The Milky Way: An Autobiography of Our Galaxy takes a tour of our home in the cosmos from an unexpected perspective. Astrophysicist and folklorist Moiya McTier presents herself not as the author, but as the lucky human vessel through which the Milky Way has chosen to tell its story. Then she lets the galaxy take it away, with humor, heart and a huge dose of snark.
The book alternates chapters between science and mythology, reflecting McTier’s dual specialties (her bio says she was the first student in Harvard University’s history to study both). “Many of you don’t realize this, but myths were some of your species’ first attempt at scientific inquiry,” the Milky Way tells us.
The Milky Way is telling its story now because it’s sick of being ignored. Once upon a time, humans looked to the glittering smudge of stars in the sky for insight into when to plant crops or avoid floods. We told stories about the Milky Way’s importance in the origin and fate of the world.
Our galaxy ate it up: For an entity that spends most of its time ripping up smaller galaxies and watching its own stars die, “your stories made me feel loved and needed and, perhaps for the first time in my long existence, more helpful than I was ruinous.” But in the last few centuries, technology and light pollution have pulled humankind away. “At first, I thought it was just a phase,” the Milky Way says. “Then I remembered … that several hundred years is actually a long time for humans.” So the Milky Way decided to remind us why it’s so important. Its autobiography covers big-picture scientific questions about galaxies, like where they come from (“When a gas cloud loves itself very much,” the Milky Way explains, “it hugs itself extra tight, and after a few hundred million years, a baby galaxy is born. Leave the storks out of it, please.”). It also gets into what galaxies are made of, how they interact with other galaxies, and how they live and die. The book then zooms out to cover the origins and possible ends of the universe, mysteries like dark matter and dark energy, and even humankind’s search for other intelligent life (SN: 8/4/20).
The author takes pains to explain scientific jargon and the technical tools that astronomers use to study the sky. A lot of popular astronomy writing glosses over how astronomers think about cosmic distance or exactly what a spectrum is, but not this book. If you’ve ever been curious about these insider details, The Milky Way has you covered.
McTier’s version of our home galaxy is heavily anthropomorphized. The Milky Way is brash, vain and arrogant in a way that may hide a secret insecurity. Its central black hole is characterized as the physical embodiment of the galaxy’s shame and regrets, a source of deep existential angst. And its relationship with the Andromeda galaxy is like a long-term, long-distance romance, with each galaxy sending stars back and forth as love notes until the two can eventually merge (SN: 3/05/21).
This could have felt gimmicky. But McTier’s efforts to make the metaphors work while keeping the science accurate and up-to-date made the premise endearing and entertaining.
I laughed twice on Page 1. I learned a new word on Page 2. I dog-eared the endnotes early on because it became instantly clear I would want to read every one. I read this book while traveling in rural upstate New York, where the sky is much clearer than at my home outside of Boston. The Milky Way reminded me to look up and appreciate my home in the universe, just like its narrator wanted.
For millions of people, COVID-19 doesn’t end with a negative test. Weeks or months after traces of the virus disappear from noses and throats, symptoms can persist or come back. New ones might pop up and stick around for months. People suffering from long COVID are unwillingly in it for the long haul — and it’s still unclear who’s at the highest risk for the condition.
Researchers don’t yet have an official definition for long COVID, and its symptoms are wide-ranging (SN: 7/29/22). Some people struggle with extreme fatigue that interferes with their daily lives. Others can’t concentrate or struggle with memory amid thick brain fog. Still others have organ damage or a persistent cough and difficulty breathing. “There are a variety of different kinds of ways that people can have long COVID. It’s not just the one thing,” says Leora Horwitz, an internal medicine physician at New York University Langone Health. “That’s what makes it so hard to study.”
This spectrum of symptoms makes pinning down who’s at high risk for long-term health problems from the disease especially hard. Some post-COVID conditions may stem from virus-induced damage or from the stress of being hospitalized with severe disease. In other cases, the body’s own immune response to the virus could drive the damage. Or the virus may be hiding somewhere in the body, possibly the gut, helping symptoms to persist (SN: 11/24/20). Different causes may have different risk groups, says Hannah Davis, cofounder of the Patient-Led Research Collaborative, a research and advocacy group studying long COVID.
There are some broad hints about who’s at risk. Studies suggest that women are more likely than men to have lingering symptoms. COVID-19 patients with more than five symptoms in the first week of infection or preexisting health conditions such as asthma may be more likely to develop long COVID. Age also appears to be a risk factor, though results are mixed regarding whether the burden falls on older people or middle-aged people. Populations that were disproportionally hit by COVID-19 overall — including Black and Hispanic people — may similarly face disparities for long COVID. And while vaccination seems to protect people from developing long COVID, Horwitz says, it’s still unclear by how much.
Age is a risk factor for severe COVID-19, and the U.S. Centers for Disease Control and Prevention lists more than 30 health problems, including cancer and lung disease, that also raise the risk. “So many researchers assume that those [risk factors] will be the same for long COVID and there’s no scientific basis for that,” Davis says. There are many more that researchers could be missing when it comes to long COVID.
Using health records and exams, and knowledge of ailments with symptoms similar to long COVID, experts are on the hunt for those risk factors.
Examining health When it comes to getting a better handle on who’s at risk for long COVID — which also goes by the wonky alias Post-Acute Sequelae of SARS-CoV-2 infection — electronic health records may hold important clues.
Horwitz is part of the U.S. National Institutes of Health’s RECOVER initiative that aims to understand the long-term impacts of COVID-19. One arm of the study involves mining millions of electronic health records to find potential patterns.
Studying millions of these records should pinpoint potential risk factors that are rare in the population overall but perhaps more common for people with long COVID, Horwitz says. “That’s hard even in a cohort study of thousands.”
But health records aren’t perfect: They depend on physicians logging that patients are having trouble sleeping or focusing, or that they’re exhausted. “The things people are complaining about, we’re really bad at writing down those diagnoses on the record,” Horwitz says. “So we miss that.” To account for health records’ deficiencies, Horwitz and colleagues are also directly studying thousands of people. Participants answer a questionnaire every three months so that the team can identify what kinds of symptoms people have and whether they’re getting better or worse.
Then blood, urine, stool and saliva samples can reveal what’s happening in the body. Tests on those samples can uncover if the coronavirus is still around and causing trouble, or if the immune system has learned to attack the body itself. Participants with abnormal test results will undergo additional, targeted testing.
“Unlike electronic health records where it’s hit or miss, like somebody might have had a CAT scan or might not, here we say, ‘OK, you have trouble breathing. We will take a look at your lungs,’” Horwitz says.
The study includes a range of participants: adults and kids, pregnant people, those currently with COVID-19 and people who died after having the disease.
Some of the potential risk factors that the team is looking for include autoimmune diseases and other viral infections. The list may grow as more people join the study. “We’re trying to balance the fishing versus making sure that we’re at least fishing for things that could be in the water,” Horwitz says.
Among short supply, though, are people who never caught the virus — important “controls” to highlight what’s different about people who got COVID-19.
So far, more than 7,000 people have signed up, and the group plans to recruit around 10,000 more. It’s a lot of data, but early results may soon start coming in.
“We’ll probably try to do an interim peek at those data this fall,” Horwitz says. “It’s tricky because we deliberately wanted to enroll 18,000 people so we would have enough power to really look at the things we care about. I don’t want to cheat and look too early, but we also know that there’s a lot of interest.”
Striking similarities Some long COVID symptoms — brain fog, fatigue and trouble sleeping — mirror another illness: myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS. Other long COVID symptoms, such as rapid heartbeat and dizziness, fall in the category of nervous system disorders called dysautonomia. Similar symptoms could belie similar risk factors.
Yet potential risk factors for those conditions are largely missing from long COVID research, says Davis, who has had long COVID since March 2020. Among the possibilities that scientists are considering are things like Epstein-Barr virus, migraines and some autoimmune diseases.
Epstein-Barr virus could be a big one, Davis says. Infections last a lifetime because the virus can go into hiding in the body and possibly reemerge. That virus has been linked to ME/CFS for decades, though its role in the disease remains unclear, Davis says. Some early hints of a link between Epstein-Barr virus and long COVID already exist. Multiple studies have found evidence in blood samples from some long COVID patients that the immune system recently battled with Epstein-Barr virus, which can cause infectious mononucleosis, a disease characterized by extreme fatigue. Other studies have found signs of the virus itself. And in 2021, Davis and colleagues found that 40 out of 580 people with symptoms of long COVID who responded to an online survey reported having a current or recent Epstein-Barr virus infection.
With ME/CFS, it’s possible that another illness caused by a different virus triggers the Epstein-Barr virus, which then causes the fatigue syndrome. Given the parallels between that condition and long COVID, some scientists are wondering if the two are actually the same disease, with the coronavirus now known as one trigger.
Examining health conditions that raise the chances of long COVID could provide answers for both diseases, says Nancy Klimas, an immunologist at Nova Southeastern University in Fort Lauderdale, Fla. That’s in part because researchers can more easily identify people who developed lingering symptoms after a bout of COVID-19 compared with unknown infections that may precede ME/CFS.
Also, “there’s a huge difference in these two fields and it’s money,” Klimas says. She now has funding from the CDC to compare long COVID patients with people who have ME/CFS. The team hopes that physical exams and specialized tests will reveal whether the two diseases are indeed the same and be a step toward understanding the mechanisms behind the lingering symptoms.
Still, since long COVID as a whole encompasses such a wide range of symptoms, it will take time to uncover who is at risk of what.
If COVID-19 were just one disease impacting the lungs, heart or brain, the research might be easier, Horwitz says. “But we have to test everything.”
A zap to the head can stretch the time between intention and action, a new study finds. The results help illuminate how intentions arise in the brain.
The study, published in the May 6 Journal of Neuroscience, “provides fascinating new clues” about the process of internal decision making, says neuroscientist Gabriel Kreiman of Harvard University. These sorts of studies are bringing scientists closer to “probing some of the fundamental questions about who we are and why we do what we do,” he says. Figuring out how the brain generates a sense of control may also have implications for people who lack those feelings. People with alien hand syndrome, psychogenic movement disorders and schizophrenia can experience a troubling disconnect between intention and action, says study coauthor Biyu Jade He of the National Institutes of Health in Bethesda, Md.
In the study, the researchers manipulated people’s intentions without changing their actions. The researchers told participants to click a mouse whenever the urge struck. Participants estimated when their intention to click first arose by monitoring a dot’s position on a clockface.
Intention to click usually preceded the action by 188 milliseconds on average, the team found. But a session of transcranial direct current stimulation, or tDCS, moved the realization of intention even earlier, stretching time out between awareness of intention and the action. tDCS electrodes delivered a mild electrical zap to participants’ heads, dialing up the activity of carefully targeted nerve cells. After stimulation, intentions arrived about 60 to 70 milliseconds sooner than usual. tDCS seemed to change certain kinds of brain activity that may have influenced the time shift, EEG recordings suggested.
The results highlight how thoughts and intentions can be separated from the action itself, a situation that appears to raise thorny questions about free will. But these tDCS zaps didn’t change the action outcome or participants’ feelings of control, only the reported timing of a person’s conscious intention.
MONTREAL — For the first time, scientists have precisely captured a map of the boisterous bang radiating from a lightning strike. The work could reveal the energies involved in powering some of nature’s flashiest light shows.
As electric current rapidly flows from a negatively charged cloud to the ground below, the lightning rapidly heats and expands the surrounding air, generating sonic shock waves. While scientists have a basic understanding of thunder’s origins, they lack a detailed picture of the physics powering the crashes and rumbles. Heliophysicist Maher Dayeh of the Southwest Research Institute in San Antonio and colleagues sparked their own lightning by firing a long, Kevlar-coated copper wire into an electrically charged cloud using a small rocket. The resulting lightning followed the conductive wire to the ground. Using 15 sensitive microphones laid out 95 meters from the strike zone, Dayeh said he and his colleagues precisely recorded the incoming sound waves. Because sound waves from higher elevations took longer to reach the microphones, the scientists could create an acoustic map of the lightning strike with “surprising detail,” Dayeh said. He presented the results May 5 at a meeting of the American Geophysical Union and other organizations.
The loudness of a thunderclap depends on the peak electric current flowing through the lightning, the researchers found. This discovery could one day allow scientists to use thunder to sound out the amount of energy powering a lightning strike, Dayeh said. SHOCK AND AWE Scientists shot a long copper wire into a lightning-prone cloud using a small rocket. The generated lightning followed the wire down to the ground, allowing the researchers to record the sound waves of the resulting thunder. The green flashes are caused by the intense heating of the copper wire. Credit: Univ. of Florida, Florida Institute of Technology, SRI
Monkeypox is not yet a global public health emergency, the World Health Organization said June 25.
The decision comes as the outbreak of the disease related to smallpox continues to spread, affecting at least 4,100 people in 46 countries as of June 24. That includes at least 201 cases in the United States. Those cases have been found in 25 states and the District of Columbia, according to the U.S. Centers for Disease Control and Prevention. “Controlling the further spread of outbreak requires intense response efforts,” and the situation should be reevaluated in a few weeks, the WHO committee evaluating the outbreak said in an announcement.
The declaration of a public health emergency would have potentially made it easier to get treatments and vaccines to people infected with or exposed to the virus. Some medications and vaccines that could help fend off monkeypox are approved for use against smallpox, and can be used against monkeypox only with special authorization.
The virus that causes monkeypox, named for its discovery in monkeys in 1958 though it is probably a virus that mainly infects rodents, is not a new threat. Countries in central Africa, where monkeypox is endemic, have had sporadic outbreaks since researchers found the first human case in 1970. Places in western Africa had few cases until 2017. But most cases outside the continent were travel-related, with limited spread to others (SN: 5/26/22).
“Monkeypox has been circulating in a number of African countries for decades and has been neglected in terms of research, attention and funding,” WHO director-general Tedros Ghebreyesus said in a statement announcing the decision. “This must change not just for monkeypox but for other neglected diseases in low-income countries as the world is reminded yet again that health is an interconnected proposition.”
Monkeypox typically kills fewer than 10 percent of people who contract it. At least one person has died in the global outbreak.
As case numbers climb, researchers are working to decipher the genetic blueprint of the virus, in hopes of uncovering whether some viral mutations might explain why the virus has quickly gained a foothold in new places.
Tracing the mutations The closest known relative of the versions of the virus behind the global outbreak comes from Nigeria, hinting that the outbreak may have got its start there.
In the newest surge in cases, scientists have uncovered more viral changes than anticipated — a sign that the virus may have been circulating undetected among people for a while, perhaps since Nigeria’s 2017–2018 monkeypox outbreak, new research suggests. What’s more, a group of enzymes known for their virus-fighting abilities in the body may be to blame for many of those mutations.
A genetic analysis of monkeypox viruses involved in the global outbreak from 15 people across seven countries shows that these viruses have an average of 50 more genetic tweaks than versions circulating in 2018 and 2019, researchers report June 24 in Nature Medicine. That’s roughly six to 12 times as many mutations as scientists would have expected the virus to develop over that time. Unlike some other types of viruses, poxviruses, which include smallpox and monkeypox viruses, typically mutate fairly slowly.
The changes have a pattern that is a hallmark of an enzyme family called APOBEC3, the researchers say. These enzymes edit DNA’s building blocks — represented by the letters G, C, A and T — in a specific way: Gs change to As and Cs to Ts. The analysis found that particular pattern in the viral sequences, suggesting that APOBEC3s are responsible for the mutations.
Ideally, so many DNA building blocks are swapped for another that a virus is effectively destroyed and can’t infect more cells. But, sometimes, APOBEC3 enzymes don’t make enough changes to knock out the virus. Such mutated, though still functional, viruses can go on to infect additional cells, and possibly another person.
A big question, though, is whether the genetic tweaks seen in the monkeypox virus are helpful, harmful or have no effect at all on the virus.
While it’s still unknown whether the enzymes are directly responsible for the changes in the monkeypox virus, similar mutations are still popping up, the team found. So, APOBEC3s may still be helping the virus change as it continues to spread. One member of the enzyme family is found in skin cells, where people with monkeypox can develop infectious pox lesions. Different symptoms Symptoms reported in the global outbreak have been generally milder than those reported in previous outbreaks, perhaps allowing the disease to spread before a person knows they’re infected.
It is not clear whether those differences in symptoms are related to changes in the virus, Inger Damon, director of the CDC’s Division of High-Consequence Pathogens and Pathology, said June 21 in a news briefing hosted by SciLine, a service for journalists and scientists sponsored by the American Association for the Advancement of Science.
Typically, in previous outbreaks, people would develop flu-like symptoms, including fever, headaches, muscle aches and exhaustion about a week or two after exposure to the virus. Then, one to three days after those symptoms start, a rash including large pus-filled lesions pops up generally starting on the face and limbs, particularly the hands, and spreads over the body. Though generally milder, those symptoms are similar to smallpox, but people with monkeypox also tend to develop swollen lymph nodes.
All patients in the U.S. outbreak have gotten rashes, Damon said, “but the lesions have been scattered or localized to a specific body site, rather than diffuse, and have not generally involved the face or the … palms of the hand or the soles of the feet.” Instead, rashes may start in the genital or anal area where they can be mistaken for sexually transmitted diseases, such as syphilis or herpes, she said.
In many cases, the rashes have not spread to other parts of the body. And the classical early symptoms such as fever have been “mild and sometimes nonexistent before a rash appears,” Damon said.
Monkeypox is transmitted from person to person through close skin-to-skin contact or by contact with contaminated towels, clothes or bedding. It may also be spread by droplets of saliva exchanged during kissing or other intimate contact. The CDC is investigating whether the virus might be spread by semen as well as skin-to-skin contact during sex, Agam Rao, a captain in the U.S. Public Health Service, said June 23 at a meeting of the CDC’s Advisory Committee on Immunization Practices.
“We don’t have any reason to suspect it is spread any other way,” such as through the air, Rao said.
In Nigeria, more monkeypox cases have been recorded among women, while the global outbreak has affected mainly men, particularly men who have sex with men. Experts warn that anyone can be infected with monkeypox, and some people face an increased risk of severe disease. Those at increased risk include children, people who are immunocompromised, pregnant people and people with eczema.
The risk of catching monkeypox through casual contact is still low in the United States, Rao said. But data she presented show that while people in the country have contracted monkeypox while traveling abroad, cases have also spread locally.
At the time, Conover was a Ph.D. student in particle physics (she’s now physics senior writer for Science News). She was part of a team building a detector in the cavern to observe elusive particles called neutrinos. It was the Fourth of July 2012. A few hundred kilometers away, scientists were announcing the discovery of another elusive subatomic particle, the Higgs boson, which physicists had been hunting for decades. As hundreds of researchers cheered in the main auditorium at the CERN particle physics lab near Geneva, Conover and the small group of physicists in the chilly French cavern cheered too, as did scientists worldwide. The Higgs boson filled in a missing piece in the standard model of particle physics, which explains just about everything known about the particles that make up atoms and transmit the forces of nature. No Higgs boson, no life as we know it.
In this issue’s cover story, “The Higgs boson at 10,” Conover looks back at the excitement around the discovery of the Higgs boson and looks ahead to the many things that researchers hope to find out with its help. She also reviews a new biography of Peter Higgs, a modest man who made clear that he was just one of many scientists who contributed to the breakthrough.
The discovery is part of Science News history too. Journalists around the world were eagerly awaiting the big announcement, which was being kept under wraps. But when Kate Travis, a Science News editor at the time, uncovered an announcement video accidentally posted early on CERN’s website, we published the big news the day before the official announcement.
“Even though its discovery is 10 years old now, that’s still new in the grand scheme of particle physics, so we’re still learning lots about it,” Conover told me. “It’s very cool that I get the opportunity to write about this particle that is still so new to science.” And it’s very cool that we get to explore it with her.
In the 1920s, laborers and amateur archaeologists at gravel quarry pits in southeastern England uncovered more than 300 ancient, sharp-edged oval tools. Researchers have long suspected that these hand axes were made 500,000 to 700,000 years ago. A new study confirms that suspicion in the first systematic excavation of the site, known as Fordwich.
Dating those tools and more recent finds suggests that humanlike folk inhabited the area between about 560,000 and 620,000 years ago, researchers report in the June Royal Society Open Science. Relatively warm conditions at that time drew hominids to what’s now northern Europe before the evolutionary rise of Neandertals and Homo sapiens. The results confirm that Fordwich is one of the oldest hominid sites in England. Previous discoveries place hominids in what’s now southeastern England at least 840,000 years ago (SN: 7/7/10) and perhaps as far back as nearly 1 million years ago (SN: 2/11/14). No hominid fossils have been found at Fordwich. It’s unclear which species of the human genus made the tools.
In 2020, archaeologist Alastair Key of the University of Cambridge and colleagues unearthed 238 stone artifacts at Fordwich that display grooves created by striking the surface with another stone. Other finds include three stones with resharpened edges, presumably used to scrape objects like animal hides.
A method for determining when sediment layers were last exposed to sunlight indicated that the newly discovered artifacts date to roughly 542,000 years ago. The previously unearthed hand axes probably came from the same sediment.
Hominids must have fashioned tools at Fordwich a bit earlier than 542,000 years ago because ancient climate data suggest that an ice age at that time made it hard to survive in northern Europe, the team concludes. Warmer conditions between 560,000 and 620,000 years ago would have enabled the hominid toolmakers to live so far north.
Not long before the end of the school year, my husband and I received an e-mail from our fifth-grader’s principal that may now be all-too-familiar to many parents. The subject line included the words, “MULTIPLE COVID CASES.”
Several students in my daughter’s class had tested positive for COVID-19. Her school acted fast. It reinstated a mask mandate for 10 days and required students not up-to-date on their COVID-19 vaccinations to quarantine.
These precautions may have helped — my daughter didn’t end up bringing the virus home. But for kids who do, COVID-19 can hopscotch through households, knocking down relatives one by one. And it’s not clear how long one infection protects you from a second round with the virus. Recent high-profile cases have put reinfections in the spotlight. Health and Human Services Secretary Xavier Becerra has had two bouts of COVID-19 in less than a month. So has The Late Show host Stephen Colbert. Back at his desk in May, he joked, “You know what they say. ‘Give me COVID once, shame on you. Give me COVID twice, please stop giving me COVID.’”
Just a few months ago, scientists thought reinfections were relatively rare, occurring most often in unvaccinated people (SN: 2/24/22). But there are signs the number may be ticking up.
An ABC News investigation that contacted health departments in every state reported June 8 that more people seem to be getting the virus again. And omicron, the variant that sparked last winter’s surge, is still spawning sneaky subvariants. Some can evade antibodies produced after infection with the original omicron strain, scientists report June 17 in Nature. That means a prior COVID-19 infection might not be as helpful against future infections as it once was (SN:8/19/21). What’s more, reinfection could even add to a person’s risk of hospitalization or other adverse outcomes, a preliminary study suggests.
Scientists are still working to pin down the rate of reinfection. Like most questions involving COVID-19 case numbers, the answer is more than a little murky. “You really need to have a cohort of people who are well followed and tested every time they have symptoms,” says Caroline Quach-Thanh, an infectious diseases specialist at CHU Sainte-Justine, a pediatric hospital at the University of Montreal.
A recent look at hundreds of thousands of COVID-19 cases among people in the province of Quebec found that roughly 4 percent were reinfections, scientists report in a preliminary study posted May 3 at medRxiv.org (SN:5/27/22). Quach-Thanh has seen an even smaller rate in her own study of health care workers first infected between March and September of 2020. Those data are still unpublished, but she points out that most of the people in her study were vaccinated. “A natural infection with three doses of vaccines protects better than just a natural infection,” she says.
As many families, mine included, gear up for summer camps and vacations, I wanted to learn more about our current COVID-19 risks. I chatted with Quach-Thanh and Anna Durbin, an infectious diseases physician at Johns Hopkins Bloomberg School of Public Health who has studied COVID-19 vaccines. Our conversations have been edited for length and clarity.
What’s the latest on reinfections? Is the picture changing? Durbin: We have to remember that the virus strain that’s circulating now is very different from the earlier strains. Whether you’ve been infected with COVID-19 or vaccinated, your body makes an immune response to fight future infections. It recognizes [the strain] your body originally saw. But as the virus changes, as it did with omicron, it becomes sort of a fuzzier picture for the immune system. It’s not recognizing the virus as well, and that’s why we’re seeing reinfections.
I’ll also say that reinfections — particularly with respiratory viruses — are very common.
How can scientists distinguish a true reinfection from a relapse of an original infection? Quach-Thanh: There are multiple ways of looking at this. The first is looking at the time elapsed between the first infection and a new positive PCR test. If it has been more than three months, it is unlikely to be just a remnant of a previous infection. We can also look at viral load. A really high viral load usually means it’s a new infection. But the best way to tell is to sequence the virus [to determine its genetic makeup] to see if it is actually a new strain.
What do we know about the health risks of reinfection? Quach-Thanh: The good thing is that most of the people who got reinfected [in the Quebec study] got a mild disease, and the risk of hospitalization and death was much lower.
When you get reinfected, you might [have symptoms] like a cold, or even sometimes a cough, and a little bit of a fever, but you usually don’t progress to complications as much as you would with your first infection — if you’re vaccinated.
Does reinfection increase your chance of developing long COVID? Durbin: I think that’s unknown, but it’s being studied.
As we look back at the omicron wave in the U.S. that happened in January and February, now is about the time we would start to see symptoms of long COVID. So far it looks promising. We seem to be seeing a lower incidence of long COVID [after reinfection with omicron] than we did with primary infection, but those data are going to continue to be collected over the next few months.
At this point in the pandemic, how cautious do we need to be? Quach-Thanh: It depends on your baseline risk of complications. If you’re healthy, if you’re doing most activities outdoors, if you’re vaccinated, life can proceed. But if you’re immune suppressed or elderly, the situation might be different. If you have symptoms, it would be advisable to not mingle in indoor settings without a mask so that you don’t contaminate other people. There are immunocompromised people who might be at risk of serious infection. We still need to keep them in mind. I think we have to be responsible, and if we’re sick, we should get tested.
Durbin: This is what I tell my friends, family and patients: This virus is here to stay. Any time you’re in a crowded place with poor ventilation and lots of people, there’s a chance there’s going to be transmission. The risk is never going to be zero. It’s a message people don’t want to hear. But as long as there are people to infect, this virus is not going away.
We have to move to acceptance, and we have to be better members of society. If we can, we should stay home when we’re sick. If we can’t stay home, we should wear a mask. We should wash our hands regularly. These are things that work to reduce transmission.
They reduce your risk of getting not just COVID-19, but also a cold or the flu.
A flexible sensor applied to the back of the neck could help researchers detect whiplash-induced concussions in athletes.
The sensor, described June 23 in Scientific Reports, is about the size of a bandage and is sleeker and more accurate than some instruments currently in use, says electrical engineer Nelson Sepúlveda of Michigan State University in East Lansing. “My hope is that it will lead to earlier diagnosis of concussions.”
Bulky accelerometers in helmets are sometimes used to monitor for concussion in football players. But since the devices are not attached directly to athletes’ bodies, the sensors are prone to false readings from sliding helmets. Sepúlveda and colleagues’ patch adheres to the nape. It is made of two electrodes on an almost paper-thin piece of piezoelectric film, which generates an electric charge when stretched or compressed. When the head and neck move, the patch transmits electrical pulses to a computer. Researchers can analyze those signals to assess sudden movements that can cause concussion.
The team tried out the patch on the neck of a human test dummy, dropping the figure from a height of about 60 centimeters. Researchers also packed the dummy’s head with different sensors to provide a baseline level of neck strain. Data from the patch aligned with data gathered by the internal sensors more than 90 percent of the time, Sepúlveda and colleagues found.
The researchers are now working on incorporating a wireless transmitter into the patch for an even more streamlined design.
There’s a lot more to the story of the Higgs boson than just one man named Higgs.
Despite the appeal of the “lone genius” narrative, it’s rare that a discovery can be attributed solely to the work of one scientist. At first, Elusive, a biography of Peter Higgs written by physicist and author Frank Close, seems to play into that misleading narrative: The book is subtitled “How Peter Higgs solved the mystery of mass.”
But the book quickly — and rightfully — veers from that path as it delves into the theoretical twists and turns that kicked off a decades-long quest for the particle known as the Higgs boson, culminating with its discovery in 2012 (SN: 7/28/12, p. 5). That detection verified the mechanism by which particles gain mass. Higgs, of the University of Edinburgh, played a crucial role in establishing mass’s origins, but he was one of many contributors.
The habitually modest and attention-averse Higgs makes the case against himself as the one whiz behind the discovery, the book notes: According to Higgs, “my actual contribution was only a key insight right at the end of the story.”
The Higgs boson itself doesn’t bestow fundamental particles with mass. Instead, its discovery confirmed the correctness of a theory cooked up by Higgs and others. According to that theory, elementary particles gain mass by interacting with a field, now known as the Higgs field, that pervades all of space.
A paper from Higgs in 1964 was not the first to propose this process. Physicists Robert Brout and François Englert just barely beat him to it. And another team of researchers published the same idea just after Higgs (SN: 11/2/13, p. 4). Crucial groundwork had already been laid by yet other scientists, and still others followed up on Higgs’ work. Higgs, however, was the one to make the pivotal point that the mass mechanism implied the existence of a new, massive particle, which could confirm the theory. Despite this complicated history, scientists slapped his name on not just the particle, the Higgs boson, but also the process behind it, traditionally called the Higgs mechanism, but more recently and accurately termed the Brout-Englert-Higgs mechanism. (Higgs has reportedly proposed calling it the “ABEGHHK’tH mechanism,” using the first letter of the last names of the parade of physicists who contributed to it, Anderson, Brout, Englert, Guralnik, Hagen, Higgs, Kibble and ’t Hooft.) The postmortem of how Higgs’ name attained outsize importance is one of the most interesting sections of Elusive, revealing much about the scientific sausage-making process and how it sometimes goes awry. Equally fascinating is the account of how the media embraced Higgs as a titan of physics based on his association with the boson, lofting him to a level of fame that, for Higgs, felt unwelcome and unwarranted.
The book admirably tackles the complexities of the Brout-Englert-Higgs mechanism and how particles gain mass, covering details that are usually glossed over in most popular explanations. Close doesn’t shy away from nitty-gritty physics terms like “perturbation theory,” “renormalization” and “gauge invariance.” The thorniest bits are most appropriate for amateur physics aficionados who desire a deeper understanding, and those bits may require a reread before sinking in.
Higgs is famously not a fan of the limelight — he disappeared for several hours on the day he won a Nobel Prize for his work on mass. The physicist sometimes seems to fade into the background of this biography as well, with multiple pages passing with no appearance or contribution from Higgs. Once the scientific community got wind of the possibility of a new particle, the idea took on a life of its own, with experimental physicists leading the charge. Higgs didn’t make many contributions to the subject beyond his initial insight, which he calls “the only really original idea I’ve ever had.”
Thus, the book sometimes feels like a biography of a particle named Higgs, with the person playing a backup role. Higgs is so reserved and so private that you get the sense that Close still hasn’t quite cracked him. While interesting details of Higgs’ life and passions are revealed — for example, his fervent objection to nuclear weapons — deeper insights are missing. In the end, Higgs is, just like the particle named after him, elusive.
