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.

For all the coronavirus variants that have thrown pandemic curve balls — including alpha, beta, gamma and delta — COVID-19 vaccines have stayed the same. That could change this fall.

On June 28, an advisory committee to the U.S. Food and Drug Administration met to discuss whether vaccine developers should update their jabs to include a portion of the omicron variant — the version of the coronavirus that currently dominates the globe. The verdict: The omicron variant is different enough that it’s time to change the vaccines. Those shots should be a dual mix that includes both a piece of the nearly identical omicron subvariants BA.4/BA.5 and the virus from the original vaccines, the FDA announced June 30.

“This doesn’t mean that we are saying that there will be boosters recommended for everyone in the fall,” Amanda Cohn, chief medical officer for vaccine policy at the U.S Centers for Disease Control and Prevention said at the meeting. “But my belief is that this gives us the right vaccine for preparation for boosters in the fall.”
The decision to update COVID-19 vaccines didn’t come out of nowhere. In the two-plus years that the coronavirus has been spreading around the world, it has had a few “updates” of its own — mutating some of its proteins that allow the virus to more effectively infect our cells or hide from our immune systems.

Vaccine developers had previously crafted vaccines to tackle the beta variant that was first identified in South Africa in late 2020. Those were scrapped after studies showed that current vaccines remained effective.

The current vaccines gave our immune systems the tools to recognize variants such as beta and alpha, which each had a handful of changes from the original SARS-CoV-2 virus that sparked the pandemic. But the omicron variant is a slipperier foe. Lots more viral mutations combined with our own waning immunity mean that once omicron can gain a foothold in the body, vaccine protection isn’t as good as it once was at fending off COVID-19 symptoms (SN: 6/27/22).

The shots still largely protect people from developing severe symptoms, but there has been an uptick in hospitalizations, especially among older people, Heather Scobie, deputy team lead of the CDC’s Surveillance and Analytics Epidemiology Task Force said at the meeting. Deaths among older age groups are also beginning to increase. And while it’s impossible to predict the future, we could be in for another tough fall and winter, epidemiologist Justin Lessler of the University of North Carolina at Chapel Hill said at the meeting. From March 2022 to March 2023, simulations project that deaths from COVID-19 in the United States might number in the tens to hundreds of thousands.

A switch to omicron-containing jabs may give people an extra layer of protection for the upcoming winter. Pfizer-BioNTech presented data at the meeting showing that updated versions of its mRNA shot gave clinical trial participants a boost of antibodies that recognize omicron. One version included omicron alone, while the other is a twofer, or bivalent, jab that mixes the original formulation with omicron. Moderna’s bivalent shot boosted antibodies too. Novavax, which developed a protein-based vaccine that the FDA is still mulling whether to authorize for emergency use, doesn’t have an omicron-based vaccine yet, though the company said its original shot gives people broad protection, generating antibodies that probably will recognize omicron.

Pfizer and Moderna both updated their vaccines using a version of omicron called BA.1, which was the dominant variant in the United States in December and January. But BA.1 has siblings and has already been outcompeted by some of them.
Since omicron first appeared late last year, “we’ve seen a relatively troubling, rapid evolution of SARS-CoV-2,” Peter Marks, director of the FDA’s Center for Biologics Evaluation and Research, said at the advisory meeting.

Now, omicron subvariants BA.2, BA.2.12.1, BA.4 and BA.5 are the dominant versions in the United States and other countries. The CDC estimates that roughly half of new U.S. infections the week ending June 25 were caused by either BA.4 or BA.5. By the time the fall rolls around, yet another new version of omicron — or a different variant entirely — may join their ranks. The big question is which of these subvariants to include in the vaccines to give people the best protection possible.

BA.1, the version already in the updated vaccines, may be the right choice, virologist Kanta Subbarao said at the FDA advisory meeting. An advisory committee to the World Health Organization, which Subbarao chairs, recommended on June 17 that vaccines may need to be tweaked to include omicron, likely BA.1. “We’re not trying to match [what variants] may circulate,” Subbarao said. Instead, the goal is to make sure that the immune system is as prepared as possible to recognize a wide variety of variants, not just specific ones. The hope is that the broader the immune response, the better our bodies will be at fighting the virus off even as it evolves.

The variant that is farthest removed from the original virus is probably the best candidate to accomplish that goal, said Subbarao, who is director of the WHO’s Collaborating Center for Reference and Research on Influenza at the Doherty Institute in Melbourne, Australia. Computational analyses of how antibodies recognize different versions of the coronavirus suggest that BA.1 is probably the original coronavirus variant’s most distant sibling, she said.

Some members of the FDA advisory committee disagreed with choosing BA.1, instead saying that they’d prefer vaccines that include a portion of BA.4 or BA.5. With BA.1 largely gone, it may be better to follow the proverbial hockey puck where it’s going rather than where it’s been, said Bruce Gellin, chief of Global Public Health Strategy with the Rockefeller Foundation in Washington, D.C. Plus, BA.4 and BA.5 are also vastly different from the original variant. Both have identical spike proteins, which the virus uses to break into cells and the vaccines use to teach our bodies to recognize an infection. So when it comes to making vaccines, the two are somewhat interchangeable.
There are some real-world data suggesting that current vaccines offer the least amount of protection from BA.4 and BA.5 compared with other omicron subvariants, Marks said. Pfizer also presented data showing results from a test in mice of a bivalent jab with the original coronavirus strain plus BA.4/BA.5. The shot sparked a broad immune response that boosted antibodies against four omicron subvariants. It’s unclear what that means for people.

Not everyone on the FDA advisory committee agreed that an update now is necessary — two members voted against it. Pediatrician Henry Bernstein of Zucker School of Medicine at Hofstra/Northwell in Uniondale, N.Y., noted that the current vaccines are still effective against severe disease and that there aren’t enough data to show that any changes would boost vaccine effectiveness. Pediatric infectious disease specialist Paul Offit of Children’s Hospital of Philadelphia said that he agrees that vaccines should help people broaden their immune responses, but he’s not yet convinced omicron is the right variant for it.

Plenty of other open questions remain too. The FDA could have authorized either a vaccine that contains omicron alone or a bivalent shot. Some data presented at the meeting hinted that a bivalent dose might spark immunity that could be more durable, but that’s still unknown. Pfizer and Moderna tested their updated shots in adults. It’s unclear what the results mean for kids. Also unknown is whether people who have never been vaccinated against COVID-19 could eventually start with such an omicron-based vaccine instead of the original two doses.

Maybe researchers will get some answers before boosters start in the fall. But health agencies needed to make decisions now, so vaccine developers have a chance to make the shots in the first place. Unfortunately, we’re always lagging behind the virus, said pediatrician Hayley Gans of Stanford University. “We can’t always wait for the data to catch up.”

A flexible electronic implant could one day make pain management a lot more chill.

Created from materials that dissolve in the body, the device encircles nerves with an evaporative cooler. Implanted in rats, the cooler blocked pain signals from zipping up to the brain, bioengineer John Rogers and colleagues report in the July 1 Science.

Though far from ready for human use, a future version could potentially let “patients dial up or down the pain relief they need at any given moment,” says Rogers, of Northwestern University in Evanston, Ill.
Scientists already knew that low temperatures can numb nerves in the body. Think of frozen fingers in the winter, Rogers says. But mimicking this phenomenon with an electronic implant isn’t easy. Nerves are fragile, so scientists need something that gently hugs the tissues. And an ideal implant would be absorbed by the body, so doctors wouldn’t have to remove it.

Made from water-soluble materials, the team’s device features a soft cuff that wraps around a nerve like toilet paper on a roll. Tiny channels snake down its rubbery length. When liquid coolant that’s pumped through the channels evaporates, the process draws heat from the underlying nerve. A temperature sensor helps scientists hit the sweet spot — cold enough to block pain but not too cold to damage the nerve.

The researchers wrapped the implant around a nerve in rats and tested how they responded to having a paw poked. With the nerve cooler switched on, scientists could apply about seven times as much pressure as usual before the animals pulled their paws away. That’s a sign that the rats’ senses had grown sluggish, Rogers says.

He envisions the device being used to treat pain after surgery, rather than chronic pain. The cooler connects to an outside power source and would be tethered to patients like an IV line. They could control the level of pain relief by adjusting the coolant’s flow rate. Such a system might offer targeted relief without the downsides of addictive pain medications like opioids, Rogers suggests (SN: 8/27/19).

Now the researchers want to explore how long they can apply the cooling effect without damaging tissues, Rogers says. In experiments, the longest that they cooled rats’ nerves was for about 15 minutes.

“If treating pain, cooling would have to go on for a much longer period of time,” says Seward Rutkove, a nerve physiologist at Harvard Medical School who wasn’t involved in the study. Still, he adds, the device is “an interesting proof of concept and should definitely be pursued.”