HIV came to NYC at least a decade before virus ID’d

A genetic study of HIV viruses from the 1970s may finally clear the name of a man long identified as the source of the AIDS epidemic in the United States. HIV came to New York City between 1969 and 1973, long before the man known as Patient Zero became infected, researchers report October 26 in Nature.

Using techniques developed to decipher badly degraded ancient DNA from fossils, researchers reconstructed the genetic instruction books of eight HIV viruses from blood samples collected in 1978 and 1979 in New York City and San Francisco. The viral DNA was so genetically diverse that the viruses must have been circulating in the cities for years, picking up variations, says evolutionary biologist Michael Worobey of the University of Arizona in Tucson.
Worobey and colleagues calculate that the virus probably first jumped to the United States in 1970 or 1971. So HIV spread for about a decade before AIDS was recognized in 1981 and found to be caused by a retrovirus in 1983.
Examining the relationships between the New York City and San Francisco viruses with HIV strains from elsewhere let researchers trace the virus’s path. The eight American samples all came from the same branch of the HIV family tree as ones from the Caribbean. That suggests that HIV spread from Africa to the Caribbean before making its way to the United States. New York HIV samples were more diverse than those from California, indicating that New York City was probably the hub of early HIV spread and the virus arrived in San Francisco later.
Worobey and colleagues also examined HIV DNA from Patient Zero. Also known as Case 57, he was part a 1984 study of gay men with AIDS in Los Angeles who had either a rare cancer called Kaposi’s sarcoma or Pneumocystis carinii pneumonia, both complications of the disease. Researchers from the Centers for Disease Control and Prevention found that many of the men had had sexual contact with each other, helping to establish that HIV is sexually transmitted.
Later, in the book And the Band Played On, author Randy Shilts identified Patient Zero as an Air Canada flight attendant named Gaëtan Dugas. It was widely interpreted that Dugas was the first case of HIV in the United States, even though the CDC never claimed — and has repeatedly refuted — that, says epidemiologist James Curran, a coauthor of the 1984 study who is now at Emory University in Atlanta. Part of the confusion may have been that Patient Zero was supposed to be identified as Patient O (for “outside of California”).

Dugas became a flight attendant in 1974 and began traveling to the United States shortly after, says Richard McKay, coauthor of the new study and a medical historian at the University of Cambridge. Dugas estimated that he had about 250 male sexual partners each year between 1979 and 1981. Shilts and others contended that Dugas was intentionally spreading the virus to others, though he was diagnosed with Kaposi’s sarcoma in 1980 before anyone knew what AIDS was or that it was caused by a virus.

Now, the genetic analysis confirms that Dugas was not carrying the earliest version of the virus. “This individual was simply one of thousands infected before HIV/AIDS was recognized,” McKay says.

The new study is a cautionary tale against trying to pin the spread of an infectious disease on any one person, says Robert Remien, a behavioral scientist at Columbia University Medical Center. “There’s no blame or cause to be laid on any of those people in those early years.”

Editor’s note: This story was updated November 10, 2016, to fix the alignment of the timeline with the phylogenetic tree and to update the number of sequential diagnoses in the Patient Zero cluster of AIDS cases.

Learning curve not so smooth

Many preschoolers take a surprisingly long and bumpy mental path to the realization that people can have mistaken beliefs — say, thinking that a ball is in a basket when it has secretly been moved to a toy box. Traditional learning curves, in which kids gradually move from knowing nothing to complete understanding, don’t apply to this landmark social achievement and probably to many other types of learning, a new study concludes.

Kids ranging in age from 3 to 5 often go back and forth between passing and failing false-belief tests for several months to more than one year, say psychologist Sara Baker of the University of Cambridge and her colleagues. A small minority of youngsters jump quickly from always failing to always passing these tests, the scientists report October 20 in Cognitive Psychology.
“If these results are replicated, it will surprise a lot of researchers that there is such a low level of sudden insight into false beliefs,” says psychologist Malinda Carpenter, currently at the Max Planck Institute for Evolutionary Anthropology in Leipzig. Early childhood researchers generally assume that preschoolers either pass or fail false-belief tests, with a brief transition between the two, explains Carpenter, who did not participate in the new study. Grasping that others sometimes have mistaken beliefs is a key step in social thinking.

False-belief understanding may start out as something that can be indicated nonverbally but not described. Human 2-year-olds and even chimpanzees tend to look toward spots where a person would expect to find a hidden item that only the children or apes have seen moved elsewhere (SN Online: 10/6/16).

Numerous investigations suggest that neurologically healthy kids between ages 3 and 5 consciously appreciate when others have formed mistaken beliefs. But those studies report average scores on false-belief tests for groups of preschoolers. That leaves unexamined how individual kids progress — or not — as mind readers.

Baker’s team generated individual scoring profiles for 52 children repeatedly assessed for false-belief understanding between ages 3 and 5. Trials occurred over roughly one to two years. Two types of false-belief tasks were alternately presented about every two to six weeks, either at a preschool, in a lab or at a child’s home.

In one task, an experimenter used pictures to help describe a situation in which someone moves an object from one location to another once a friend leaves — say, taking a ball from a basket and putting it in a toy box. Children were asked where the friend would later look for the object.
In a second task, children observed a container’s unexpected contents, such as a sock in a crayon box or a toy cow in an egg carton. Kids reported what they originally thought was inside the container and what another person would think is inside it.

Nine children, including some of the youngest ones, passed their first three trials. All except one of the nine continued to pass trials at a high rate. The remaining 43 children failed at least one of the first three trials. A statistical analysis calculated the likelihood that a series of scores for a particular child reflected gains, losses or no change in false-belief understanding.

Five of the 43 children achieved rapid insights into false beliefs, consistently passing trials immediately after a string of failed trials. Another 22 youngsters showed different patterns of improvement, such as going from a 12 percent likelihood of passing trials to a 50 percent chance by the study’s end. None of them moved gradually and steadily from failing to passing false belief tests. Smooth learning curves are statistical illusions created by averaging group scores, the researchers suspect.

Four kids started out failing false-belief tests and showed no signs of improvement over time. Another 10 children sometimes passed and sometimes failed throughout the study. Statistical profiles were inconclusive for two children.

Related findings, although based on group statistics, nonetheless suggest that grade-schoolers shift among various problem-solving strategies when learning mathematical concepts (SN: 3/17/01, p. 172). Baker’s statistical method could enhance the study of how individual children develop math skills and other forms of reasoning, says psychologist Rose Scott of the University of California, Merced.

Supersolids produced in exotic state of quantum matter

A mind-bogglingly strange state of matter may have finally made its appearance. Two teams of scientists report the creation of supersolids, which are both liquid and solid at the same time. Supersolids have a crystalline structure like a solid, but can simultaneously flow like a superfluid, a liquid that flows without friction.

Research teams from MIT and ETH Zurich both produced supersolids in an exotic form of matter known as a Bose-Einstein condensate. Reports of the work were published online at arXiv.org on October 26 (by the MIT group) and September 28 (by the Zurich group).
Bose-Einstein condensates are created when a group of atoms, chilled to near absolute zero, huddle up into the same quantum state and begin behaving like a single entity. The scientists’ trick for creating a supersolid was to nudge the condensate, which is already a superfluid, into simultaneously behaving like a solid. To do so, the MIT and Zurich teams created regular density variations in the atoms — like the repeating crystal structure of a more typical solid — in the system. That density variation stays put, even though the fluid can still flow.

The new results may be the first supersolids ever created — at least by some definitions. “It’s certainly the first case where you can unambiguously look at a system and say this is both a superfluid and a solid,” says Sarang Gopalakrishnan of the College of Staten Island of the City University of New York. But the systems are far from what physicists predicted when they first dreamt up the strange materials.

Scientists originally expected supersolids to appear in helium-4 — an isotope of the element helium and the same gas that fills balloons at children’s birthday parties. Helium-4 can be chilled and pressurized to produce a superfluid or a solid. Supersolid helium would have been a mixture of these two states.

Previous claims of detecting supersolid helium-4, however, didn’t hold up to scrutiny (SN Online: 10/12/2012). So, says Nikolay Prokof’ev of the University of Massachusetts Amherst, “now we have to go to the artificial quantum matter.” Unlike helium-4, Bose-Einstein condensates can be precisely controlled with lasers, and tuned to behave as scientists wish.

The two groups of scientists formed their supersolids in different ways. By zapping their condensate with lasers, the MIT group induced an interaction that gave some of the atoms a shove. This motion caused an interference between the pushed and the motionless atoms that’s similar to the complex patterns of ripples that can occur when waves of water meet. As a result, zebralike stripes — alternating high- and low-density regions — formed in the material, indicating that it was a solid.
Applying a different method, the ETH Zurich team used two optical cavities — sets of mirrors between which light bounces back and forth repeatedly. The light waves inside the cavities caused atoms to interact and thereby arrange themselves into a crystalline pattern, with atoms separated by an integer number of wavelengths of light.

Authors of the two studies declined to comment on the research, as the papers have been submitted to embargoed journals.

“Experimentally, of course, these are absolutely fantastic achievements,” says Anatoly Kuklov of the College of Staten Island. But, he notes, the particles in the supersolid Bose-Einstein condensates do not interact as strongly as particles would in supersolid helium-4. The idea of a supersolid is so strange because superfluid and solid states compete, and in most materials atoms are forced to choose one or the other. But in Bose-Einstein condensates these two states can more easily live together in harmony, making the weird materials less counterintuitive than supersolid helium-4 would be.

Additionally, says Prokof’ev, “some people will say ‘OK, well, this does not qualify exactly for supersolid state,’” because the spacing of the density variations was set externally, rather than arising naturally as it would have in helium.

Still, such supersolids are interesting for their status as a strange and new type of material. “These are great works,” says Kuklov. “Wide attention is now being paid to supersolidity.”

Zap to the head leads to fat loss

SAN DIEGO — A nerve-zapping headset caused people to shed fat in a small preliminary study.

Six people who had received the stimulation lost on average about 8 percent of the fat on their trunks in four months, scientists reported November 12 at the annual meeting of the Society for Neuroscience.

The headset stimulated the vestibular nerve, which runs just behind the ears. That nerve sends signals to the hypothalamus, a brain structure thought to control the body’s fat storage. By stimulating the nerve with an electrical current, the technique shifts the body away from storing fat toward burning it, scientists propose.
Six overweight and obese people received the treatment, consisting of up to four one-hour-long sessions of stimulation a week. Because it activates the vestibular system, the stimulation evoked the sensation of gently rocking on a boat or floating in a pool, said study coauthor Jason McKeown of the University of California, San Diego.

After four months, body scans measured the trunk body fat for the six people receiving the treatment and three people who received sham stimulation. All six in the treatment group lost some trunk fat, despite not having changed their activity or diet. In contrast, those in the sham group gained some fat. Researchers suspect that metabolic changes are behind the difference. “The results were a lot better than we thought they’d be,” McKeown said.

Earlier studies had found that vestibular nerve stimulation causes mice to drop fat and pack on muscle, resulting in what McKeown called Schwarzenegger mice. Though small, the current study suggests that the approach has promise in people. McKeown and colleagues have started a company based on the technology and plan to test it further, he said.

How a ring of mountains forms inside a crater

Building mountains in minutes requires deep rocks and a big bang.

Rings of mountainous peaks sit inside large impact craters, but scientists weren’t sure how these features formed. One explanation proposed that these mountains form from deep rocks jolted to the surface by the impact. Another theory suggested that uplift caused surface rocks to congregate in heaps around the crater.

Rocks extracted from ground zero of the impact that devastated the dinosaurs have now resolved this debate. That crater’s peak ring is made up of deep rocks, researchers report in the Nov. 18 Science.
Confirming this explanation of peak ring formation will help scientists study the depths of other planets, says study coauthor Sean Gulick, a geophysicist at the University of Texas at Austin. It will also help better estimate the environmental damage wrought by the dinosaur-killing impact.、
“Unlike tectonic mountains that take millions of years to form, these mountains are made in less than 10 minutes,” Gulick says. Knowing the forces involved in sculpting those mountains will allow scientists to better estimate the total energy released during the catastrophic crash.
The Chicxulub impactor whacked into Mexico’s Yucatán Peninsula around 66 million years ago, leaving behind a 200-kilometer-wide hole in the ground. Rising around 600 meters from the crater floor — though now buried under sediment – is the peak ring. While similar rings of mountains have been spotted inside large craters on other planetary bodies such as the moon and Mercury, Chicxulub is the only crater on Earth with an intact peak ring structure. And “it’s a lot cheaper to get to the one in Mexico,” Gulick says.

Last spring, Gulick and colleagues drilled into Chicxulub’s peak ring off the coast of Mexico using a special ship that can convert into a stable platform using three long legs. Rock samples, collected from about 750 to 1,300 meters below the seafloor, contained bits of granite and other minerals that would have been buried many kilometers belowground just before the impact. That means that the same process that built the peak ring must have churned those deep rocks to the surface, the researchers concluded.
That result does not mesh with the idea that the peak ring material instead came from much closer to the surface. Under that theory, after impact, surface material slides down the crater rim onto the floor. The middle of the floor then rebounds upward due to the removal of the weight of the overlying rock. That uplift shifts the fallen material, forming a peak ring.
Instead, the dynamic collapse theory of peak ring formation explains what happened at Chicxulub, researchers say. After the initial strike, churned-up material rushed in to fill the deep void left by the impact, like water when a stone is dropped into a pond. The flowing material met in the middle of the crater and surged upward into a towering central peak that then collapsed outward, dumping rocks previously buried several kilometers underground onto the crater’s surface.
These rocks became more porous and less dense during their dramatic rise, the researchers found. While typical deep rocks in the region have an average density of more than 2.6 grams per cubic centimeter, the peak ring rocks average just 2.41 grams per cubic centimeter and are heavily fractured.

“About 10 percent of the rock is pores, so there’s lots of space,” Gulick says. Microbes, he proposes, may have moved into those holes as life repopulated the impact site. Early life on Earth may have even gotten its first foothold in the porous rock inside similar impact craters, he speculates.

The high porosity of the Chicxulub rock could also explain why the moon’s crater-riddled crust is highly porous and help solve other planetary mysteries as well, says Ross Potter, a planetary scientist at Brown University.

“Impact craters are excavating material from depth, so they’re very good probes into the interior of planetary bodies,” he says. “You may be able to find very interesting samples that tell you a lot about not only the cratering process itself, but also the interior of the planet and how the planet formed.”

For some early monks, impaired hearing amplified sounds of silence

SAN ANTONIO — Early Christian monks’ vows of silence may have attracted not only the devout but also a fair number of hearing-impaired men with a sacred calling.

A team led by bioarchaeologist Margaret Judd of the University of Pittsburgh found that a substantial minority of Byzantine-era monks buried in a communal crypt at Jordan’s Mount Nebo monastery display skeletal signs of hearing impairments. Judd presented these results November 19 at the annual meeting of the American Schools of Oriental Research.
Judd has directed excavations at Mount Nebo since 2007. Her new results focus on a two-chambered crypt containing skeletons of at least 57 men presumed to have been monks. Oil lamps found in the crypt date to the 700s.

About 16 percent of these men displayed damage to middle ear bones caused by infections known as otitis media. This condition frequently occurs in childhood and can lead to lasting hearing problems even if the infection clears up quickly (SN Online: 3/10/10). Monks showing signs of otitis media probably suffered mild to moderate hearing loss.

Damage to one middle ear bone, the stapes, in two other individuals likely caused severe hearing loss in one ear each. In another case, a fracture above the left eye could have damaged middle ear bones, Judd proposed. Finally, one skull’s thickened bone may have resulted from Paget’s disease, a viral infection in adulthood that can impair hearing.

Hearing loss would have had little effect on monks’ daily lives, since they communicated with hand signals, nods and other gestures, Judd said. Even if some developed hearing ailments after joining the monastery, those conditions must have largely gone undetected by affected monks and their peers who rarely or never spoke, she suggested.

Scientific success depends on finding light in darkness

Without light, we cannot see. That’s why “dark galaxies” have eluded astronomers for so long. Two years ago, these star-starved entities were virtually unknown. But scientists now have better ways of seeing, even in dim conditions. New telescopes that can detect the faint light from these mysterious galaxies have enabled scientists to chalk up a considerable list: Dark galaxies seem to be much more common than anyone had thought. One rivals the Milky Way in size but holds only a hundredth as many stars.

Cataloging these dark galaxies, as Christopher Crockett reports (SN: 12/10/16, p. 18), is just the beginning. Scientists still don’t know how such galaxies might have formed or how their small populations of stars can fend off the gravitational grabs of other galaxies. Understanding dark galaxies will take more time and more intense study of their faint light.
Cleverly built telescopes may allow us to examine the cosmic darkness, but a different type of cleverness entirely is required to delve into the minds of animals. Specifically, researchers trying to understand the evolutionary roots of mathematics must resort to complex tests for evaluating how animals judge quantities, Susan Milius reports in “Animals give clues to the origins of human number crunching.” (SN: 12/10/16, p. 22).

Counting seems an all-too-human concept, and yet many creatures can reliably pick out a greater number of treats. Figuring out how animals are making such a choice (is it surface area? volume? number?) has frustrated researchers and occasionally triggered disagreements. But the latest studies show signs that many animals do have some quantitative sense, even if it’s far less sophisticated than our own.

Much less illuminating are the results that supposedly would have provided the final answer about heart health risks posed by the anti-inflammatory pain medicine Celebrex. Like Vioxx, which was taken off the market years ago after it was linked to heart problems, Celebrex (generic name celecoxib) is what’s known as a COX-2 inhibitor. Many experts were concerned that the problems with Vioxx might also show up in people who took Celebrex. But there were little data, so the U.S. Food and Drug Administration asked for a large study to clear up the question. When the results were reported in November at a meeting of the American Heart Association, they brought little resolution, Laura Beil reports in “Popular painkiller doesn’t have more heart risks than others, study claims” (SN: 12/10/16, p. 6). Despite finding no elevated heart risk from Celebrex use, and fewer gastrointestinal side effects compared with ibuprofen and naproxen, the study was not done as cleverly as it needed to be. It enrolled people already at low risk of heart problems, for one. Dosages of medicines shifted during the long study. Many taking Celebrex dropped out before the study was completed. Far from settling the issue, the research leaves many questions unanswered.

In so many areas, science succeeds — seeing into the darkness, exploring the unknown and investigating fantastical ideas. But sometimes the signal is faint, the tools we use too crude, the logic shaky, the deeper understanding still elusive. That’s when scientists need to be more clever, more persistent, more wedded to reason and committed to revealing whatever truths can be found out there in the light.

Stellar vomiting produces dark galaxies, simulations suggest

Brilliant births and destructive deaths of stars might take a runt of a galaxy and stretch it to become a ghostly behemoth, new computer simulations show. This process could explain the origin of recently discovered dark galaxies, which can be as wide as the Milky Way but host roughly 1 percent as many stars.

Since 2015, astronomers have found hundreds of these shadowy systems lurking in and around several clusters of galaxies (SN: 12/10/16, p. 18). How these dark galaxies form is a puzzle. But prolific star formation and blast waves from exploding stars could be responsible, researchers suggest in a paper to appear in Monthly Notices of the Royal Astronomical Society Letters.
“The mystery is: Are these galaxies like the Milky Way, or are they dwarf galaxies?” says study coauthor Arianna Di Cintio, an astrophysicist at the University of Copenhagen in Denmark. “Our mechanism could be a nice formation scenario for these galaxies and prove that they are dwarfs.”

Di Cintio and colleagues ran computer simulations of galaxy evolution and found that some runts can be inflated by stellar energy. Radiation from young massive stars heats up interstellar gas, preventing it from forming more stars. And a flurry of supernova explosions can toss that gas out of the galaxy. The gravity of the galaxy drops, and so does its ability to hold on to stars and dark matter, an enigmatic substance thought to help hold galaxies together. “Dark matter particles fly outward and start the expansion,” says Di Cintio. “This happens to the stellar population as well.”

Those galaxies that remain as runts in the simulations go through this process just once, whereas giant dark galaxies regurgitate their gas multiple times. And that provides a way to test this idea, says Di Cintio. First astronomers need to find dark entities far away from galaxy clusters where the environment can also take its toll. Then researchers can estimate the ages of stars in the galaxy to see if there have been multiple bursts of star formation. If this hypothesis is correct, dark galaxies might also be loaded up with lots of hydrogen gas that allows them to sustain several rounds of gas purging.

“It is very interesting to see that, in some cases, [supernovas] can be efficient enough to expand dwarf galaxies,” says Nicola Amorisco, also at the University of Copenhagen. He helped put forth an idea that dark galaxies start as runts that get stretched because of rapid rotation. Recent observations also show that some dark systems have masses that are similar to dwarf galaxies (though one is as hefty as the Milky Way). “It is even possible that a combination of — or the interplay between — a few different mechanisms could be responsible,” says Amorisco. “It will be very exciting to understand whether that is the case.”

Cells avoiding suicide may play role in spread of cancer

SAN FRANCISCO — Mostly dead is still partly alive, even for cells on the brink of suicide, new research suggests.

Near-death experiences may play a role in embryo development and help cancer cells that survive chemotherapy spread throughout the body, Denise Montell, a cell biologist at the University of California, Santa Barbara, reported December 6 at the annual meeting of the American Society for Cell Biology.

Montell described a recently discovered process called anastasis that saves cells in the midst of committing a type of cellular suicide known as apoptosis. She and others are only beginning to unravel how the process works. Preliminary results indicate that cells simultaneously kill themselves and hold on to a lifeline in case conditions improve, she said.
Scientists had thought that once a cell going through apoptosis activated an executioner molecule known as a caspase, the cell would surely die, said Claire Walczak, a cell biologist at Indiana University in Bloomington. But cells sometimes call off their attempted suicides at the last moment, even after the executioner starts working, cell biologist Ho Lam Tang discovered in 2008 while a graduate student at the Chinese University of Hong Kong. Tang, now at Johns Hopkins University, named the process anastasis, which in Greek means “rising to life.”

Tang’s discovery that apoptosis is reversible “was really shocking,” said Walczak. “It’s a really nice illustration of how adaptable cells are.”

Tang initially made the discovery by treating an immortal type of cancer cells, called HeLa cells, with a drug that stimulates apoptosis. Once the cells were dying, Tang washed away the drug and some of the cells recovered.

“That experiment is essentially what we do to patients” undergoing chemotherapy treatment, said J. Marie Hardwick, a cell and molecular biologist at Johns Hopkins. She reported with Tang last year in Scientific Reports that fruit fly egg cells can come back from apoptosis and even produce an adult fly.

Cancer patients are given a dose of chemotherapy drugs or radiation that causes cells to commit apoptosis. Then the treatments are stopped for a short time to allow the patient to recover. If cancer cells can come back through anastasis, they may cause a resurgence of the disease, Hardwick suggests. Many of the cells brought back by anastasis have genetic defects. “If you’ve already attempted to die, you’ve got problems,” Hardwick says.
Some cells that survive apoptosis brought on by stresses such as heat or irradiation can go on to divide and “do basically anything a normal cell can do,” Montell said. But unpublished work from her lab indicates that cells brought back to life by anastasis may never go back to their untreated state and may carry permanent memories of their near-death experiences, she said at the cell biology meeting.

Montell and colleagues compared gene activity in untreated cells and ones taken to the brink of death and allowed to recover for varying amounts of time. Cell survival genes are already being made while the cell is preparing to kill itself, her team discovered.

“Dying cells are actually hedging their bets. They’re on the brink of death. They don’t know if things are going to get better or get worse,” Montell said. After recovery, the reanimated cells begin to move and to stimulate blood vessel production. Those are things cells do when healing a wound, but they are also actions taken by tumor cells.

“This would be an extremely unbeneficial response if the cells in question happen to be cancer cells,” Montell said. The findings suggest that stopping anastasis may lead to more effective cancer treatments.

In some other cases, stimulating anastasis may benefit patients, Montell said, such as by saving heart cells after a heart attack or brain cells after a stroke. Those cells don’t divide much so there’s less risk of cancer and recovered cells could restore heart and brain function.

Scientists don’t know exactly how anastasis works — few researchers are even aware it happens — so it may take some time before anyone is able to start or stop anastasis at will, Hardwick said.

Disabling enzyme could block Zika

SAN FRANCISCO — Disrupting the Zika enzyme NS3 could help stop the virus. NS3 causes problems when it gloms on to centrioles, structures inside cells needed to divvy up chromosomes when cells divide, Andrew Kodani, a cell biologist at Boston Children’s Hospital, reported December 6 at the American Society for Cell Biology’s annual meeting.

Zika, dengue and other related viruses, known as flaviviruses, all use a version of NS3 to chop joined proteins apart so they can do their jobs. (Before chopping, Zika’s 10 proteins are made as one long protein.) But once NS3 finishes slicing virus proteins, it moves to the centrioles and can interfere with their assembly, Kodani and colleagues found. Something similar happens in some genetic forms of microcephaly.

Kodani and colleagues found that small amounts of a chemical called anthracene can prevent NS3 from tinkering with the centrioles. So far the work has been done only in lab dishes.