ORLANDO, Fla. — Weight gain may depend on how an individual’s genes react to certain diets, a new study in mice suggests.
Four strains of mice fared differently on four different diets, William Barrington of North Carolina State University in Raleigh reported July 15 at the Allied Genetics Conference.
One strain, the A/J mouse, was nearly impervious to dietary changes. Those mice didn’t gain much weight or have changes in insulin or cholesterol no matter what they ate: a fat-and-carbohydrate-laden Western diet, traditional Mediterranean or Japanese diet (usually considered healthy) or very low-carbohydrate, fat-rich fare known as the ketogenic diet. In contrast, NOD/ShiLtJ mice gained weight on all but the Japanese diet. Those mice’s blood sugar shot up — a hallmark of diabetes — on a Mediterranean diet, but decreased on the Japanese diet.
FVB/NJ mice didn’t get fat on the Western diet, but became obese and developed high cholesterol and other health problems on the ketogenic diet. The opposite was true for C57BL/6J mice. They became obese and developed cholesterol and other problems linked to heart disease and diabetes in people on the Western diet, but not on the ketogenic diet. They also fattened up on the Mediterranean diet.
The results indicate that “there’s no universally healthy diet,” Barrington said. The findings echo results of a human study in which blood sugar rose in some people after eating some foods, even when the same food had no effect on other people (SN: 1/9/16, p. 8). Such individual reactions to food suggest that diets should be personalized.
Barrington and colleagues are working to find the genes that control the mouse strains’ varying responses to what they eat. There is still no way to predict how people will fare on a given diet, he said.
MANCHESTER, England — The human nose harbors not only a deadly enemy — Staphylococcus aureus — but also its natural foe. Scientists have now isolated a compound from that foe that might combat MRSA, the methicillin-resistant strain of S. aureus.
“We didn’t expect to find this. We were just trying to understand the ecology of the nose to understand how S. aureus causes problems,” bacteriologist Andreas Peschel of the University of Tübingen in Germany said at a news briefing July 26 during the EuroScience Open Forum. Investigating the intense interspecies competition in the nose — where microbes fight for space and access to scant sugars and amino acids — might offer a fertile alternative to searching for new drug candidates in soil microbes. Antibiotic researcher Kim Lewis of Northeastern University in Boston agrees in general that the approach might produce new drug discovery leads. But so far the human microbiome has produced only a handful of potential new antibiotics (including lactocillin). If “the compound they found is membrane-acting, [it] will be useful for topical applications, but not as a systemic antibiotic,” he wrote in an e-mail. And new systemic antibiotics are needed most, he says. Despite being a relatively nutrient-poor environment, the human nose is home to more than 50 species of bacteria. One of these is S. aureus, a dominant cause of hospital-acquired infections such as MRSA, as well as infections of the blood and heart. But there’s a huge variability in the nasal microbe scene between individuals: while S. aureus is present in the nasal passages of roughly 30 percent of people, the other 70 percent don’t have any sign of it.
Trying to explain this difference led Peschel and colleagues to study “the ecology of the nose.” They suspected that other nasal inhabitants, well-tuned to compete in that harsh niche, might be blocking S. aureus from colonizing the nose in those who don’t carry it.
From nasal secretion samples, the team isolated 90 strains of different Staphylococcus species. Of these, one bacterium, S. lugdunensis, killed S. aureus when the two were grown together in a dish. Introducing a variety of mutations into S. lugdunensis produced a strain that didn’t kill. The missing gene, the team showed, normally produced an antibiotic, which the researchers named lugdunin; it represents the first example of a new class of antibiotic.
Lugdunin was able to fend off MRSA as well as a strain of Enterococcus resistant to the antibiotic vancomycin. Neither bacteria developed resistance. The team also pitted S. lugdunensis against S. aureus in test tube and mouse studies, with S. lugdunensis besting S. aureus. Only 5.9 percent of 187 hospital patients had S. aureus in their noses if they also carried S. lugdunensis, the team found, while S. aureus was present in 34.7 percent of those without S. lugdunensis. Peschel and colleagues also reported the results July 28 in Nature. Lugdunin cleared up a staph skin infection in mice, but it’s unclear how the compound works. Researchers could not rule out that it damages the cell membrane, which could limit its use in humans to a topical antibiotic. Peschel and coauthor Bernhard Krismer also suggest that the bacterium itself might be a good probiotic, applied nasally, to fend off staph infections in vulnerable hospital patients.
For the first time in the United States, free-flying genetically modified mosquitoes have federal approval to take wing in Florida. But when, and if, that will happen is still up in the air. Local officials will make the final decision — possibly not until after the November elections.
The World Health Organization has recognized these mosquitoes as possible tools for fighting the spread of mosquito-borne Zika virus. But the U.S. Food and Drug Administration’s decision, announced August 5, covers only a specific, preliminary test release of GM mosquitoes on Key Haven in the Florida Keys, where no locally transmitted Zika cases have been reported. This trial of OX513A mosquitoes, genetically engineered by the British company Oxitec, “would be unlikely to result in adverse effects on the environment or human health,” the FDA ruled. If Key West commissioners approve it, the trial would release abundant GM male Aedes aegypti species carrying a gene that will cause their offspring to die. In tests in Brazil, Panama and the Cayman Islands, months of releasing these mosquitoes has reduced the wild populations of Ae. aegypti mosquitoes by 90 percent or more. As a result, a Brazil neighborhood has seen mosquito-borne dengue cases plummet (SNOnline: 7/15/16).
To see whether OX513A could work in the United States, too, the test release would now need approval from the Florida Keys Mosquito Control District Board of Commissioners. Opponents of GM organisms have protested the idea, so the five commissioners have arranged for a nonbinding referendum question to appear on the November ballot. Commissioners plan to wait until the community has weighed in before making their final decision, says mosquito control district spokeswoman Beth Ranson.
If the mosquito plan gets a thumbs up, Oxitec could release mosquitoes in December, said Hadyn Parry, the company’s chief executive officer. Monitoring and testing could take six months and results would go back to the FDA with an application to allow the mosquitoes to be released commercially — and more broadly — in the United States for mosquito control.
As Zika rages in Puerto Rico, and with Miami reporting the first locally mosquito-transmitted cases on the U.S. mainland, debate over the controversial mosquito has taken on new urgency. Tom Frieden, director of the U.S. Centers for Disease Control and Prevention, has noted that efforts to eradicate mosquitoes in an area in Miami have fallen short (SNOnline: 8/1/16).
Ae. aegypti mosquitoes resist many pesticides, bite during the day, love human houses, and can breed in plant saucers and other small pools of water. Virtually a domestic animal, this species bites people almost exclusively. It’s suspected to be the main spreader of Zika virus, and also does a fine job of infecting people with dengue, chikungunya and yellow fever viruses. Oxitec GM mosquitoes, developed in 2002, would target Floridian pests via a new twist in the decades-old strategy of male sterilization. Mid-20th century entomologists sterilized screwworms by irradiating them and releasing the decoy males in overwhelming clouds. So many wild females mated with these sterile males that eventually the gruesome screwworm pests of livestock disappeared from the United States.
OX513A, with their mix of old-fashioned strategy and newfangled genetic tinkering, has kicked up anti-GMO feeling, even though it’s not the first U.S. approval of testing a GM insect in pest control. That honor goes to pink bollworms in the Southwest in 2009, though their release passed largely unnoticed outside the pest-control community. But when the FDA released a favorable draft opinion in March, saying the GM-mosquito test would probably have “no significant impact” on people or the environment, more than 2,000 people typed comments on the public FDA site. Many were vehemently opposed to the plan, peppering their comments with multiple exclamation points and the occasional “OMG!!!”
Some commenters worried about blood contact from the bite of a GM organism, possible allergies should someone accidentally swallow one and unknown consequences to the environment.
Oxitec posted explanations responding to those fears: Almost all mosquitoes released would be males, which don’t bite; males will die three or four days after release; their offspring are engineered to die without unnatural amounts of tetracycline — a lab-provided supplement — in their diets. Angry public comments, however, largely dismissed these reassurances as corporate-funded research.
Another commenter wondered whether a successful test, driving down the Ae. aegypti population on the Keys, could make room for some other insect menace. That’s a reasonable question, says Phil Lounibos of the University of Florida in Vero Beach. He has studied competition between Ae. aegypti and the relentlessly biting Asian tiger mosquito, Aedes albopictus. These tiger mosquitoes were once rare on the Keys, but he has found that they can take over from Ae. aegypti, in part by sexual deception. Tigers that mate with Ae. aegypti females render the females sterile and have thus conquered other parts of Florida. Even though Ae. aegypti is recognized as a more potent vector for human disease, the tigers can carry many of the same viruses (including Zika), Lounibos warns (SNOnline: 5/16/16).
As far as ecological concerns go, entomologist Bruce Tabashnik of the University of Arizona in Tucson, has no problem with eradicating Ae. aegypti from the Florida Keys or anywhere else in the Americas. “It’s an invasive species,” he says. “There are no ecological ethics violated.”
Tabashnik was part of the research team monitoring the first GM insect release in the United States: sterile male pink bollworms. Males of this invasive pest species that prey on cotton in the Southwest were sterilized by radiation. However, Oxitec had inserted a gene that made them fluoresce red so monitors could tell the friendlies from the wild targets. Tabashnik recalls no particular public outcry over the experiment. It took place in a sparsely populated area and, instead of mosquitoes, involved a kind of moth only a cotton farmer could hate.
So far outrage, or even interest, in other tweaked pest-control animals seems minimal compared with GM-mosquito fever. A proposed test of Oxitec’s GM diamondback moth in New York has inspired fewer comments. Tests of a non-GM but still tinkered-with mosquito — Ae. albopictus developed to carry Wolbachia bacteria that interfere with mating — were first approved in 2012 for release in American Samoa. Later tests have released these bacteria-carrying mosquitoes in California and other sites in the mainland United States.
WASHINGTON — When bacteria lose genes needed to make enzymes for important chemical reactions, defeat isn’t inevitable. Sometimes other enzymes will take on new roles to patch together a work-around chain of reactions that does the job, biologist Shelley Copley reported August 4 at the 2nd American Society for Microbiology Conference on Experimental Microbial Evolution.
Bacteria that can adapt in this way are more likely to survive when living conditions change, passing along these new tricks to their descendants. So studying these biochemical gymnastics is helping scientists to understand how evolution works on a molecular level. Working with different strains of Escherichia coli bacteria, Copley and colleagues deleted genes responsible for making crucial enzymes. The team then watched the microbes replicate for many generations to see how they worked around those limitations.
Most enzymes are highly specialized: They only work well to speed up one type of reaction, the way a key fits only one lock. But some enzymes are more like master keys — they can boost multiple reactions, though they tend to specialize in one. These so-called “promiscuous” enzymes can switch away from their specialty if conditions change.
Copley’s team found that new enzymes would sub in to replace the missing ones. For instance, E. coli missing an enzyme needed to make vitamin B6 synthesized the vitamin using a different set of enzymes. But surprisingly, the promiscuous enzymes didn’t end up directly triggering the same reaction as the enzymes they replaced. Instead, the replacement enzymes cobbled together a different (often longer) work-around series of reactions that ultimately achieved the same function.
“We were rerouting metabolism,” said Copley, of the University of Colorado Boulder.
By modifying the bacteria’s genes and forcing the microbes to survive with a more limited chemical toolkit, Copley’s work gives a more detailed look at the biochemistry underlying evolution, says biologist Gavin Sherlock of Stanford University, who was not involved in the research. Betul Kacar, a synthetic biologist at Harvard University, says promiscuity could also be a window into the past, giving hints about enzymes’ previous roles earlier in evolutionary history. The role that an enzyme jumps in to play in a pinch could have once been its main job. “Trying to understand how novel pathways arise, what kind of mechanistic underlying forces shape those trajectories, is quite essential,” she says.
Bacteria can piece together all sorts of alternative routes in response to missing enzymes, depending on specific environmental conditions, Copley said. The ones that are most successful are more efficient —they have fewer steps, or they yield more of the desired reaction product.
Climate change flaunted its deadly side during the 2003 European heat wave, which killed over 70,000 people across the continent. In London and Paris alone, global warming led to 570 more heat-related deaths than would be expected without human-caused warming, researchers estimate in the July Environmental Research Letters.
Daniel Mitchell of the University of Oxford and colleagues ran thousands of climate simulations with and without the influence of greenhouse gases emitted by humans. The simulations showed that 70 percent of heat-related deaths in central Paris during the heat wave and 20 percent in Greater London could be attributed to climate change. The study is the first to quantify climate change’s role in the event and will inform policy makers on the risks climate change poses, the researchers say.
Even if you’ve never lived in rattlesnake territory, you know what the sound of a snake’s rattle means: Beware! A shake of its rattle is an effective way for a snake to communicate to a potential predator that an attack could result in a venomous bite.
For more than a century, scientists have posited how that rattle might have evolved. The rattle is composed of segments of keratin (the same stuff that makes up human hair), and specialized muscles in a snake’s tail vibrate those segments rapidly to create the rattling sound. The rattlesnake’s rattle is a trait that evolved only once in the past and is now found in only two closely related genera of snakes that live in North and South America. But plenty of other species of snakes also vibrate their tails as a warning to potential predators.
Bradley Allf and colleagues at the University of North Carolina in Chapel Hill think that the tail vibration and the evolution of the rattle might be connected. They gathered 155 snakes of 56 species — 38 species from the Viperidae family, which includes rattlesnakes, and 18 species from the largest snake family, Colubridae — from museums, zoos and private collectors. Working with captive snakes let them control conditions, such as temperature, that can affect tail vibration. With each snake, one of the researchers tried to get it to behave defensively by waving a stuffed animal in front of it. The team videotaped the snakes as they vibrated their tails, or not.
The researchers plotted the snakes’ tail vibration duration and rate against how closely related a species was to rattlesnakes. One group of snakes that lives in the Americas was taken out of the analysis because its tail vibrations were so similar to those of rattlesnakes; it appears that these species are mimicking the dangerous snakes that live near them (not a bad strategy for survival). Among the rest of the snakes analyzed, those that were more closely related had tail behavior that was more similar to that of rattlesnakes.
“Our results suggest that tail vibration by rattleless ancestors of rattlesnakes may have served as the signal precursor to rattlesnake rattling behavior,” the researchers write in the October issue of the American Naturalist. “If ancestral tail vibration was a reliable cue to predators that a bite was imminent, then this behavior could have become elaborated as a defensive signal.”
Allf and his colleagues propose a couple of ways that this could have happened. Perhaps snakes that made noise with their tails were better at startling predators, and this may have prompted such noise-making tail features to spread and eventually become refined into what is now a rattle. Or maybe snakes that shook their tails longer and faster developed calluses of keratin. If these calluses provided better warning, that may have somehow evolved into a rattle.
“Thus, the rattlesnake rattle might have evolved via elaboration of a simple behavior,” they conclude.
A barrage of rocks hitting the solar system 3.9 billion years ago could have dramatically reshaped Earth’s geology and atmosphere. But some of the evidence for this proposed bombardment might be shakier than previously believed, new research suggests. Simplifications made when dating moon rocks could make it appear that asteroid and comet impacts spiked around this time even if the collision rate was actually decreasing, scientists report the week of September 12 in the Proceedings of the National Academy of Sciences.
Many scientists think that a period of relative calm after Earth formed 4.6 billion years ago was interrupted by a period called the Late Heavy Bombardment, when rocky debris pummeled Earth and the other planets. The moon’s cratered surface holds the best evidence for this event; scientists have measured radioactive decay of argon gas trapped inside moon rocks to date when craters on the moon were formed. Many of the hundreds of moon rocks analyzed appear to be around 3.9 billion years old. That suggests the number of rocks hitting the moon suddenly spiked at that time — evidence for a Late Heavy Bombardment.
Geochemists Patrick Boehnke and Mark Harrison of UCLA took a second look at the data. Measuring argon from the same rock at different temperatures leeches the gas from different parts of the rock’s crystals; if all those age values align, researchers can be relatively confident they’re getting an accurate age. But many of the lunar samples previously analyzed gave different ages depending on the temperature at which their argon content was measured.
Instead of colliding sharply once and sitting undisrupted, which might give more uniform age data at different temperatures, these lunar rocks were probably tossed around and slammed into other rocks many times, Boehnke says. So assigning one impact age to those rocks might be an oversimplification.
Boehnke and Harrison created a model to simulate how this simplification might affect the patterns seen when scientists looked at the ages of many rocks. The team modeled 1,000 rocks and assigned each one an impact age. Some rocks hadn’t been knocked around and had a clear impact age. Others had been smashed repeatedly, which changed their argon content and obscured the actual impact age assigned by the model.
The model assumed that asteroid collisions decreased over time — that more of the rocks were older and fewer were newer. But still, collision ages appeared to spike 3.9 billion years ago thanks to the fuzziness introduced by the disrupted rocks. So the apparent asteroid increase at that time might just be a quirk due to the way the argon dating data were compiled and analyzed, not an indication of something dramatic actually happening. “We can’t say the Late Heavy Bombardment didn’t happen,” Boehnke says. Nor do the results invalidate the technique of argon dating, which is used widely by geologists. Instead, Boehnke says, it points to the need for more nuanced interpretation of lunar rock data.
“A lot of data that shows this complexity is being interpreted in a very simplistic way,” he says.
Planetary scientist Simone Marchi says he finds the paper “certainly convincing in saying that we have to be very careful” when interpreting argon dating data from lunar samples.
But there’s other evidence for a Late Heavy Bombardment that doesn’t rely on argon dating, such as dating from more stable radioactive elements and analysis of overlapping craters on the moon, says Marchi, of the Southwest Research Institute in Boulder, Colo. He supports the idea of a gentler Late Heavy Bombardment 4.1 billion years ago, instead of a dramatic burst 3.9 billion years ago (SN: 8/23/14, p.13).
Other recent work has also pointed out limitations in argon dating, says Noah Petro, a planetary geologist at NASA Goddard Space Flight Center in Greenbelt, Md., who wasn’t part of the study. Collecting new samples and analyzing old ones with newer techniques could help scientists update their view of the early solar system. “We’re at this point with the moon right now where we’re finding the limitations of what we think we know.”
The first time Jessica Cantlon met Kumang at the Seneca Park Zoo, the matriarch orangutan regurgitated her previous meal right into Cantlon’s face. “I was retching,” Cantlon recalls. “It was so gross.” But Cantlon was there to kick off a series of behavioral experiments, and her students, who would be working with Kumang regularly, were watching. “Does anyone have any towels?” she remembers asking, knowing she had to keep her cool.
Cantlon’s deliberate nature and whatever-it-takes attitude have served her well. As a cognitive neuroscientist at the University of Rochester in New York, she investigates numerical thinking with some of the most unpredictable and often difficult study subjects: nonhuman primates, including orangutans, baboons and rhesus macaques, and — most remarkably — children as young as age 3. Both groups participate in cognitive tests that require them, for example, to track relative quantities as researchers sequentially add items to cups and to distinguish between quantities of assorted dots on touch screens. The kids also go into the functional MRI scanner where, in a feat impressive to parents everywhere, they lie completely still for 20 to 30 minutes so Cantlon and colleagues can get pictures of their brains. “She takes steps carefully, and she thinks very hard about where she is going,” says Daniel Ansari, a developmental cognitive neuroscientist at the University of Western Ontario in London, Canada, who is familiar with Cantlon’s work. “She goes for the big questions and big methodological challenges.”
The central question in Cantlon’s research is: How do humans understand numbers and where does that understanding come from? Sub-questions include: What are the most primitive mathematical concepts? What concepts do humans and other primates share? Are these shared concepts the foundation for fancier forms of mathematical reasoning? In addressing these questions, Cantlon draws on a wide range of methods. “Very few people can combine work on cognitive skills — studies from the point of view of behavior — with imaging work in very young children, and very few people do that same combination in nonhuman primates,” says Elissa Newport, who chaired the brain and cognitive sciences department at Rochester for more than a decade and now leads the Center for Brain Plasticity and Recovery at Georgetown University.
As a graduate student, Cantlon determined that neuroimaging studies would add an independent source of data to the cognitive questions under exploration in Elizabeth Brannon’s lab at Duke University. So she identified collaborators and taught herself functional MRI. “By the time she graduated, she had something like four dissertations’ worth of work,” says Brannon, now of the University of Pennsylvania.
In the years since, Cantlon has identified a type of “protocounting” in baboons; they can keep tabs on approximate quantities of peanuts as researchers increase those quantities (SN Online: 5/17/15). In her most attention-grabbing work, Cantlon studied activity in the brains of children while they watched Sesame Street clips that dealt with number concepts — an unexpected success that proved everyday, relatively unaltered stimuli can yield meaningful data. An ongoing study in Cantlon’s lab seeks to find out how monkeys, U.S. kids and adults, and the Tsimané people of Bolivia, who have little formal education, distinguish between quantities. Do they determine the number of dots presented on the computer screen or do they rely on a proxy such as the total area covered by the dots? The work explores how the brain understands everyday concepts, but it could also inform strategies in math education. “If we understand the fundamental nature of the human brain and mind, that might give us a better insight into how to communicate number concepts to kids,” Cantlon says.
Growing up outside of Chicago, Cantlon enjoyed digging deep into a topic and becoming an expert. She and a friend turned themselves into ice skating superfans one summer, reading up on the Olympic skaters and checking videos out of the local library. In another project, Cantlon decided to learn everything possible about the price of gold. When she moved to a school where she could no longer take Latin, she taught and tested herself. Despite the fact that neither of her parents went to college, no one ever questioned that Cantlon would go. She studied anthropology as an undergraduate at Indiana University in Bloomington. “I was interested in the question of where we come from,” Cantlon says. “I was interested in studying people.” During college, she went on an archaeological dig in Belize and studied lemurs in Madagascar. For a year after graduation, she observed mountain gorillas in Rwanda, detailing their behavior every 10 minutes. “What they were thinking was something that was constantly on my mind,” she says. “‘How are we similar? Are you thinking what I’m thinking?’” Though she might have succeeded in any number of careers, she wanted exploration to be a big part of her life: “I don’t think doing a less exotic type of work would have been as satisfying.”
Today, Cantlon, who at age 40 recently earned tenure, doesn’t spend much time in the field. And even in the lab, she leaves much of the data collection to her graduate students and research assistants. “At this point, we are a well-oiled system,” she says, referring to the brain scan studies on kids. To make the kids comfortable, Cantlon’s team does trial runs in a mock scanner, describing it as a spaceship and providing “walkie-talkies” for any necessary communication. To keep them interested, the researchers treat it as a team activity and offer a ton of positive reinforcement, with prizes including Lego sets and a volcano-making kit. The kids receive pictures of their brains, which typically interest the parents most. The older of Cantlon’s two daughters, a 5-year-old extrovert named Cloe, has participated in behavioral tests and will no doubt be excited for her first brain scan.
The Sesame Street study was in part inspired by a paper by Uri Hasson, a neuroscientist at Princeton University who imaged the brains of volunteers while they watched The Good, the Bad and the Ugly. To better understand brain development, Cantlon wanted to see how brain activity compared in kids and adults exposed to math in a natural way. Of particular interest was a region called the intraparietal sulcus, or IPS, thought to play a role in symbolic number processing. The results, reported in PLOS Biology in 2013, showed that kids with IPS activity more closely resembling adults’ activity performed better on mathematical aptitude tests.
“It was the clearest, cleanest — did not have to come out this way — result,” Cantlon says.
Cantlon is notable for her diverse set of tools, says Steve Piantadosi, a computational neuroscientist and colleague at Rochester. “But she has something which is even more powerful than that. If you have different hypotheses and you want to come up with the perfect experiment that distinguishes them, that is something she is very good at thinking about. She is a great combination of critical and creative.”
To add another methodological approach, Cantlon next plans to collaborate with Piantadosi to develop computational models that explain the operations the brain performs as it counts or compares quantities. She would also like to add data analyses from wild primates into the mix. When researchers talk about the evolution of a primitive number sense, they often speak about foraging activity — identifying areas of the forest with more food, for example. But Cantlon wonders whether social interactions also require some basic understanding of quantities.
As for a recent question from a colleague about what risky project she’ll pursue now that she has tenure, Cantlon says nothing in particular comes to mind: “I feel like we’ve been doing the crazy things all along.”
ORLANDO, Fla. — New evidence from separate labs supports the controversial idea that an overlooked and unexpected Culex mosquito might spread Zika virus.
The southern house mosquito, Culex quinquefasciatus, is common in the Americas. Constância Ayres, working with Brazil’s Oswaldo Cruz Foundation in Recife, previously surprised Zika researchers with the disturbing proposal that this mosquito might be a stealth spreader of Zika. But two U.S. research groups tested the basic idea and couldn’t get the virus to infect the species. Now, preliminary results from Ayres’ and two other research groups are renewing the discussion. The data, shared September 26 at the International Congress of Entomology, suggest that Zika can build up in the house mosquito’s salivary glands — a key step in being able to transmit disease. Basic insect physiology is only part of the puzzle, though. Even if the mosquitoes prove competent at passing along Zika, there remain questions of whether their tastes, behavior and ecology will lead them to actually do so.
In the current outbreak, the World Health Organization has focused on mosquitoes in a different genus, Aedes, particularly Ae. aegypti, as the main disease vector. But Ayres had announced months ago the discovery of the virus in Brazil’s free-flying house mosquitoes (SN Online: 7/28/16).
At the congress, Ayres’ foundation colleague Duschinka Guedes reported that captive mosquitoes fed Zika-tainted blood had virus growing in their own guts and salivary glands within days. The virus doesn’t spread every time a mosquito slurping contaminated blood gets virus smeared on its mouthparts, though. To move from the mosquito to what it bites, viruses have to infect the insect midgut, then travel to the salivary glands and build up enough of a population for an infective dose drooling into the next victim. When Guedes offered the infected mosquitoes a special card to bite, they left telltale virus in the salivary traces, a sign of what they could do when biting — and infecting — a real animal.
Researchers from China and Canada who were not originally on the symposium program also stepped up to share their results, some of which are unpublished. Some tasks are still in early stages, but both labs showed Zika virus building up in some kind of Culex mosquitoes.
At the Beijing Institute of Microbiology and Epidemiology, Tong-Yan Zhao found the virus peaking in the house mosquitoes eight days after their first contaminated drink. As a test of the infectious powers of the mosquitoes, researchers let the Zika-carrying insects bite baby lab mice. Later, the virus showed up in the brains of eight out of nine lab mice. The results were reported September 7 in Emerging Microbes & Infections. From Brock University in St. Catharines, Canada, Fiona Hunter has found signs that 11 out of 50 wild-caught Culex pipiens pipiens mosquitoes picked up the virus somewhere on their bodies. So far, she has completely analyzed one mosquito and reports that the virus was indeed in its saliva.
These positive results contradict Culex tests at the University of Texas Medical Branch in Galveston. Those tests, with U.S. mosquitoes, found no evidence that C. quinquefasciatus can pick up and pass along a Zika infection, says study coauthor Scott Weaver. Stephen Higgs of Kansas State University in Manhattan and his colleagues got similar results. “We’re pretty good at infecting mosquitoes,” Higgs says, so he muses over whether certain virus strains won’t infect mosquitoes from particular places.
The main risk from Culex at the moment is distraction, warned Roger Nasci of North Shore Mosquito Abatement District in Northfield, Ill. After the talks, he rose from the audience to say that Ae. aegypti is a known enemy and limited resources should not be diverted from fighting it.
George Peck, who runs mosquito control for Clackamas County in Oregon, isn’t convinced that the high virus concentrations dosing the test mosquitoes are realistic. Yet he’s watching the issue because like much of northern North America, Clackamas doesn’t have the Ae. aegypti vector to worry about. But it does have plenty of Culex mosquitoes.
Baby humans’ brain cells take awhile to get situated after birth, it turns out. A large group of young nerve cells moves into the frontal lobe during infants’ first few months of life, scientists report in the Oct. 7 Science. The mass migration might help explain how human babies’ brains remain so malleable for a window of time after birth.
Most of the brain’s nerve cells, or neurons, move to their places in the frontal lobe before birth. Then, as babies interact with the world, the neurons link together into circuits controlling learning, memory and social behavior. Those circuits are highly malleable in early infancy: Connections between neurons are formed and severed repeatedly. The arrival of new neurons during the first few months of life could help account for the circuits’ prolonged flexibility in babies, says study coauthor Eric Huang, a neuropathologist at the University of California, San Francisco. “The fact that [the neurons] are migrating for months and months is remarkable,” says Stephen Noctor, a neuroscientist at the University of California, Davis who wasn’t involved in the work.
Huang and colleagues noticed a group of cells making proteins related to migration when looking at slices of postmortem infant brains under an electron microscope. To catch these neurons in the act of moving, though, the team used rare samples of brain tissue collected and donated immediately after infants’ deaths. The team infected those tissues with a virus tagged with a glowing protein. When the virus infected the brain cells, they glowed green. Then the researchers could track the migrating neurons’ path across the brain. The neurons started as a cluster in the subventricular zone, a layer inside the brain where new neurons are born, and then formed a chain moving into the frontal lobe, Huang’s team found. Once the migrating neurons settled down later in development, they mostly became inhibitory interneurons. This type of neuron acts like a stoplight for other neurons, keeping signaling in check. Huang’s team found migrating neurons in the brains of babies up to about seven months old, with migration peaking around 1.5 months and then tapering off.
“In the first six months, that’s kind of [infants’] critical period when they slowly develop their response to [their] environment. They start to engage with emotions,” says Huang. “Our results provide a cellular basis for postnatal human brain development and how cognition might be developed.”
By replenishing the frontal lobe’s supply of building blocks midway through construction, the new neurons might help babies’ brain circuits stay malleable longer. The mass migration after birth means that experiences in infancy could affect where these neurons end up — and, by extension, the connections they form.
The finding raises additional questions about the timing of the event, Noctor says — like when the migrating cells were born and how long an individual cell takes to move.
