Publisher Health

Many people don’t realize that the trillions of bacteria, viruses, and fungi residing within the gastrointestinal tract — collectively called the gut microbiome — are connected to overall health, and specifically to cancer.
Manipulating the gut microbiome to produce “beneficial” commensal microbes, which protect the host from pathogens and can boost immune responses, among other things, could potentially help patients respond better to cancer drugs called immune checkpoint inhibitors, a type of immunotherapy.
To that end, researchers at the University of Michigan have developed a new dietary fiber formulation that improves the potency of immunotherapies against cancer by modulating the gut microbiome. In the future, cancer patients treated with immune checkpoint blockers may benefit from consuming this inulin gel dietary fiber, said James Moon, the John G. Searle Associate Professor of Pharmaceutical Sciences in the College of Pharmacy. The findings appear in the June 24 issue Nature Biomedical Engineering.
Inulin, a dietary fiber found in chicory root, Jerusalem artichoke and other plants, is a prebiotic that helps produce colon-residing commensal bacteria. By formulating inulin into a more colon-targeted inulin gel formulation, the team was able to provide a rich source of nutrients to allow beneficial gut microbes to expand more in the gastrointestinal tract.
The inulin gel improved immune checkpoint inhibitor therapy in rodents with colon carcinoma as well as melanoma. For instance, when inulin gel was combined with an immune checkpoint inhibitor in a colon carcinoma rodent model, the rate of tumor eradication doubled (100% improvement), compared with the immune checkpoint inhibitor therapy alone.
“Consumption of the inulin gel expanded and increased the number of beneficial microbes in tumor-bearing mice,” said Kai Han, postdoctoral fellow and first author of the study. “These are beneficial commensal microbes that are found in cancer patients who respond well to immune checkpoint inhibitors.

A bout with flu virus can be hard, but when Streptococcus pneumonia enters the mix, it can turn deadly.
Now researchers have found a further reason for the severity of this dual infection by identifying a new virulence mechanism for a surface protein on the pneumonia-causing bacteria S. pneumoniae. This insight comes more than three decades after discovery of that surface protein, called pneumococcal surface protein A, or PspA.
This new mechanism had been missed in the past because it facilitates bacterial adherence only to dead or dying lung epithelial cells, not to living cells. Heretofore, researchers typically used healthy lung cell monolayers to search for bacterial adhesins that aid infection. Virus killing of lung cells during flu was found to set the stage for S. pneumonia attachment to the airway, thereby worsening disease and pneumonia.
The research, published in the journal Cell Reports, was led by Carlos Orihuela, Ph.D., and David Briles, Ph.D., professor and professor emeritus in the University of Alabama at Birmingham Department of Microbiology. Orihuela and Briles say their findings provide further explanation for how an infection by influenza A flu virus — followed by S. pneumoniae superinfection — causes severe pneumonia and a high death rate. The mechanism also points to possible improvements for disease treatment and vaccination.
A historical example of the deadly synergy of flu infection followed by S. pneumoniae superinfection is found in banked lung samples from the 1918 Spanish influenza pandemic that killed 40 million to 50 million people — the vast majority of these samples showed co-infection or secondary infection with S. pneumonia.
The UAB research on PspA began with some head-scratching results from experimental lung infections of mice with influenza A, followed by either wild-type S. pneumonia that has the intact PspA gene, or a mutant S. pneumoniae that lacks PspA. Lung homogenates from mice infected with the wild-type had much higher numbers of S. pneumonia bacteria than lungs infected with the mutant. However, when researchers washed the interiors of the lungs and collected that bronchoalveolar lavage fluid, they counted similar numbers of the wild-type S. pneumonia and the mutant.
“This unexpected result was interpreted to mean that wild-type S. pneumoniae were more resistant to dislodgement than S. pneumonia with a pspA gene deletion, and it served as rationale for further experimentation,” Orihuela said.
From this clue, the researchers were able to show that PspA functions as an adhesin to dying host cells, in addition to its several other previously established virulence mechanisms. The researchers also detailed the molecular mechanism of this bacterial adherence.
Both influenza A infection and release of the S. pneumoniae toxin pneumolysin cause death of lung epithelial cells. As they are dying, cells’ phosphatidylserine residues get flipped to the outer cell membrane, where they bind the host enzyme glyceraldehyde-3-phosphate dehydrogenase, or GAPDH. In turn, the S. pneumoniae PspA on the surface of the bacteria binds to the GAPDH. PspA-GAPDH-mediated binding to lung cells increased S. pneumoniae localization in the lower airway, and this was enhanced by pneumolysin exposure or co-infection with influenza A virus.
Tests with fragments of the PspA protein showed that a 52-amino acid portion of the protein — from amino acid 230 to 281 — was required for GAPDH binding. Instilling one of those binding fragments into the lungs of influenza-infected mice reduced the disease severity of S. pneumoniae superinfection, presumably through binding competition.
“Our findings support the targeting of regions of PspA for therapeutic and vaccine development against influenza A/Streptococcus pneumoniae superinfections,” Orihuela said. “Importantly, and despite more than 30 years since its discovery, PspA was not previously shown to function as an adhesin. Thus, our finding of PspA’s role in adherence substantially advances our knowledge on the interactions of S. pneumoniae with its host.”
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Materials provided by University of Alabama at Birmingham. Original written by Jeff Hansen. Note: Content may be edited for style and length.

To better understand the role of bacteria in health and disease, National Institutes of Health researchers fed fruit flies antibiotics and monitored the lifetime activity of hundreds of genes that scientists have traditionally thought control aging. To their surprise, the antibiotics not only extended the lives of the flies but also dramatically changed the activity of many of these genes. Their results suggested that only about 30% of the genes traditionally associated with aging set an animal’s internal clock while the rest reflect the body’s response to bacteria.
“For decades scientists have been developing a hit list of common aging genes. These genes are thought to control the aging process throughout the animal kingdom, from worms to mice to humans,” said Edward Giniger, Ph.D., senior investigator, at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study published in iScience. “We were shocked to find that only about 30% of these genes may be directly involved in the aging process. We hope that these results will help medical researchers better understand the forces that underlie several age-related disorders.”
The results happened by accident. Dr. Giniger’s team studies the genetics of aging in a type of fruit fly called Drosophila. Previously, the team showed how a hyperactive immune system may play a critical role in the neural damage that underlies several aging brain disorders. However, that study did not examine the role that bacteria may have in this process.
To test this idea, they raised newborn male flies on antibiotics to prevent bacteria growth. At first, they thought that the antibiotics would have little or no effect. But, when they looked at the results, they saw something interesting. The antibiotics lengthened the fly’s lives by about six days, from 57 days for control flies to 63 for the treated ones.
“This is a big jump in age for flies. In humans, it would be the equivalent of gaining about 20 years of life,” said Arvind Kumar Shukla, Ph.D., a post-doctoral fellow on Dr. Giniger’s team and the lead author of the study. “We were totally caught off guard and it made us wonder why these flies took so long to die.”
Dr. Shukla and his colleagues looked for clues in the genes of the flies. Specially, they used advanced genetic techniques to monitor gene activity in the heads of 10, 30, and 45-day old flies. In a previous study, the team discovered links between the age of a fly and the activity of several genes. In this study, they found that raising the flies on antibiotics broke many of these links.

Ultrasound can overcome some of the detrimental effects of ageing and dementia without the need to cross the blood-brain barrier, Queensland Brain Institute researchers have found.
Professor Jürgen Götz led a multidisciplinary team at QBI’s Clem Jones Centre for Ageing Dementia Research who showed low-intensity ultrasound effectively restored cognition without opening the barrier in mice models.
The findings provide a potential new avenue for the non-invasive technology and will help clinicians tailor medical treatments that consider an individual’s disease progression and cognitive decline.
“Historically, we have been using ultrasound together with small gas-filled bubbles to open the almost-impenetrable blood-brain barrier and get therapeutics from the bloodstream into the brain,” Professor Götz said.
The new research involved a designated control group who received ultrasound without the barrier-opening microbubbles.
“The entire research team was surprised by the remarkable restoration in cognition,” he said.

An updated analysis of American COVID-19 deaths throughout 2020 reveals an even bigger drop in average life expectancy as well as still-substantial disparities by race and ethnicity.
Lead author Theresa Andrasfay, a postdoctoral scholar at the USC Leonard Davis School of Gerontology, and coauthor Noreen Goldman of Princeton University first examined the pandemic’s effect on American life expectancy in October 2020. Their initial study, published in Proceedings of the National Academy of Sciences in January 2021, showed the largest single-year decline in life expectancy in at least 40 years and the lowest life expectancy estimated since 2003.
The updated analysis, which included the more than 380,000 US COVID-19 deaths in 2020 and used 2018 life expectancies as a comparison, indicates that COVID-19 reduced overall life expectancy by 1.31 years (up from the initial estimate of 1.13 years lost) to 77.43 years. The reductions in average lifespan are more than three times as large for Latinos (3.03 years) and twice as large for the Black population (1.90 years) compared to whites (0.94 years).
“Impacts on life expectancy are likely to be even larger once excess mortality from other causes is taken into account.” Andrasfay cautioned.
The changing geography of the pandemic’s impact since last fall has made a significant difference in total average life expectancy loss as well as for whites, who were previously projected to lose 0.68 years on average.
“Since our October 2020 projections, disproportionately white Midwestern and Mountain states experienced surges in COVID-19 cases and deaths,” Andrasfay explained. “As a result, the disparities are not quite as large as we initially projected, but are still striking.”
As noted in the previous study, Black and Latino Americans have experienced a disproportionate burden of coronavirus infections and deaths, reflecting persistent structural inequalities that heighten risk of exposure to and death from COVID-19. The particularly large decrease in average life expectancy among Latinos likely stems from social and economic inequities that result in both higher exposure to infection and higher fatality among those infected. Compared to Black and white populations, Latinos have lower rates of health insurance, are more likely to live in multi-generational or crowded households and are more likely to hold frontline jobs with COVID-19 exposure risks, Andrasfay noted.
“Life expectancy is a metric of population-level mortality in a given year, and it is sensitive to deaths at younger ages,” Andrasfay explained. “Though COVID-19 disproportionately killed older Americans, substantial numbers of younger Black and Latino Americans had their lives taken by COVID-19, which contributed to greater life expectancy reductions for these populations.”
Andrasfay and Goldman also examined data from the first few months of 2021, which showed that average life expectancy is still affected by the pandemic.
“Though it is too early to estimate 2021 life expectancy, the deaths that occurred in just the first three months of 2021 already indicate that 2021 will have reduced life expectancy compared to pre-pandemic levels, and substantial racial and ethnic disparities in these reductions will persist,” Andrasfay said. “The ultimate impact of COVID-19 on 2021 US life expectancy will depend on whether there is sufficient and equitable vaccination across the US. Looking to the future beyond COVID-19, reducing racial disparities in life expectancy requires investments beyond healthcare, including a commitment to make the economy more equitable.”
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Materials provided by University of Southern California. Original written by Beth Newcomb. Note: Content may be edited for style and length.

Toxoplasma gondii, the parasite responsible for toxoplasmosis, is capable of infecting almost all cell types. It is estimated that up to 30% of the world’s population is chronically infected, the vast majority asymptomatically. However, infection during pregnancy can result in severe developmental pathology in the unborn child. Like the other members of the large phylum of Apicomplexa, Toxoplasma gondii is an obligate intracellular parasite which, to survive, must absolutely penetrate its host’s cells and hijack their functions to its own advantage. Understanding how the parasite manages to enter host cells offers new opportunities to develop more effective prevention and control strategies than those currently available. A team from the University of Geneva (UNIGE), in collaboration with the University of Zurich (UZH) and the Paul Scherrer Institute (PSI) in Villigen, Switzerland, have identified the key role of RON13, a protein of the parasite, which is essential for the invasion process. The three-dimensional structure and the site of action of this enzyme are atypical, thus offering the possibility of designing specific inhibitors to stop the infection. These results are published in the journal Nature Communications.
Specific types of enzymes named kinases are key regulators of a wide range of basic biological processes. “These enzymes modify proteins by adding or removing phosphate groups that, like a switch, turn cellular functions on or off as needed,” explains Oscar Vadas, a lecturer in the Department of Microbiology and Molecular Medicine at UNIGE Faculty of Medicine, a specialist in protein biochemistry and co-author of this study. “Kinases are great targets for drug development because, on the one hand, they are relatively easy to inhibit and, on the other hand, they are involved in many pathologies. They are therefore the subject of intense research.” Identifying a kinase essential to the survival of a pathogen would thus pave the way for the development of new therapies.
A kinase seen from all its angles
The identification of RON13, a Toxoplasma gondii kinase, quickly became a very attractive subject of study in light of its major role in the invasive capacity of the parasite. “To understand the biological processes controlled by this enzyme, both at the cellular and molecular level, we combined several state-of-the-art technologies,” explains Professor Adrian Hehl of UZH. Cryo-electronic microscopy identified an additional modular structure that was absent in all other kinases previously studied, but essential for RON13 activity. Expansion microscopy demonstrated morphological changes in the parasite using high-resolution images. In addition, proteomics was used to identify the kinase targets that are released into host cells to promote its invasion, and genetics was performed to study the impact of the absence of this kinase on the parasite’s growth.
“These sophisticated analyses were also made possible thanks to the high-precision technology facilities of the UNIGE Faculty of Medicine, which were made available to the research teams,” says Dominique Soldati-Favre, Director of UNIGE Faculty of Medicine Department of Microbiology and Molecular Medicine, who directed this work. “By pooling together all our expertise, we were able to identify precisely the interactions at work and understand the structure of this kinase at the atomic level,” underlines Volodymyr Korkhov, a professor at PSI.
Without RON13, there is no invasion
RON13 is a kinase located in a unique compartment of the parasite, an organelle containing proteins to be injected into the host. Without RON13, host cells infection is impossible. “To confirm these results, we infected mice with a strain of the parasite that does not express RON13: it became completely harmless, to the extent that the mice did not show any specific immune response,” explains Dominique Soldati-Favre.
Moreover, these very particular characteristics make RON13 insensitive to an inhibitor that is effective on the majority of kinases. “From a therapeutic point of view, this is excellent news,” says Oscar Vadas. “This means that we can target it very precisely without affecting human kinases, thus limiting the side effects of the treatment.” Moreover, although this work focused on the toxoplasmosis parasite, other pathogens of the Apicomplexa phylum share the same invasion process. It is therefore conceivable that a kinase similar to RON13 plays an essential role in infection by other parasites, and in particular by Plasmodium falciparum, the agent responsible for malaria.
This work was carried out thanks to the support of the Carigest SA Foundation and the Swiss National Science Foundation (SNSF).
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Materials provided by Université de Genève. Note: Content may be edited for style and length.

A few dozen human genes rapidly evolved in ancient East Asia to thwart coronavirus infections, scientists say. Those genes could be crucial to today’s pandemic.Researchers have found evidence that a coronavirus epidemic swept East Asia some 20,000 years ago and was devastating enough to leave an evolutionary imprint on the DNA of people alive today.The new study suggests that an ancient coronavirus plagued the region for many years, researchers say. The finding could have dire implications for the Covid-19 pandemic if it’s not brought under control soon through vaccination.“It should make us worry,” said David Enard, an evolutionary biologist at the University of Arizona who led the study, which was published on Thursday in the journal Current Biology. “What is going on right now might be going on for generations and generations.”Until now, researchers could not look back very far into the history of this family of pathogens. Over the past 20 years, three coronaviruses have adapted to infect humans and cause severe respiratory disease: Covid-19, SARS and MERS. Studies on each of these coronaviruses indicate that they jumped into our species from bats or other mammals.Four other coronaviruses can also infect people, but they usually cause only mild colds. Scientists did not directly observe these coronaviruses becoming human pathogens, so they have relied on indirect clues to estimate when the jumps happened. Coronaviruses gain new mutations at a roughly regular rate, and so comparing their genetic variation makes it possible to determine when they diverged from a common ancestor.The most recent of these mild coronaviruses, called HCoV-HKU1, crossed the species barrier in the 1950s. The oldest, called HCoV-NL63, may date back as far as 820 years.But before that point, the coronavirus trail went cold — until Dr. Enard and his colleagues applied a new method to the search. Instead of looking at the genes of the coronaviruses, the researchers looked at the effects on the DNA of their human hosts.Over generations, viruses drive enormous amounts of change in the human genome. A mutation that protects against a viral infection may well mean the difference between life and death, and it will be passed down to offspring. A lifesaving mutation, for example, might allow people to chop apart a virus’s proteins.But viruses can evolve, too. Their proteins can change shape to overcome a host’s defenses. And those changes might spur the host to evolve even more counteroffensives, leading to more mutations.When a random new mutation happens to provide resistance to a virus, it can swiftly become more common from one generation to the next. And other versions of that gene, in turn, become rarer. So if one version of a gene dominates all others in large groups of people, scientists know that is most likely a signature of rapid evolution in the past.In recent years, Dr. Enard and his colleagues have searched the human genome for these patterns of genetic variation in order to reconstruct the history of an array of viruses. When the pandemic struck, he wondered whether ancient coronaviruses had left a distinctive mark of their own.He and his colleagues compared the DNA of thousands of people across 26 different populations around the world, looking at a combination of genes known to be crucial for coronaviruses but not other kinds of pathogens. In East Asian populations, the scientists found that 42 of these genes had a dominant version. That was a strong signal that people in East Asia had adapted to an ancient coronavirus.But whatever happened in East Asia seemed to have been limited to that region. “When we compared them to populations around the world, we couldn’t find the signal,” said Yassine Souilmi, a postdoctoral researcher at the University of Adelaide in Australia and a co-author of the new study.The scientists then tried to estimate how long ago East Asians had adapted to a coronavirus. They took advantage of the fact that once a dominant version of a gene starts being passed down through the generations, it can gain harmless random mutations. As more time passes, more of those mutations accumulate.Dr. Enard and his colleagues found that the 42 genes all had about the same number of mutations. That meant that they had all rapidly evolved at about the same time. “This is a signal we should absolutely not expect by chance,” Dr. Enard said.They estimated that all of those genes evolved their antiviral mutations sometime between 20,000 and 25,000 years ago, most likely over the course of a few centuries. It’s a surprising finding, since East Asians at the time were not living in dense communities but instead formed small bands of hunter-gatherers.Aida Andres, an evolutionary geneticist at the University College London who was not involved in the new study, said she found the work compelling. “I’m quite convinced there’s something there,” she said.Still, she didn’t think it was possible yet to make a firm estimate of how long ago the ancient epidemic took place. “The timing is a complicated thing,” she said. “Whether that happened a few thousand years before or after — I personally think it’s something that we cannot be as confident of.”Scientists looking for drugs to fight the new coronavirus might want to scrutinize the 42 genes that evolved in response to the ancient epidemic, Dr. Souilmi said. “It’s actually pointing us to molecular knobs to adjust the immune response to the virus,” he said.Dr. Anders agreed, saying that the genes identified in the new study should get special attention as targets for drugs. “You know that they’re important,” she said. “That’s the nice thing about evolution.”

It points the way to some possible means of fighting it.Childhood obesity has increased significantly in the United States during the past four decades. In 1980, about 5 percent of the country’s children between 2 and 19 were experiencing obesity, according to the C.D.C.; as of 2018, more than 19 percent were — and an additional 16 percent were considered overweight. Because children are far more likely to gain an unhealthful amount of weight while out of school over the summer, experts were worried last spring when in-person schooling was suspended indefinitely because of the pandemic. They feared extended closures might “exacerbate the epidemic of childhood obesity and increase disparities in obesity risk,” as researchers from the Mailman School of Public Health at Columbia University and colleagues put it in a paper in the journal Obesity in June 2020. That, in turn, would mean more children living with related conditions such as Type 2 diabetes, hypertension and fatty-liver disease.Those concerns were warranted, according to a May study in Pediatrics. Based on measurements of body mass index taken for more than 500,000 children between the ages of 2 and 17 during visits to the Children’s Hospital of Philadelphia Care Network, researchers found that, on average, between January 2019 and December 2020 the prevalence of obesity increased by almost 2 percentage points overall, from 13.7 percent to 15.4 percent. (In the most recent years for which national data is available, the increase has been 1 percentage point or less.) Black and Latino children, as well as those from families with lower incomes, displayed sharper increases than children from other groups did. Such gains early in life make it more likely that children will have higher B.M.I.s when they grow up. (Obesity already affects more than 40 percent of American adults.) “This isn’t just baby fat that’s going to go away,” says Brian Jenssen, the study’s lead author and a pediatrician at Children’s. “That’s why I think this is so alarming.”Illustration by Mario MenesesAnalyzing what children do differently during the school year compared with the summer months has led researchers to single out factors that can contribute to unhealthful weight gain. Schools often serve more nutritionally balanced meals than children get at home. At school, students eat on a regular schedule and find it difficult to snack throughout the day. Schools also offer opportunities for physical activity, which are more limited for children who live in neighborhoods that lack outdoor amenities or are unsafe. “In downtown Baltimore, where our murder rate is so high, you’re not letting your kid go out and play in a park,” says Maureen Black, a psychologist and professor of pediatrics, epidemiology and public health at the University of Maryland School of Medicine. That tends to mean that children spend more time in front of screens, sedentary and often snacking. A lack of school structure can also contribute to altered sleep-wake patterns, which have been associated with unhealthful weight gain.But while it has been possible to identify ways that schools can help prevent B.M.I. increases, it has been harder to figure out how to replicate those conditions when classes aren’t in session. For example, only about three million of the 22 million children who receive free or reduced-price lunch during the school year get the meals they’re eligible for over the summer. Those meals are typically more balanced nutritionally than the cheaper, calorie-dense fare that families resort to when food is scarce. Inconsistent access to food can also cause physiological changes that heighten the risk of obesity; school closures and job losses during the pandemic greatly increased the number of children without a stable source of nutrition. In June 2020, more than 27 percent of U.S. households with children were experiencing food insecurity; in about two-thirds of them, there was evidence that the children, in addition to adults, weren’t getting enough to eat — more than 5.5 times the number who reported those circumstances in all of 2018, according to the Brookings Institution. In addition, many families with sufficient resources were buying more ultraprocessed, shelf-stable foods for comfort and in preparation for possible lockdowns or supply shortages. The crisis did force federal, state and local agencies to improvise novel ways of getting more balanced meals to children outside a school setting. To limit infection risk and reach more students, for instance, the U.S.D.A. offered waivers to what is known as its “congregant feeding” requirement that children eat on-site. This allowed caregivers to pick up multiple days’ worth of meals; some districts converted school buses running along their regular routes into a food-delivery service. The agency also made all children eligible for free lunch through September 2021, eliminating the paperwork required to qualify and the stigma that often comes with it, says Eliza Kinsey, a professor of epidemiology at the Mailman School of Public Health and an author of the Obesity paper. Such “program flexibility,” she points out, “could be applied in other, non-Covid contexts,” such as during the summer or for other disruptions like hurricane and wildfire closures. It stands to reason that broadening access to nutritious foods would help prevent childhood obesity going forward. But schools also play a central role in the collection of nationally representative health data for children, a process that has been disrupted by school closures. We don’t know yet if the nearly 2 percentage point increase observed in the Philadelphia area will be similar across the country — or how much expanded feeding programs have mitigated the many and varied risk factors for obesity imposed by the pandemic. Still, other pediatric hospital networks have reported worrying increases not just in obesity but also in the conditions that go with it. In a study published in April in the journal Diabetes Care, researchers noted a sharp increase in 2020, compared with previous years, of the number of children who showed up at Children’s Hospital Los Angeles with a severe form of new-onset Type 2 diabetes called diabetic ketoacidosis. That might be because children were eating poorer-​quality food and moving less, according to the lead author, Lily Chao, interim medical diabetes director at the hospital. It could also be that worries about the coronavirus induced families to delay seeking treatment for their children’s symptoms until they were in diabetic ketoacidosis.A better understanding of how and why the pandemic affected children — not just physically but also emotionally and academically — would improve the ability of pediatricians, parents and policymakers to facilitate their recovery. Unfortunately, what is clear is that for children whose B.M.I. increased, “there are no magic bullets,” Black says. And, she adds, “it’s not healthy for kids to think about losing weight.” Rather than try to undo a past B.M.I. increase, a better strategy is to try to slow future ones and establish healthy habits. There is some good news in the fact that children tend to experience a growth spurt during puberty, says Risa Wolf, a pediatric endocrinologist at the Johns Hopkins Hospital; this can enable them to redistribute added weight on a taller frame. Wolf suggests parents focus on trying to build physical activity into their kids’ daily routine; the C.D.C. recommends 60 minutes for school-age children. And cutting fruit juice and soda from children’s diets is an easy way to significantly reduce sugar and calorie intake, Chao says. But the Pediatrics findings, Jenssen argues, also highlight how the problem of obesity can come from societal causes: The children who had the largest B.M.I. increases in his study were 5- to 9-year-olds. “They’re not making those individual choices,” he says. “They’re influenced by the environment.” Which means policies that improve the post-pandemic availability of nutritious meals and recreation can still positively influence their trajectory. Rebecca Franckle, a public health researcher at Boston College, was an author of a May report about how pandemic adaptations could be expanded to improve U.S.D.A. summer feeding programs for Healthy Eating Research, a nonprofit organization. “There’s huge opportunity,” she says, “for prevention when it comes to kids versus adults.” Kim Tingley is a contributing writer for the magazine.

Scientists are studying the case of a man in Bristol who has recovered from 290 days being positive with SARS-CoV-2. Dave, 72, is a driving instructor and musician who’s spent the last 10 months with an active coronavirus infection, visiting hospital seven times. His immune system was vulnerable to the virus after a leukaemia diagnosis and chemotherapy treatment. Dave was eventually treated with a new mixture of anti-viral drugs provided by the US company Regeneron on compassionate grounds. Now scientists at the University of Bristol are studying Dave’s case to try and understand how Covid acts and mutates within the body. The BBC’s Jon Kay reports.