That’s the takeaway of a new study of snail fever, or schistosomiasis, a tropical disease that affects more than 250 million people worldwide. It’s caused by a water-borne parasite that reproduces inside some snails. Parasite larvae burrow through people’s skin and can cause infertility, cognitive problems and even cancer. Today, most countries manage the disease with a drug that kills the parasite in human hosts. Some nations also control snail populations to hamstring the parasite’s life cycle, but that’s a less popular approach.
But snail control turns out to be more effective than drugs for curbing snail fever, researchers report July 21 in PLOS Neglected Tropical Diseases. The scientists compared a range of disease management strategies in 83 countries in the last century that included killing snails, using drugs or changing infrastructure (such as sanitation services). Projects using snail control cut disease by over 90 percent; those without it, by less than 40 percent.
The researchers suggest a blend of drug therapy and snail management to eradicate disease in the future.
Blue whirl Bloo werl n. A swirling flame that appears in fuel floating on the surface of water and glows blue.
An unfortunate mix of electricity and bourbon has led to a new discovery. After lightning hit a Jim Beam warehouse in 2003, a nearby lake was set ablaze when the distilled spirit spilled into the water and ignited. Spiraling tornadoes of fire leapt from the surface. In a laboratory experiment inspired by the conflagration, a team of researchers produced a new, efficiently burning fire tornado, which they named a blue whirl. To re-create the bourbon-fire conditions, the researchers, led by Elaine Oran of the University of Maryland in College Park, ignited liquid fuel floating on a bath of water. They surrounded the blaze with a cylindrical structure that funneled air into the flame to create a vortex with a height of about 60 centimeters. Eventually, the chaotic fire whirl calmed into a blue, cone-shaped flame just a few centimeters tall, the scientists report online August 4 in Proceedings of the National Academy of Sciences.
“Firenadoes” are known to appear in wildfires, when swirling winds and flames combine to form a hellacious, rotating inferno. They burn more efficiently than typical fires, as the whipping winds mix in extra oxygen, which feeds the fire. But the blue whirl is even more efficient; its azure glow indicates complete combustion, which releases little soot, or uncombusted carbon, to the air.
The soot-free blue whirls could be a way of burning off oil spills on water without adding much pollution to the air, the researchers say, if they can find a way to control them in the wild.
Editor’s note: When reporting results from the functional MRI scans of dogs’ brains, left and right were accidentally reversed in all images, the researchers report in a correction posted April 7 in Science. While dogs and most humans use different hemispheres of the brain to process meaning and intonation — instead of the same hemispheres, as was suggested — lead author Attila Andics says the more important finding still stands: Dogs’ brains process different aspects of human speech in different hemispheres. Dogs process speech much like people do, a new study finds. Meaningful words like “good boy” activate the left side of a dog’s brain regardless of tone of voice, while a region on the right side of the brain responds to intonation, scientists report in the Sept. 2 Science.
Similarly, humans process the meanings of words in the left hemisphere of the brain, and interpret intonation in the right hemisphere. That lets people sort out words that convey meaning from random sounds that don’t. But it has been unclear whether language abilities were a prerequisite for that division of brain labor, says neuroscientist Attila Andics of Eötvös Loránd University in Budapest.
Dogs make ideal test subjects for understanding speech processing because of their close connection to humans. “Humans use words towards dogs in their everyday, normal communication, and dogs pay attention to this speech in a way that cats and hamsters don’t,” says Andics. “When we want to understand how an animal processes speech, it’s important that speech be relevant.” Andics and his colleagues trained dogs to lie still for functional MRI scans, which reveal when and where the brain is responding to certain cues. Then the scientists played the dogs recordings of a trainer saying either meaningful praise words like “good boy,” or neutral words like “however,” either in an enthusiastic tone of voice or a neutral one. The dogs showed increased activity in the left sides of their brains in response to the meaningful words, but not the neutral ones. An area on the right side of the brain reacted to the intonation of those words, separating out enthusiasm from indifference.
When the dogs heard praising words in an enthusiastic tone of voice, neural circuits associated with reward became more active. The dogs had the same neurological response to an excited “Good dog!” as they might to being petted or receiving a tasty treat. Praise words or enthusiastic intonation alone didn’t have the same effect.
Humans stand out from other animals in their ability to use language — that is, to manipulate sequences of sounds to convey different meanings. But the new findings suggest that the ability to hear these arbitrary sequences of sound and link them to meaning isn’t a uniquely human ability.
“I love these results, as they point to how well domestication has shaped dogs to use and track the very same cues that we use to make sense of what other people are saying,” says Laurie Santos, a cognitive psychologist at Yale University.
While domestication made dogs more attentive to human speech, humans have been close companions with dogs for only 30,000 years. That’s too quickly for a trait like lateralized speech processing to evolve, Andics thinks. He suspects that some older underlying neural mechanism for processing meaningful sounds is present in other animals, too.
It’s just hard to test in other species, he says — in part because cats don’t take as kindly to being put inside MRI scanners and asked to hold still.
A beautiful but unproved theory of particle physics is withering in the harsh light of data.
For decades, many particle physicists have devoted themselves to the beloved theory, known as supersymmetry. But it’s beginning to seem that the zoo of new particles that the theory predicts —the heavier cousins of known particles — may live only in physicists’ imaginations. Or if such particles, known as superpartners, do exist, they’re not what physicists expected.
New data from the world’s most powerful particle accelerator — the Large Hadron Collider, now operating at higher energies than ever before — show no traces of superpartners. And so the theory’s most fervent supporters have begun to pay for their overconfidence — in the form of expensive bottles of brandy. On August 22, a group of physicists who wagered that the LHC would quickly confirm the theory settled a 16-year-old bet. In a session at a physics meeting in Copenhagen, theoretical physicist Nima Arkani-Hamed ponied up, presenting a bottle of cognac to physicists who bet that the new particles would be slow to materialize, or might not exist at all. Whether their pet theories are right or wrong, many theoretical physicists are simply excited that the new LHC data can finally anchor their ideas to reality. “Of course, in the end, nature is going to tell us what’s true,” says theoretical physicist Yonit Hochberg of Cornell University, who spoke on a panel at the meeting.
Supersymmetry is not ruled out by the new data, but if the new particles exist, they must be heavier than scientists expected. “Right now, nature is telling us that if supersymmetry is the right theory, then it doesn’t look exactly like we thought it would,” Hochberg says. Since June 2015, the LHC, at the European particle physics lab CERN near Geneva, has been smashing protons together at higher energies than ever before: 13 trillion electron volts. Physicists had been eager to see if new particles would pop out at these energies. But the results have agreed overwhelmingly with the standard model, the established theory that describes the known particles and their interactions.
It’s a triumph for the standard model, but a letdown for physicists who hope to expose cracks in that theory. “There is a low-level panic,” says theoretical physicist Matthew Buckley of Rutgers University in Piscataway, N.J. “We had a long time without data, and during that time many theorists thought up very compelling ideas. And those ideas have turned out to be wrong.”
Physicists know that the standard model must break down somewhere. It doesn’t explain why the universe contains more matter than antimatter, and it fails to pinpoint the origins of dark matter and dark energy, which make up 95 percent of the matter and energy in the cosmos.
Even the crowning achievement of the LHC, the discovery of the Higgs boson in 2012 (SN: 7/28/2012, p. 5), hints at the sickness within the standard model. The mass of the Higgs boson, at 125 billion electron volts, is vastly smaller than theory naïvely predicts. That mass, physicists worry, is not “natural” — the factors that contribute to the Higgs mass must be finely tuned to cancel each other out and keep the mass small (SN Online: 10/22/13).
Among the many theories that attempt to fix the standard model’s woes, supersymmetry is the most celebrated. “Supersymmetry was this dominant paradigm for 30 years because it was so beautiful, and it was so perfect,” says theoretical physicist Nathaniel Craig of the University of California, Santa Barbara. But supersymmetry is becoming less appealing as the LHC collects more collisions with no signs of superpartners.
Supersymmetry solves three major problems in physics: It explains why the Higgs is so light; it provides a particle that serves as dark matter; and it implies that the three forces of the standard model (electromagnetism and the weak and strong nuclear forces) unite into one at high energies.
If a simple version of supersymmetry is correct, the LHC probably should have detected superpartners already. As the LHC rules out such particles at ever-higher masses, retaining the appealing properties of supersymmetry requires increasingly convoluted theoretical contortions, stripping the idea of some of the elegance that first persuaded scientists to embrace it. “If supersymmetry exists, it is not my parents’ supersymmetry,” says Buckley. “That kind of means it can’t be the most compelling version.”
Still, many physicists are adopting an attitude of “keep calm and carry on.” They aren’t giving up hope that evidence for the theory — or other new particle physics phenomena — will show up soon. “I am not yet particularly worried,” says theoretical physicist Carlos Wagner of the University of Chicago. “I think it’s too early. We just started this process.” The LHC has delivered only 1 percent of the data it will collect over its lifetime. Hopes of quickly finding new phenomena were too optimistic, Wagner says. Experimental physicists, too, maintain that there is plenty of room for new discoveries. But it could take years to uncover them. “I would be very, very happy if we were able to find some new phenomena, some new state of matter, within the first two or three years” of running the LHC at its boosted energy, Tiziano Camporesi of the LHC’s CMS experiment said during a news conference at the International Conference on High Energy Physics, held in Chicago in August. “That would mean that nature has been kind to us.”
But other LHC scientists admit they had expected new discoveries by now. “The fact that we haven’t seen something, I think, is in general quite surprising to the community,” said Guy Wilkinson, spokesperson for the LHCb experiment. “This isn’t a failure — this is perhaps telling us something.” The lack of new particles forces theoretical physicists to consider new explanations for the mass of the Higgs. To be consistent with data, those explanations can’t create new particles the LHC should already have seen.
Some physicists — particularly those of the younger generations — are ready to move on to new ideas. “I’m personally not attached to supersymmetry,” says David Kaplan of Johns Hopkins University. Kaplan and colleagues recently proposed the “relaxion” hypothesis, which allows the Higgs mass to change — or relax — as the universe evolves. Under this theory, the Higgs mass gets stuck at a small value, never reaching the high mass otherwise predicted.
Another idea, which Craig favors, is a family of theories by the name of “neutral naturalness.” Like supersymmetry, this idea proposes symmetries of nature that solve the problem of the Higgs mass, but it doesn’t predict new particles that should have been seen at the LHC. “The theories, they’re not as beautiful as just simple supersymmetry, but they’re motivated by data,” Craig says.
One particularly controversial idea is the multiverse hypothesis. There may be innumerable other universes, with different Higgs masses in each. Perhaps humans observe such a light Higgs because a small mass is necessary for heavy elements like carbon to be produced in stars. People might live in a universe with a small Higgs because it’s the only type of universe life can exist in.
It’s possible that physicists’ fears will be realized — the LHC could deliver the Higgs boson and nothing else. Such a result would leave theoretical physicists with few clues to work with. Still, says Hochberg, “if that’s the case, we’ll still be learning something very deep about nature.”
This issue marks the second year that Science News has reached out to science notables and asked: Which up-and-coming scientist is making a splash? Whose work impresses you? Tell us about early- to mid-career scientists who have the potential to change their fields and the direction of science more generally.
This year, we expanded the pool of people we asked. We reached out to Nobel laureates again and added recently elected members of the National Academy of Sciences. That allowed us to consider shining lights from a much broader array of fields, from oceanography and astronomy to cognitive psychology. Another difference this year: We spent time face-to-face with many of those selected, to get a better sense of them both as scientists and as people. The result is the SN 10, a collection of stories not only about science, but also about making a life in science. They are stories of people succeeding because they have found what they love, be it working in the lab on new ways to probe molecular structures or staring up to the stars in search of glimmers of the early universe. In my interviews with chemist Phil Baran, I was struck by his drive to do things in new ways, whether devising chemical reactions or developing ideas about how to fund research. (If you can, he says, go private.) Laura Sanders, who met with neuroscientist Jeremy Freeman, was intrigued by his way of seeing a problem (siloed data that can’t be easily shared or analyzed) and figuring out solutions, even if those solutions were outside his area of expertise.
Of course, there are many ways to identify noteworthy scientists — and there’s plenty more fodder out there for future years. Our approach was to seek standouts, asking who deserved recognition for the skill of their methods, the insights of their thinking, the impacts of their research. Not all of the SN 10’s work has made headlines, but they all share something more important: They are participants in building the science of the future.
Notably, many of them do basic research. I think that’s because it’s the type of work that other scientists notice, even if it’s not always on the radar of the general public. But that’s where fundamental advances are often made, as scientists explore the unknown.
That edge of what’s known is where Science News likes to explore, too. Such as the bet-ending, head-scratching results from the Large Hadron Collider, which have failed to reveal the particles that the equations of supersymmetry predict. As Emily Conover reports in “Supersymmetry’s absence at LHC puzzles physicists,” that means that either the theory must be more complicated than originally thought, or not true, letting down those who looked to supersymmetry to help explain a few enduring mysteries, from the nature of dark matter to the mass of the Higgs boson.
Other mysteries may be closer to a solution, as Sanders reports in “New Alzheimer’s drug shows promise in small trial.” A new potential treatment for Alzheimer’s disease reduced amyloid-beta plaques in patients. It also showed hints of improving cognition. That’s standout news, a result built on decades of basic research by many, many bright young scientists.
In smart homes of the future, computers may identify inhabitants and cater to their needs using a tool already at hand: Wi-Fi. Human bodies partially block the radio waves that carry the wireless signal between router and computer. Differences in shape, size and even gait among household members yield different patterns in the received Wi-Fi signals. A computer can analyze the signals to distinguish dad from mom, according to a report posted online August 11 at arXiv.org.
Scientists built an algorithm that was nearly 95 percent accurate when attempting to discern two adults walking between a wireless router and a computer. For six people, accuracy fell to about 89 percent. Scientists tested the setup on men and women of various sizes, but it should work with children as well, says study coauthor Bin Guo of Northwestern Polytechnical University in Xi’an, China.
In a home rigged with Wi-Fi and a receiver, the system could eventually identify family members and tailor heating and lighting to their preferences — maybe even cue up a favorite playlist.
Two trillion galaxies. That’s the latest estimate for the number of galaxies that live — or have lived — in the observable universe, researchers report online October 10 at arXiv.org. This updated headcount is roughly 10 times greater than previous estimates and suggests that there are a lot more galaxies out there for future telescopes to explore.
Hordes of relatively tiny galaxies, weighing as little as 1 million suns, are responsible for most of this tweak to the cosmic census. Astronomers haven’t directly seen these galaxies yet. Christopher Conselice, an astrophysicist at the University of Nottingham in England, and colleagues combined data from many ground- and space-based telescopes to look at how the number of galaxies in a typical volume of the universe has changed over much of cosmic history. They then calculated how many galaxies have come and gone in the universe.
The galactic population has dwindled over time, as most of those 2 trillion galaxies collided and merged to build larger galaxies such as the Milky Way, the researchers suggest. That’s in line with prevailing ideas about how massive galaxies have been assembled. Seeing many of these remote runts, however, is beyond the ability of even the next generation of telescopes. “We will have to wait at least several decades before even the majority of galaxies have basic imaging,” the researchers write.
Crucial immune system proteins that make it harder for viruses to replicate might also help the attackers avoid detection, three new studies suggest. When faced with certain viruses, the proteins can set off a cascade of cell-to-cell messages that destroy antibody-producing immune cells. With those virus-fighting cells depleted, it’s easier for the invader to persist inside the host’s body.
The finding begins to explain a longstanding conundrum: how certain chronic viral infections can dodge the immune system’s antibody response, says David Brooks, an immunologist at the University of Toronto not involved in the research. The new studies, all published October 21 in Science Immunology, pin the blame on the same set of proteins: type 1 interferons. Normally, type 1 interferons protect the body from viral siege. They snap into action when a virus infects cells, helping to activate other parts of the immune system. And they make cells less hospitable to viruses so that the foreign invaders can’t replicate as easily.
But in three separate studies, scientists tracked mice’s immune response when infected with lymphocytic choriomeningitis virus, or LCMV. In each case, type 1 interferon proteins masterminded the loss of B cells, which produce antibodies specific to the virus that is being fought. Normally, those antibodies latch on to the target virus, flagging it for destruction by other immune cells called T cells. With fewer B cells, the virus can evade capture for longer.
The proteins’ response “is driving the immune system to do something bad to itself,” says Dorian McGavern, an immunologist at the National Institute of Neurological Disorders and Stroke in Bethesda, Md., who led one of the studies.
The interferon proteins didn’t directly destroy the B cells; they worked through middlemen instead. These intermediaries differed depending on factors including the site of infection and how much of the virus the mice received. T cells were one intermediary. McGavern and his colleagues filmed T cells actively destroying their B cell compatriots under the direction of the interferon proteins. When the scientists deleted those T cells, the B cells didn’t die off even though the interferons were still hanging around. Another study found that the interferons were sending messages not just through T cells, but via a cadre of other immune cells, too. Those messages told B cells to morph into cells that rapidly produce antibodies for the virus. But those cells die off within a few days instead of mounting a longer-term defense.
That strategy could be helpful for a short-term infection, but less successful against a chronic one, says Daniel Pinschewer, a virologist at the University of Basel in Switzerland who led that study. Throwing the entire defense arsenal at the virus all at once leaves the immune system shorthanded later on.
But interferon activity could prolong even short-term viral infections, a third study showed. There, scientists injected lower doses of LCMV into mice’s footpads and used high-powered microscopes to watch the infection play out in the lymph nodes. In this case, the interferon stifled B cells by working through inflammatory monocytes, white blood cells that rush to infection sites.
“The net effect is beneficial for the virus,” says Matteo Iannacone, an immunologist at San Raffaele Scientific Institute in Milan who led the third study. Sticking around even a few days longer gives the virus more time to spread to new hosts.
Since all three studies looked at the same virus, it’s not yet clear whether the mechanism extends to other viral infections. That’s a target for future research, Iannacone says. But Brooks thinks it’s likely that other viruses that dampen antibody response (like HIV and hepatitis C) could also be exploiting type 1 interferons.
Joining a gang doesn’t necessarily make a protein a killer, a new study suggests. This clumping gets dangerous only under certain circumstances.
A normally innocuous protein can be engineered to clump into fibers similar to those formed by proteins involved in Alzheimer’s, Parkinson’s and brain-wasting prion diseases such as Creutzfeldt-Jakob disease, researchers report in the Nov. 11 Science. Cells that rely on the protein’s normal function for survival die when the proteins glom together. But cells that don’t need the protein are unharmed by the gang activity, the researchers discovered. The finding may shed light on why clumping proteins that lead to degenerative brain diseases kill some cells, but leave others untouched. Clumpy proteins known as prions or amyloids have been implicated in many nerve-cell-killing diseases (SN: 8/16/08, p. 20). Such proteins are twisted forms of normal proteins that can make other normal copies of the protein go rogue, too. The contorted proteins band together, killing brain cells and forming large clusters or plaques.
Scientists don’t fully understand why these mobs resort to violence or how they kill cells. Part of the difficulty in reconstructing the cells’ murder is that researchers aren’t sure what jobs, if any, many of the proteins normally perform (SN: 2/13/10, p. 17).
A team led by biophysicists Frederic Rousseau and Joost Schymkowitz of Catholic University Leuven in Belgium came up with a new way to dissect the problem. They started with a protein for which they already knew the function and engineered it to clump. That protein, vascular endothelial growth factor receptor 2, or VEGFR2, is involved in blood vessel growth. Rousseau and colleagues clipped off a portion of the protein that causes it to cluster with other proteins, creating an artificial amyloid.
Masses of the protein fragment, nicknamed vascin, could aggregate with and block the normal activity of VEGFR2, the researchers found. When the researchers added vascin to human umbilical vein cells grown in a lab dish, the cells died because VEGFR2 could no longer transmit hormone signals the cells need to survive. But human embryonic kidney cells and human bone cancer cells remained healthy. Those results suggest that some forms of clumpy proteins may not be generically toxic to cells, says biophysicist Priyanka Narayan of the Whitehead Institute for Biomedical Research in Cambridge, Mass. Instead, rogue clumpy proteins may target specific proteins and kill only cells that rely on those proteins for survival.
Those findings may also indicate that prion and amyloid proteins, such as Alzheimer’s nerve-killing amyloid-beta, normally play important roles in some brain cells. Those cells would be the ones vulnerable to attack from the clumpy proteins. The newly engineered ready-to-rumble protein may open new ways to inactivate specific proteins in order to fight cancer and other diseases, says Salvador Ventura, a biophysicist at the Autonomous University of Barcelona. For instance, synthetic amyloids of overactive cancer proteins could gang up and shut down the problem protein, killing the tumor.
Artificial amyloids might also be used to screen potential drugs for anticlumping activity that could be used to combat brain-degenerating diseases, Rousseau suggests.
It was barely more than half a century ago that the Nobel Prize–winning virologist Sir Frank Macfarlane Burnet mused about the demise of contagions. “To write about infectious disease,” he wrote in 1962, “is almost to write of something that has passed into history.”
If only. In the past several decades, over 300 infectious pathogens have either newly emerged or emerged in new places, causing a steady drumbeat of outbreaks and global pandemic scares.
Over the course of 2016, their exploits reached a crescendo. Just as the unprecedented outbreak of Ebola in West Africa was collapsing in early 2016, the World Health Organization declared Zika virus, newly erupted in the Americas, an international public health emergency. What would balloon into the largest outbreak of yellow fever in Angola in 30 years had just begun. A few months later, scientists reported the just-discovered “superbug” mcr-1 gene in microbes collected from humans and pigs in the United States (SN Online: 5/27/16). The gene allows bacteria to resist the last-ditch antibiotic colistin, bringing us one step closer to a looming era of untreatable infections that would transform the practice of medicine. Its arrival presaged yet another unprecedented event: the convening of the United Nations General Assembly to consider the global problem of antibiotic-resistant bugs. It was only the fourth time over its 70-plus-year history that the assembly had been compelled to consider a health challenge. It’s “huge,” says University of Toronto epidemiologist David Fisman. But even as UN delegates arrived for their meeting in New York City in September, another dreaded infection was making headlines again. The international community’s decades-long effort to end the transmission of polio had unraveled. In 2015, the WHO had declared Nigeria, one of the three last countries in the world that suffered the infection, free of wild polio. By August 2016, it was back. Millions would have to be vaccinated to keep the infection from establishing a foothold. Three fundamental, interrelated factors fuel the microbial comeback, experts say. Across the globe, people are abandoning the countryside for life in the city, leading to rapid, unplanned urban expansions. In crowded conditions with limited access to health care and poor sanitation, pathogens like Ebola, Zika and influenza enjoy lush opportunities to spread. With more infections mingling, there are also more opportunities for pathogens to share their virulence genes.
At the same time, global demand for meat has quadrupled over the last five decades by some estimates, driving the spread of industrial livestock farming techniques that can allow benign microbes to become more virulent. The use of colistin in livestock agriculture in China, for example, has been associated with the emergence of mcr-1, which was first discovered during routine surveillance of food animals there. Genetic analyses suggest that siting factory farms full of chickens and pigs in proximity to wild waterfowl has played a role in the emergence of highly virulent strains of avian influenza. Crosses of Asian and North American strains of avian influenza caused the biggest outbreak of animal disease in U.S. history in 2014–2015. Containing that virus required the slaughter of nearly 50 million domesticated birds and cost over $950 million. Worryingly, some strains of avian influenza, such as H5N1, can infect humans. The thickening blanket of carbon dioxide in the atmosphere resulting from booming populations of people and livestock provides yet another opportunity for pathogens to exploit. Scientists around the world have documented the movement of disease-carrying creatures including mosquitoes and ticks into new regions in association with newly amenable climatic conditions. Climate scientists predict range changes for bats and other animals as well. As the organisms spread into new ranges, they carry pathogens such as Ebola, Zika and Borrelia burgdorferi(a bacterium responsible for Lyme disease) along with them. Since we can rarely develop drugs and vaccines fast enough to stanch the most dangerous waves of disease, early detection will be key moving forward. Researchers have developed a welter of models and pilot programs showing how environmental cues such as temperature and precipitation fluctuations and the insights of wildlife and livestock experts can help pinpoint pathogens with pandemic potential before they cause outbreaks in people. Chlorophyll signatures, a proxy for the plankton concentrations that are associated with cholera bacteria, can be detected from satellite data, potentially providing advance notice of cholera outbreaks.
Even social media chatter can be helpful. Innovative financing methods, such as the World Bank’s recently launched Pandemic Emergency Financing Facility — a kind of global pandemic insurance policy funded by donor countries, the reinsurance market and the World Bank — could help ensure that resources to isolate and contain new pathogens are readily available, wherever they take hold. Right now, emerging disease expert Peter Daszak points out, “we wait for epidemics to emerge and then spend billions on developing vaccines and drugs.” The nonprofit organization that Daszak directs, EcoHealth Alliance, is one of a handful that instead aim to detect new pathogens at their source and proactively minimize the risk of their spread.
Burnet died in 1985, two years after the discovery of HIV, one of the first of the latest wave of new pathogens. His vision of a contagion-free society was that of a climber atop a foothill surrounded by peaks, mistakenly thinking he’d reached the summit. The challenge of surviving in a world of pathogens is far from over. In many ways, it’s only just begun.
