says Sela, an immunologist. In the future, he says, information about the strain could help doctors predict how a patient’s illness will unfold and decide on the best treatment.

The new study “adds fuel to an active debate” about the role of accessory genes, says Alan McNally, a microbiologist at the University of Birmingham in England — whether or not the collections of genetic add-ons that bacteria maintain are shaped by natural selection, the process that fuels evolution. This research suggests that for some kinds of bacteria, genetic customization might aid survival of certain strains by enabling them to provoke a tailored immune response.

But more research needs to be done to link the strain-to-strain variation in immune response to the accessory genome, he says, as this study looked at only a few extra genes, not the entire accessory genome.

Volcano-fueled holes in Earth’s ozone layer 252 million years ago may have repeatedly sterilized large swaths of forest, setting the stage for the world’s largest mass extinction event. Such holes would have allowed ultraviolet-B radiation to blast the planet. Even radiation levels below those predicted for the end of the Permian period damage trees’ abilities to make seeds, researchers report February 7 in Science Advances.

Jeffrey Benca, a paleobotanist at the University of California, Berkeley, and his colleagues exposed plantings of modern dwarf pine tree (Pinus mugo) to varying levels of UV-B radiation. Those levels ranged from none to up to 93 kilojoules per square meter per day. According to previous simulations, UV-B radiation at the end of the Permian may have increased from a background level of 10 kilojoules (just above current ambient levels) to as much as 100 kilojoules, due to large concentrations of ozone-damaging halogens spewed from volcanoes (SN: 1/15/11, p. 12).

Exposure to higher UV-B levels led to more malformed pollen, the researchers found, with up to 13 percent of the pollen grains deformed under the highest conditions. And although the trees survived the heightened irradiation, the trees’ ovulate cones — cones that, when fertilized by pollen, become seeds — did not. But the trees weren’t permanently sterilized: Once removed from extra UV-B exposure, the trees could reproduce again.

The finding supports previous research suggesting that colossal volcanic eruptions in what’s now Siberia, about 300,000 years before the onset of the extinction event, probably triggered the die-off of nearly all marine species and two-thirds of species living on land (SN: 9/19/15, p. 10). Repeated pulses of volcanism at the end of the Permian may have led to several periods of irradiation that sterilized the forests, causing a catastrophic breakdown of food webs, the researchers say — an indirect but effective way to kill.

AUSTIN, Texas — Stretchy sensors that stick to the throat could track the long-term recovery of stroke survivors.

These new Band-Aid‒shaped devices contain motion sensors that detect muscle movement and vocal cord vibrations. That sensor data could help doctors diagnose and monitor the effectiveness of certain treatments for post-stroke conditions like difficulty swallowing or talking, researchers reported February 17 in a news conference at the annual meeting of the American Association for the Advancement of Science. Up to 65 percent of stroke survivors have trouble swallowing, and about a third of survivors have trouble carrying on conversations.
The devices can monitor speech patterns more reliably than microphones by sensing tissue movement rather than recording sound. “You don’t pick up anything in terms of ambient noise,” says study coauthor John Rogers, a materials scientist and bioengineer at Northwestern University in Evanston, Ill. “You can be next to an airplane jet engine. You’re not going to see that in the [sensor] signal.”

Developed by Rogers’ team, the sensors have built-in 12-hour rechargeable batteries and continually stream motion data to a smartphone. Researchers are now testing the sensors with real stroke patients to see how the devices can be made more user-friendly. For instance, Rogers’ team realized that patients were unlikely to wear sensors that were too easily visible. By equipping the patches with more sensitive motion sensors, they can be worn lower on a person’s neck, hidden behind a buttoned-up shirt, and still pick up throat motion.

These kinds of sensors could also track the recovery of neck cancer patients, who commonly develop swallowing and speaking problems caused by radiation therapy and surgery, Rogers says. The devices can also measure breathing and heart rates to monitor sleep quality and help diagnose sleep apnea. Rogers expects this wearable tech to be ready for widespread use within the next year or two.

With fevers, chills and aches, the flu can pound the body. Some influenza viruses may hammer the brain, too. Months after being infected with influenza, mice had signs of brain damage and memory trouble, researchers report online February 26 in the Journal of Neuroscience.

It’s unclear if people’s memories are affected in the same way as those of mice. But the new research adds to evidence suggesting that some body-wracking infections could also harm the human brain, says epidemiologist and neurologist Mitchell Elkind of Columbia University, who was not involved in the study.
Obvious to anyone who has been waylaid by the flu, brainpower can suffer at the infection’s peak. But not much is known about any potential lingering effects on thinking or memory. “It hasn’t occurred to people that it might be something to test,” says neurobiologist Martin Korte of Technische Universität Braunschweig in Germany.

The new study examined the effects of three types of influenza A — H1N1, the strain behind 2009’s swine flu outbreak; H7N7, a dangerous strain that only rarely infects people; and H3N2, the strain behind much of the 2017–2018 flu season misery (SN: 2/17/18, p. 12). Korte and colleagues shot these viruses into mice’s noses, and then looked for memory problems 30, 60 and 120 days later.

A month after infection, the mice all appeared to have recovered and gained back weight. But those that had received H3N2 and H7N7 had trouble remembering the location of a hidden platform in a pool of water, the researchers found. Mice that received no influenza or the milder H1N1 virus performed normally at the task.
Researchers also studied the brain tissue of the infected mice under a microscope and found that the memory problems tracked with changes in nerve cells. A month after H7N7 or H3N2 infection, mice had fewer nerve cell connectors called dendritic spines on cells in the hippocampus, a brain region involved in memory. Electrical experiments on the nerve cell samples in dishes also suggested the cells’ signal-sending abilities were impaired.
What’s more, these mice’s brains looked inflamed under the microscope, full of immune cells called microglia that were still revved up 30 and 60 days after infection. Cell counts revealed that mice that had suffered through H3N2 or H7N7 had more active microglia than mice infected with H1N1 or no virus at all. That lingering activity was surprising, Korte says; most immune cells in the body usually settle down soon after an infection clears.

These memory problems and signs of brain trouble were gone by 120 days, which translates to about a decade in human time, Korte says. “I’m not saying that everyone who has influenza is cognitively impaired for 10 years,” he says, noting that human brains are much more complex than those of mice. “The news is more that we should not only look at lung functionality after the flu, but also cognitive effects, weeks and months after infection.”

H7N7 can infect brain cells directly. But H1N1 and H3N2 don’t typically get into the brain (and Korte and colleagues confirmed that in their experiments). Some flu viruses may be causing brain trouble remotely, perhaps through inflammatory signals in the blood making their way into the brain, the study suggests. If that pathway is confirmed, then many types of infections could cause similar effects on the brain. “It is plausible that this is a general phenomenon,” Elkind says.

Deep in the Bale Mountains of Ethiopia, wildlife workers trek up above 9,800 feet to save some of the world’s most rare carnivores, Ethiopian wolves.

“It’s cold, tough work,” says Eric Bedin, who leads the field monitoring team in its uphill battle.

In this sparse, sometimes snowy landscape, the lanky and ginger-colored wolves (Canis simensis) reign as the region’s apex predators. Yet the combined threats of rabies, canine distemper and habitat reduction have the animals cornered.

Bedin and his colleagues, traveling by horse and on foot through dramatically shifting temperatures and weather, track these solitary hunters for weeks at a time. Team members know every wolf in most packs in these mountains. The team has vaccinated some wolves against rabies, only to have hopes dashed when the animals died of distemper months later.
“These guys work their asses off to protect these wolves,” says Claudio Sillero, a conservation biologist at the University of Oxford who heads up the Ethiopian Wolf Conservation Programme, of which the field monitoring team is an integral part. Down the line, humans stand to benefit from all this work too.

Sillero and his colleagues have been at this for 30 years. They’ve seen four major outbreaks of rabies alone, each leaving dozens of carcasses across the highlands and cutting some populations by as much as 75 percent.

Today, fewer than 500 Ethiopian wolves exist — around half of them in the Bale Mountains. A new oral rabies vaccine program aims to give the endangered animals a fighting chance. It may be their best hope for survival, Sillero says.

Later this year, if all goes well, oral vaccines hidden in hunks of goat meat will be scattered across wolf ranges and eaten by the animals. One dose every two years should bolster immunity against rabies among these iconic animals immortalized on several of their country’s postage stamps.
One Health
Vaccinating endangered animals en masse in the wild is rarely attempted. Making the case for vaccination takes years of testing. And even when the case is strong for stepping in, the tools needed to vaccinate wildlife aren’t often available, says Tonie Rocke, an epizootiologist with the U.S. Geological Survey in Madison, Wis. On the opposite side of the globe from Bale, on North America’s Great Plains, Rocke’s lab is testing an oral vaccine to protect prairie dogs and endangered ferrets from plague.
A recent synergy has made these new oral vaccine efforts possible: improvements in vaccine technology (developed for humans and domesticated animals) and growing public and scientific interest in “One Health.” The conservation buzzword refers to efforts to help one species that also benefit others, including humans.

The researchers pushing for a green light in Ethiopia point to the one shining success in oral vaccines for wild animals, and to its One Health benefits. From 1978 to 2010, oral vaccines sprinkled across parts of Europe eliminated rabies in red foxes. Europe’s rabies cases in humans and other animals dropped by 80 percent from 1984 to 2014. But rabies is still common in certain parts of the world, including Ethiopia. Worldwide, more than 59,000 people die from the disease each year.

Successes on the plateaus of Bale and the prairies of North America could open the door for other vaccines to protect threatened species. Vaccines against Ebola in great apes and white-nose syndrome in bats are in the works.

But introducing vaccines into natural environments is a hard sell and can come with controversy and unexpected consequences.
A last resort
To the average U.S. vet or dog owner, vaccination is a no-brainer. But for endangered species, the stakes are high. Some conservationists are reluctant to intervene with disease-preventing vaccines in the wild, says Karen Laurenson, an epidemiologist and veterinarian with the Frankfurt Zoological Society.

Disease has its place in ecosystems. It can control population levels and put pressure on species to develop natural resistance, says Laurenson, who started working with the wolf project in the mid-1990s. Using a vaccine to take a disease out of the mix could leave a population vulnerable to future outbreaks should the vaccine become ineffective or stop being used. In an ecosystem with multiple power players, one vaccinated predator could gain an unnatural advantage over its competitors.

Some vaccines also bring direct risks. Injectable vaccines often require trapping the animal — a costly endeavor that’s stressful and dangerous for both wild animals and the humans doing the vaccinating. Oral vaccines could be scooped up and eaten by other animals. Plus, for an oral or injectable attenuated vaccine, which contains a living but harmless version of a virus, there’s a slim possibility that evolutionary pressure could eventually drive the virus, now distributed through the population, to become lethal again.

Because room for error is slim for a species on the brink of extinction, most instances of vaccine use have been limited to emergency responses during ongoing outbreaks.

Projects that don’t go well can have lasting repercussions. In 1990, researchers tried to vaccinate some packs of endangered African wild dogs (Lycaon pictus) in Tanzania and Kenya against rabies, assuming the disease was behind a recent dip in numbers. Every dog in the study died. The stress of getting vaccinated, shot by dart from a distance, may have made the dogs more susceptible to disease, though that theory was never proven. The incident increased skepticism about vaccines and caused some African countries to tighten vaccine regulations. “It left a terrible legacy,” says veterinarian Richard Kock of the University of London.

The long game
The uphill battle faced by Sillero’s team involves more than the challenges of canvassing the Ethiopian highlands. Making a case to government officials that oral vaccines are necessary conservation tools took decades of fieldwork, genetic testing and meetings upon meetings. “The credit really goes to Claudio and the others for persisting,” Laurenson says. “Even when the doors have been shut, sometimes they’ve kept banging.”

Sillero arrived in Ethiopia in 1987 to study the wolves. A rabies outbreak hit in late 1989. Just as it does in dogs and humans, the disease attacks a wolf’s brain, causing aggressive behavior and, eventually, death. Canine distemper appeared in 1992. Marked by severe diarrhea, vomiting and coughing, the disease appears to hit wolves harder than dogs, Sillero says. The Ethiopian packs have faced four more major flare-ups of rabies and two of distemper. Two of the eight populations of wolves he came to study have gone extinct in that time.

“This is a human-caused problem, not a natural dynamic,” Laurenson says. Each year, shepherds and farmers move higher up into the wolves’ habitat, bringing grazing livestock. These people also bring domesticated dogs — the primary carriers of rabies and canine distemper (SN Online: 9/30/16). In one area of Ethiopia, wolf habitat shrunk by 34 percent from 1985 to 2003. Islands of wolf populations persist in remote highland areas surrounded by oceans of free-ranging dogs.

Vaccinating the wolves was plan B, after the lower-risk approach of vaccinating domestic dogs didn’t cut it. Because the dogs roam far and wide, dog vaccination programs didn’t reach enough animals to generate prolonged protection and prevent outbreaks in wolves. “I’m sure we were improving the situation and reducing the chance of spillovers in wild carnivores, but we weren’t preventing them altogether,” Sillero says.

Going with oral vaccines was plan C. In 2003, the government approved use of an injectable vaccine only in response to outbreaks. Sillero’s team first had to collect samples and send them to international labs to confirm that an outbreak was happening. The researchers were always behind. An oral option that proactively protects the animals started to sound like a smart way to go.

Deliver the dose
On paper, the wolves look like good candidates for an oral vaccine intervention. Few other animals brave the highlands habitat, so the odds are low that a vaccine distributed in bait would get eaten by the wrong creatures. And not vaccinating is arguably riskier than making the effort. Consecutive rabies and distemper outbreaks recently cut one of the smallest known wolf populations down to two individuals, Sillero’s team reported in December in Emerging Infectious Diseases.

The Ethiopian team chose to test an oral rabies vaccine, called SAG2, that had been used successfully in red foxes. Twenty million baits had been dropped across Europe with no vaccine-induced rabies cases or reported deaths. SAG2 also passed safety tests in a slew of different species, including African wild dogs. “That work was absolutely fundamental,” Laurenson says.
Getting the vaccine into the animals is the trickiest part. Animals have to bite into the bait to puncture an internal packet that contains the vaccine, rather than swallow the bait whole. “You’ve got to make the bait such that the [wolf] would chew it,” says Anthony Fooks, a vaccine researcher who runs a U.K. government lab that handles sample tests for the wolf project.

So Sillero and his team launched a series of pilot studies of an oral SAG2. “We set up cafeteria-type experiments, with different baits and delivery methods,” Sillero says. The researchers dropped 445 baits in locations around Bale. Hiding the vaccine in goat meat and distributing the goods at night worked better than other options, the team reported in 2016 in Vaccine. Of 21 wolves trapped a couple of weeks later, 14, or 67 percent, carried a biomarker showing the vaccine was in the wolf’s system. Of those, 86 percent had developed immunity against rabies. The impact on other wildlife was low: Only a few raptors snatched up vaccines meant for the wolves.

With all that data in hand, Sillero’s team finally won over Ethiopia’s Wildlife Conservation Authority in December, receiving an official thumbs-up to move forward. This month, 4,000 vaccines arrived; the mass vaccination program could get off the ground this summer.

It’ll be the first mass oral vaccination program to target an endangered species in the wild. The basic plan: Distribute the oral vaccines at night once every two years, vaccinate at least 40 percent of a chosen wolf population and use motion-sensing cameras to see if each pack’s high-ranking males and females — the primary pup producers — take the bait. It’s important to keep the top producers healthy.
Drones and peanut butter
Having a readily available oral vaccine for the wolves was a lucky break for the researchers in Ethiopia. A research team in the United States had no such luck. Tonie Rocke and her colleagues had to develop their own oral plague vaccine for prairie dogs. The team devised a raccoon poxvirus that produces plague proteins once inside the prairie dog body. The proteins train the immune system to fight the plague-causing Yersinia bacteria.

Saving plague-ridden prairie dogs (Cynomys spp.) is an indirect way to protect the real target: an endangered predator, black-footed ferrets (Mustela nigripes) of the Great Plains. The ferrets survive on a diet of mostly prairie dogs and had nearly gone extinct in the 1970s due to centuries of habitat loss, prey declines and plague.
On top of captive breeding and reintroduction programs to keep the ferret species afloat, the U.S. Fish and Wildlife Service traps and vaccinates wild ferrets directly. But it’s not enough.

Rocke and her colleagues went ahead and developed a peanut butter–flavored oral plague vaccine. They distributed it by drones and four-wheelers in small test plots in seven states to limit prairie dog carriers. (Plague can threaten prairie dog populations too, so everybody wins.)

Last June, the researchers published the results of these successful small-scale field trials in EcoHealth. A prairie dog’s odds of surviving in plague-ridden areas just about doubled. And the peanut butter pellets were as good at reducing plague levels as traditional insecticides that kill plague-carrying fleas. It’s unclear just how many prairie dogs in colonies need to be vaccinated to protect the ferrets from plague.

Getting the vaccine approved wasn’t as tortuous as it has been in Ethiopia. Collaborators at Colorado Parks and Wildlife already had a cheap way to make the baits, and in 2017, Colorado Serum Company licensed the product through the U.S. Department of Agriculture.

This year, Rocke hopes to conduct larger-scale field trials to determine the levels of immunity required for success in a mass vaccination. Ultimately, the application will be limited — just selected populations of prairie dogs that are either in ferret territory or endangered themselves, such as the Utah prairie dog (C. parvidens). Plague infects a handful of humans and domesticated animals each year as well, and the team is looking into using the vaccine in areas where humans spend time, like national parks.
Encouraging others
Success for one species could be good news for others. Similar preventative strategies might work in other threatened animals, including other members of the dog family dealing with rabies and ungulates like zebras at risk of catching anthrax while grazing. Researchers are testing preventative vaccines to protect wild Hawaiian monk seals from a seal-specific distemper virus.

Oral vaccines aren’t the only nontraditional delivery method. Rocke’s lab is working on a topical vaccine against white-nose syndrome, which threatens bats (SN Online: 3/31/16), and one to combat rabies in common vampire bats (Desmodus rotundus). Vampire bats in particular nuzzle each other during social grooming. “It’s an easy way to get the vaccine distributed amongst members of the colony,” Rocke says.

In October in PLOS Neglected Tropical Diseases, her lab reported that the vaccine works in captured big brown bats (Eptesicus fuscus), but it still hasn’t been tested in vampire bats, key rabies carriers in South America. Rocke and colleagues hope to start trials in vampire bats this year in Mexico and Peru.

Great apes can fall victim to some of the same pathogens as humans, such as measles and Ebola. In March 2017 in Scientific Reports, a research team published successful lab tests of an oral vaccine against Ebola in captive chimpanzees (Pan troglodytes). The vaccine relies on the rabies virus to deliver Ebola proteins that elicit an immune response in chimps, but it hasn’t been tested in the field yet.

Such a vaccine should be used selectively, Kock says. Vaccinating great apes against Ebola in preserves where the animals might encounter human carriers makes sense. But vaccinating gorillas across large forests in the Congo “is just silly,” he says.

Protecting isolated species on the brink of extinction is where vaccines could do the most good. Endangered Amur tigers (Panthera tigris altaica) have been hit hard by canine distemper, their numbers falling to around 500 individuals in their Siberian habitat. Vaccines have been debated as a potential option and injectables have been tested in captive tigers.

Sillero doesn’t expect to see any oral options developed against distemper in the future, because there’s not a big economic incentive. Unlike rabies, the disease doesn’t cause problems in humans. So he’s working with the shots available. Genetic analyses of locally circulating distemper strains published in July 2017 suggest the injectable distemper vaccines should work for the Ethiopian wolves, Fooks says. Sillero’s team is testing one in the field now. Preliminary data suggest the shot elicits a good immune response.
What’s good for the wildlife
Greater awareness about the overlap of human, livestock and wildlife health on shared lands underlies many of these projects. Ethiopia has one of the highest rabies death rates among humans in the world, and lowering the disease prevalence in any animals that humans come in contact with has benefit.

“This will have positive impacts for the threatened animals, for the welfare of domestic dogs and livestock, and for the health and finance of the human community,” Sillero argues. The One Health mind-set is also behind programs run in a few areas of Ethiopia’s northern highlands, to teach local farmers how to build more efficient stoves that require less firewood, and thus, less foraging in wolf territory.

“Vaccination and eradication of things like rabies … needs a whole of society approach,” Kock says. “It cannot be done piecemeal.”

For Ethiopia’s impending oral vaccine launch that has been so many years in the making, Sillero is optimistic. But he’s still holding his breath.

“I have to see the wolves taking up the baits before I can congratulate the team,” he says. “But I think we’re nearly there.”

In the United States, cartoon characters are a no-no in cigarette ads, and candy- or fruit-flavored cigarettes can’t be sold. But that’s not the case for e-cigarettes, and these youth-appealing tactics are luring teens who have never used tobacco products to give e-cigs and even cigarettes a try, a new study suggests.

Researchers analyzed surveys of nearly 7,000 kids ages 12 to 17 who had never used a tobacco product as of 2013 to 2014. Teens who recalled seeing or liking e-cigarette ads were 1.6 times as likely to be open to trying e-cigs or to actually try them the next year as kids who didn’t remember the ads, researchers report online March 26 in JAMA Pediatrics. E-cig ads often feature celebrities, cartoons (one product shows a unicorn vomiting a rainbow) or references to sweet flavors, such as Skittles.
Past research has shown a link between traditional cigarette advertisements and receptive nonsmoking adolescents going on to light up. Nearly nine out of 10 smokers tried their first cigarette by age 18. Gearing traditional cigarette ads toward teens has been restricted since 1998.

In 2016, more than 2.1 million U.S. middle and high school students reported using e-cigarettes. That same year, an estimated 20.5 million — or four in five — were exposed to e-cigarette ads.

But e-cigarette ads are doing more than hyping vaping, the study suggests. The ads also appeared to nudge some teens and young adults to take up cigarette smoking. Of a larger group of about 10,500 kids ages 12 to 21 who had never used tobacco products, 18 percent recalled seeing or liking e-cigarette ads but not cigarette ads. Five percent of those teens had started to smoke by the next year.

Extrapolating to the U.S. population, “105,000 12- to 21- year olds appear to have smoked their first cigarette because of the influence of e-cigarette advertising,” says John Pierce, a behavioral epidemiologist at the University of California, San Diego.
Previous research has found that teens who use e-cigarettes are more likely to smoke traditional cigarettes (SN: 9/19/15, p. 14). The fact that e-cigarette ads may up the risk of smoking “raises an unprecedented concern for adolescent tobacco control,” addiction psychologist Adam Leventhal and epidemiologist Jessica L. Barrington-Trimis, both of the University of Southern California’s Keck School of Medicine in Los Angeles, write in an accompanying editorial in the journal.

In an interview, Leventhal adds that restricting such advertising is an important target for public health campaigns and policies to limit youth use of tobacco products.

Birds can sense Earth’s magnetic field, and this uncanny ability may help them fly home from unfamiliar places or navigate migrations that span tens of thousands of kilometers.

For decades, researchers thought iron-rich cells in birds’ beaks acted as microscopic compasses (SN: 5/19/12, p. 8). But in recent years, scientists have found increasing evidence that certain proteins in birds’ eyes might be what allows them to see magnetic fields (SN: 10/28/09, p. 12).

Scientists have now pinpointed a possible protein behind this “sixth sense.” Two new studies — one examining zebra finches published March 28 in Journal of the Royal Society Interface, the other looking at European robins published January 22 in Current Biology — both single out Cry4, a light-sensitive protein found in the retina. If the researchers are correct, this would be the first time a specific molecule responsible for the detection of magnetic fields has been identified in animals.
“This is an exciting advance — we need more papers like these,” says Peter Hore, a chemist at the University of Oxford who has studied chemical reactions involved in bird navigation.

Cry4 is part of a class of proteins called cryptochromes, which are known to be involved in circadian rhythms, or biological sleep cycles (SN: 10/02/17, p. 6). But at least some of these proteins are also thought to react to Earth’s magnetic field thanks to the weirdness of quantum mechanics (SN: 7/23/16, p. 8). The protein’s quantum interactions could help birds sense this field, says Atticus Pinzon-Rodriguez, a biologist at the University of Lund in Sweden who was involved with the zebra finch study.

To figure out which of three cryptochromes is responsible for this quantum compass, Pinzon-Rodriguez and his colleagues examined the retinas, muscles and brains of 39 zebra finches for the presence of the three proteins Cry1, Cry2 and Cry4.
The team found that while levels of Cry1 and Cry2 followed a rhythmic pattern that rose and fell over the day, Cry4 levels remained constant, indicating the protein was being produced steadily.

“We assume that birds use magnetic compasses any time of day or night,” says Lund biologist Rachel Muheim, a coauthor on the zebra finch study.

European robins also showed constant levels of Cry4 during a 24-hour cycle, and higher levels during their migratory season. And the researchers in that study found Cry4 in an area of the robin’s retina that receives a lot of light — a position that would help it work as a compass, the study says.

“We have quite a lot of evidence, but [Cry4] is not proven,” says Henrik Mouritsen, an animal navigation expert at the Institute of Biology and Environmental Sciences in Oldenburg, Germany, who participated in the robin study. More definitive evidence might come from observing birds without a functioning Cry4 protein, to see if they still seem to have an internal compass.

Even then, Hore says, we still may not understand how birds actually perceive magnetic fields. To know, you’d have to be a bird.

There’s a fine line between immersive and unnerving when it comes to touch sensation in virtual reality.

More realistic tactile feedback in VR can ruin a user’s feeling of immersion, researchers report online April 18 in Science Robotics. The finding suggests that the “uncanny valley” — a term that describes how humanoid robots that look almost but not quite human are creepier than their more cartoonish counterparts — also applies to virtual touch (SN Online: 11/22/13).
Experiment participants wearing VR headsets and gripping a controller in each hand embodied a virtual avatar holding the two ends of a stick. At first, users felt no touch sensation. Then, the hand controllers gave equally strong vibrations every half-second. Finally, the vibrations were finely tuned to create the illusion that the virtual stick was being touched in different spots. For instance, stronger vibrations in the right controller gave the impression that the stick was nudged on that side.

Compared with scenarios in which users received either no touch or even buzzing sensations, participants reported feeling far less immersed in the virtual environment when they received the realistic, localized touch. This result demonstrates the existence of a tactile uncanny valley, says study coauthor Mar Gonzalez-Franco, a human-computer interaction researcher at Microsoft Research in Redmond, Washington.

But when users were shown a marble touching the virtual stick wherever they felt the localized touch, the participants found this realistic tactile feedback highly immersive rather than bothersome. The finding indicates that rich tactile feedback in VR may need to be paired with other sensory cues that explain the source of the sensation to avoid spooking users, Gonzalez-Franco says.

Better understanding how realistic touch sensations can break the VR illusion may help developers create more engaging virtual environments for games and virtual reality therapy, says Sean Follmer, a human-computer interaction researcher at Stanford University not involved in the study.