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Prime Minister Mario Draghi issued a decree requiring that workers in health care facilities be vaccinated, a move that will test the legal limits of his government’s efforts to stem coronavirus outbreaks.ROME — Giulio Macciò tested negative for the coronavirus and spent weeks receiving treatment for emphysema in a sealed-off hospital under the care of doctors and lung specialists — and a nurse who had refused to be vaccinated. On March 11, he unexpectedly died. A post-mortem swab found that he had contracted the virus, as had 14 other patients and the unvaccinated nurse who spent her shifts in his midst.“It makes no sense that a person whose job is to heal the sick gives them Covid and kills them,” said Mr. Macciò’s son, Massimiliano Macciò, who filed a complaint against the San Martino hospital in the northern Italian city of Genoa. He believes that the nurse, one of an estimated 400 who have refused vaccination against Covid-19 at the hospital, infected his father, who died unvaccinated at 79.As vaccination rollouts build momentum, businesses everywhere are grappling with whether they can require the inoculation of their employees, raising thorny ethical, constitutional and privacy issues around Europe and the United States. But that quandary becomes all the more urgent when the person is your health care worker.In Italy, the original Western front in the war against Covid, a rash of outbreaks in hospitals where medical workers have chosen not to be inoculated has raised fears that their stance is endangering public health. It has also prompted a forceful response from an Italian government that is struggling to get vaccinations on track.On Wednesday, Prime Minister Mario Draghi tested the legal limits of his government’s ability to address the problem by issuing a decree requiring that workers in health care facilities be vaccinated. It also allowed hospital employers to suspend without pay any health care workers who refuse to do so.Some legal analysts have said that requiring Covid-19 inoculation for health workers could violate Italy’s privacy laws, and that firing or forcing any who decline it to take unpaid leave could be unconstitutional because of a specific article that protects people who refuse health treatments.A coronavirus ward at the Papa Giovanni XXIII hospital in Bergamo in March last year.Fabio Bucciarelli for The New York TimesBut recent court rulings have interpreted the law differently, and Mr. Draghi has made clear that for a country that has suffered more than 100,000 Covid deaths, the breach of safety cannot be tolerated.“It is absolutely not OK that unvaccinated workers are in contact with the sick,” he said at a news conference last week while announcing his government’s intention to “intervene” when asked about the reports of unvaccinated health care workers.For much of the pandemic, nurses and doctors stood as national heroes who sacrificed their waking hours, safety and sometimes lives to protect their compatriots. It has shocked Italians that in some major hospitals up to 15 percent of those medical professionals — who were given preference in the vaccination rollout ahead of older people — have shunned inoculation.“It’s really humiliating for the medical and health worker class that you have to force people to vaccinate themselves,” said Roberto Burioni, a virologist at San Raffaele University in Milan.He added that while firing workers is exceedingly difficult in Italy, he hoped the decree will bite into the salaries of any vaccine skeptics, especially considering the large amount of data demonstrating that the vaccines’ efficacy is worth the risk. He also worried that the high number of health professionals refusing to get vaccinated had troubling implications.“Unfortunately there is huge part of doctors who are deeply ignorant,” said Mr. Burioni, who suggested that perhaps “the selection process for bringing people to gain a medical degree and then the medical license is not effective enough.”Transporting coffins in Bergamo last year. Italy has had more than 100,000 Covid-19 deaths.Fabio Bucciarelli for The New York TimesWhile Italy’s populists, including the Five Star Movement and League parties, exploited vaccine skepticism for political gain in recent years, the country is not even considered the most vaccine-skeptic in Europe, a dubious distinction that usually falls to France. Italy also had a fast start in vaccinations at the beginning of the year precisely because the previous government prioritized medical workers.In January, the health minister, Roberto Speranza, said on television that Italy, like its European partners, believed it was better to persuade people to get vaccinated than to require them to. “Those who had to deal with the virus, our health care workers, are even more aware than the others,” he said. “I think willingness will be enough.”But Italy’s vaccination program has hit speed bumps. First, the pharmaceutical company AstraZeneca failed to make good on millions of promised doses. The previous government, led by the Five Star Movement, fell, and Mr. Draghi came in promising to help accelerate vaccinations and the country’s economic recovery.He has pushed for bans on vaccine exports from the European Union to contend with the shortages. He has sought to mobilize new categories of vaccinators and centralize Italy’s response to make up for the failure of some of the country’s hardest-hit regions to inoculate the most vulnerable, older citizens. On Tuesday, Mr. Draghi himself received an AstraZeneca dose after joining a temporary Europe-wide suspension of the vaccine amid concerns about its safety.“It is absolutely not OK that unvaccinated workers are in contact with the sick,” said Prime Minister Mario Draghi, center.Angelo Carconi/EPA, via ShutterstockBut the anti-vax health workers have struck a deep nerve.In a nursing home outside Rome, nearly all of the health care workers chose not to be vaccinated, and a cluster erupted around three workers and 27 out of the 36 older guests. Roberto Agresti, the home’s owner, feared the worst for them. “If we had a law forcing everyone to get vaccinated, the virus would have passed without us even noticing it,” he said.In the southern city of Brindisi, the local health authority has opened disciplinary proceedings against 12 health care workers who expressly refused vaccination. It is also investigating why about 140 health care workers, including doctors, nurses, pediatricians and specialists, declined shots of the Pfizer vaccine.“We don’t want to punish workers — we need them,” said Giuseppe Pasqualone, who leads the local health authority. “But the risk of contagion not only for them but for fragile patients is very high.”Officials at the San Martino hospital, where Mr. Macciò died, said it was not clear whether the unvaccinated nurse was the source of the cluster, but they acknowledged that it was a problem.Salvatore Giuffrida, the director of the hospital, Europe’s fourth largest, said he favored a vaccination requirement because it would also keep medical workers healthy and would strengthen defensive lines as a brutal third wave spreads through northern Italy.“We cannot afford not having them on the job,” he said. “The objective is not to lose soldiers during a war in a nation that complains about not having health care workers.”He estimated that 15 percent of his nursing staff, about 400 nurses, was unvaccinated. Simply removing those nurses from the wards, or redirecting them to switchboards as some have proposed, would be “a cure worse than the disease,” he said, because it would result in the reduction of 250 beds.He and other directors said that Italy’s strict privacy laws kept the hospitals from knowing which doctors and nurses were unvaccinated.Paolo Petralia, the director general of the Lavagna hospital in Chiavari, the site of another outbreak this month, said 90 percent of his doctors were vaccinated, along with about 80 percent of nurses and aides.“They are protected by privacy laws,” he said, citing a recent pronouncement by Italy’s data protection authority that the vaccination status of health workers should be unknown. “But this right exists until it does not limit another person’s right,” Mr. Petralia said.Lining up at a drive-through vaccination center in Milan this month.Alessandro Grassani for The New York TimesSome Italian courts have agreed. In 2017, Italy made some vaccinations compulsory for children, including for measles, and barred the unvaccinated from attending school — a decision backed by Italy’s constitutional court because it also safeguarded public health. In the northern city of Belluno, a court ruled in mid-March that a nursing home that employed several health care workers who chose not to get vaccinated could force them to take paid leave.Mr. Macciò, whose father died in Genoa, said it made no sense that the people entrusted to care for his father were allowed to potentially harm him. He said he had complained to the doctors, who told him their hands were tied because the nurses were protected by privacy rules.But amid Italy’s frustration, and the new decree, something appears to be changing. Mr. Macciò said the police had asked for his help in identifying the nurses he saw when going to pick up his father’s belongings.“I hope some good comes of it,” he said of his father’s death. “These people should change their job.”Emma Bubola

What’s the difference between a giggle and a belly laugh? Or a yelp and an all-out scream? In many species, including humans, the volume and duration of a verbal sound conveys as much information as the noise itself.
A group of scientists, led by Scripps Research, has discovered a node in the brains of male mice that modulates the sounds they make in social situations. This discovery, published in Nature, could help identify similar locations in the human brain, and potentially lead to a better understanding of social disorders such as autism or depression.
“Identifying this node gives us signatures of what to look for when human behavior goes awry,” says Lisa Stowers, PhD, a neuroscientist and professor at Scripps Research who led the study. “It’s giving us clues to how information is organized in the brain, and how different features of information can be separated out in different brain regions.”
As part of their courtship behavior, male mice produce “songs.” These complicated whistles, which are too high for the human ear to detect, are louder and longer when the female mouse is nearby or when her scent is stronger. The researchers identified a specific type of neuron in a part of the hypothalamus called the lateral preoptic area that controls the emotional regulation of these sounds.
“The hypothalamus and the rest of the limbic system control body functions such as hunger, thirst and temperature regulation, as well as the basic features of emotional behavior like sex and fear,” Stowers says. “It is fitting that the emotional aspect of these social noises are generated in this region of the brain.”
By directly stimulating the right nodes from these neurons, the scientists could trigger the whole array of noises that go into a mouse song. Varying the level of stimulation allowed them to control how enthusiastic those sounds were.
When the researchers blocked these nodes, male mice encountering a female would attempt to court her in silence. (Female mice responded by kicking the males and running away.) If the researchers bypassed these nodes and activated the next node downstream, the male mice only made long, loud noises.
“They’re basically just shouting,” Stowers says. “By finding these neurons, it’s telling us that this part of the brain is doing this emotional scaling and persistence. If you take that away, then you lose all of that affect, all of that emotional range, and the ability to have effective social communication.”
Most research on noise production in the brain has focused on language development, Stowers says. But the sounds that even an infant can make — a giggle, a cry, a scream — don’t have to be learned and are just as vital for communication. Identifying how the brain decides on these responses is the first step to understanding where things can go wrong in social behavioral disorders such as autism and depression.
“We are starting to get a detailed look at where in the brain different types of computations are being made,” Stowers says. “Now that we know that this simple behavior is regulated in the hypothalamus, we can study whether others behaviors are also using similar circuits and if so, perhaps find a common mechanism — and drug target — for when emotions are not generated appropriately.”
Funding was provided by the Dorris Neuroscience and Skaggs Scholarships, the Anandamahidol Foundation Fellowship, Career Award at the Scientific Interface from BWF and the National Institutes of Health (R01NS097772, R01DA049787, R01NS108439).

Streptococcus pyogenes is one of the most important bacterial causes of human skin infections. If S. pyogenes invades deep into the tissue, it can cause life-threatening illnesses, such as sepsis and toxic shock. With its limited supply of carbohydrates, the skin is generally an effective barrier against infection and not a good surface for the survival of S. pyogenes. To survive successfully and invade deep into the tissue, bacteria must be able to find a source of nutrients and also evade the skin’s immune defenses.
Now, an international team led by Osaka University, Japan, in collaboration with Keio University, Japan, and University of California San Diego, USA, has discovered a way this disease organism obtains nutrition from the skin surface. This knowledge could lead to new therapeutic approaches to tackle infections. The team recently published the work in Cell Reports.
It was already known that some bacteria break down arginine (an amino acid — one of the building blocks of proteins) via a biochemical pathway named the arginine deaminase (ADI) pathway. The team confirmed that S. pyogenes can survive using arginine even when starved of glucose. When they deleted the bacterial gene (named arcA) encoding the first enzyme in the ADI pathway, the S. pyogenes lost that ability and also became less toxic towards human skin cells grown in culture.
When arginine is supplied, the ADI pathway of S. pyogenes is activated but there are also widespread changes in gene expression. Some genes are down-regulated but large numbers of genes are up-regulated, including genes associated with virulence of S. pyogenes, such as those that produce bacterial toxins.
Using mouse skin as a model system for human skin, the team showed for the first time that S. pyogenes can use arginine to survive on the skin surface. S. pyogenes lacking the arcA gene survived poorly and were less virulent on mouse skin, confirming the importance of this pathway in the disease process. In contrast, in blood (containing plentiful glucose), the altered S. pyogenes appeared no different to normal S. pyogenes since the ADI pathway was not needed.
“We showed that arginine from stratum corneum-derived filaggrin was a key substrate for the ADI pathway of S. pyogenes,” says lead researcher Dr. Yujiro Hirose. “In mice that do not produce filaggrin, less arginine is available and the S. pyogenes bacteria do not utilize ADI pathway to cause the skin lesion.”
“This represents a significant step forward in understanding how S. pyogenes survives on the skin,” explains Dr. Hirose. “We expect our study will lead to novel treatment strategies: if we can block arginine metabolism in S. pyogenes it should restrict the pathogen’s survival and virulence.”
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After the optical frequency comb made its debut as a ruler for light, spinoffs followed, including the astrocomb to measure starlight and a radar-like comb system to detect natural gas leaks. And now, researchers have unveiled the “agricomb” to measure, ahem, cow burps.
The agricomb could help optimize agricultural processes to reduce production of heat-trapping greenhouse gases.
Researchers from the National Institute of Standards and Technology (NIST) and Kansas State University (KSU) used NIST’s agricomb to simultaneously measure emissions of methane, ammonia, carbon dioxide and water vapor from the atmosphere around a beef cattle feedlot in Kansas. The NIST apparatus — a two-comb system — identifies trace gases based on the exact shades and amounts of infrared light absorbed by the atmosphere when the comb light is sent back and forth across open-air paths.
Described in Science Advances, the demonstration was the first use of frequency combs in an agricultural setting. The portable system was set up inside a trailer parked next to the feedlot. The laser light was specially amplified and filtered to target specific gases.
Researchers measured gases along two 100-meter paths both upwind and downwind from pens containing about 300 cows. The experiment focused on methane and ammonia because emissions from livestock, mainly cattle, are the largest U.S. source of anthropogenic methane, a major greenhouse gas, and ammonia is an important atmospheric pollutant.
The measurements captured emissions from both the cattle’s digestive processes and manure on the ground. The agricomb measured both methane and ammonia concentrations at parts-per-million levels with a precision of 25 parts per billion. The agricomb results for methane were comparable to those from a commercial sensor that sampled the air at multiple inlets along the edges of the feedlot. The comb system was particularly useful for ammonia because this gas is sticky and difficult to measure with inlet-based systems. In addition, the agricomb can measure many gases simultaneously, which is challenging for conventional systems.
Finally, while the commercial sensors measured precise background levels faster, the agricomb more precisely captured downwind plumes and could then better characterize the gas sources, according to the paper. The increased precision will be critical for planned future measurements of methane from sparsely distributed cows in a pasture, which is a much more challenging problem.
The agreement of the old and new techniques inspires confidence that the agricomb can be used to accurately quantify gases in agricultural contexts, the paper suggests. Advantages of the agricomb include sensitivity to a broad range of infrared light, high precision, calibration-free detection of multiple gases at once, and flexibility of the measurement setup. Pairing two combs with different spacings of “teeth” for identifying exact colors of light makes the analysis more precise.
Estimating methane emissions from livestock is challenging because of variations in management practices and cattle characteristics in commercial farms. In addition, what the cattle eat affects emissions but is unaccounted for in national inventories, leading to large uncertainties in greenhouse gas emission models, according to the paper. The cattle at the Kansas feedlot ate a mix of hay and corn silage.
“For the future our plan is to work with KSU to do a pasture measurement, where the cattle eat native grasses,” NIST physicist Brian Washburn said. “The different feed, plus microbial activity in grassland soils that consumes methane, may mean less atmospheric methane production in the pasture than in the feedlot. The cattle spend about 75% of their life in the pasture, so this measurement would be more representative of the net methane production. This would also be a harder measurement, since it would take place over a larger area, about 500 meters by 500 meters, with fewer animals, about 40 head.”
The researchers suggest the agricomb can support precision agriculture — the use of new technology to boost yields — by measuring many gases simultaneously over large spatial scales, making it possible to design cleaner and more productive farms.
This work was funded in part by the National Science Foundation, the ARPA-E MONITOR program, the William and Joan Porter Endowment, and the Habiger Heritage Fund.

A Northwestern University-led research team has developed a novel skin-mounted sticker that absorbs sweat and then changes color to provide an accurate, easy-to-read diagnosis of cystic fibrosis within minutes.
While measuring chloride levels in sweat to diagnose cystic fibrosis is standard, the soft, flexible, skin-like “sweat sticker” offers a stark contrast to current diagnostic technologies, which require a rigid, bulky, wrist-strapped device to collect sweat.
After developing the sweat sticker at Northwestern, the researchers validated it in clinical pilot studies involving cystic fibrosis patients and healthy volunteers at the Cystic Fibrosis Center at the Ann & Robert H. Lurie Children’s Hospital of Chicago. The sticker showed enhanced performance in collected sweat volume and equivalent accuracy to traditional platforms.
The research and study findings will be published on March 31 as the cover feature article in the journal Science Translational Medicine.
By softly adhering to the body, the millimeter-thick sticker makes direct but gentle contact with the skin without harsh adhesives. Not only does this make the sticker more comfortable and imperceptible to the wearer, this intimate coupling also enables the sticker to collect 33% more sweat than current clinical methods. The high collection rate ensures that one test will consistently collect a large enough sample to provide an accurate result.
The sticker also has built-in colorimetric sensors that detect, measure and analyze chloride concentration in real time using a smartphone camera, bypassing the need for expensive laboratory equipment and excruciating wait times. This opens possibilities for testing outside of hospitals in the home setting, which could provide relief to parents in rural or low-resource areas without access to clinical centers with specialized diagnostic tools.

Comorbidities such as heart disease, respiratory disease, renal disease and cancer lead to an increased risk of death from Covid-19 according to new research from the University of East Anglia (UEA) and the Norfolk and Norwich University Hospital (NNUH).
At the start of the pandemic, there was concern that specific medications for high blood pressure could be linked with worse outcomes for Covid-19 patients.
Previous research from the UEA team showed this wasn’t the case and that medications for high blood pressure could, in fact, improve Covid-19 survival rates and reduce the severity of infection.
New findings, published today in the Journal of the American Medical Association (JAMA) Network Open, additionally show that it is comorbidities such as heart disease, respiratory disease, renal disease, cancer, obesity and increasing age — and having more than one disease or chronic condition at the same time — that lead to increased mortality and severity of disease.
The team reviewed 52 separate studies involving over 100,000 patients in this, the most comprehensive study of its kind to date.
They studied the outcomes for patients taking antihypertensives — looking particularly at ‘critical’ outcomes such as being admitted to intensive care or being put on a ventilator, and death.
Their meta analysis showed a significantly lower risk of hospitalisation or death for people taking blood pressure medications Angiotensin-Converting Enzyme inhibitors (ACEi) or Angiotensin Receptor Blockers (ARB).
But they also found that risks for hospitalisation and death were much higher for people with comorbidities.
Lead researcher Dr Vassilios Vassiliou, from UEA’s Norwich Medical School and Honorary Consultant Cardiologist at NNUH, said: “What a meta analysis gives us is the really big picture. We looked at the combined findings of 52 separate studies involving over 100,000 patients. It is the most comprehensive study of its kind to date.
“With these increased numbers, what we can see very clearly now, is that it is the comorbidities such as cardiac disease or respiratory disease, cancer or obesity amongst others that lead to an increased mortality.
“And we can confirm that the blood pressure medications themselves are protective — not only for people who have high blood pressure, but for people with a range of other comorbidities as well,” he added.
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Mount Sinai researchers have identified genetic and cellular mechanisms of Crohn’s disease, providing new insights for future treatments that could offer a tailored approach to patients with the chronic inflammatory disease, according to a study published in Nature on March 31.
The researchers found that blocking the common cytokine receptor subunit gp130 may benefit some patients with Crohn’s disease and could complement a standard treatment for moderate to severe Crohn’s disease known as anti-tumor necrosis factor (TNF) treatment. This treatment uses medications known as TNF inhibitors to block white blood cells producing the protein TNF, which causes the inflammation.
Crohn’s disease is a chronic inflammatory intestinal disease with frequent abnormal healing and complications that narrow or constrict passage through the digestive tract. Complications associated with Crohn’s disease are driven by communication between cells called macrophages that detect and destroy harmful bacteria or organisms, and cells known as fibroblasts that aid with wound healing. Mount Sinai researchers analyzed inflamed and normal tissues of the small intestine in humans, and zebrafish models of intestinal injury, and showed that a dysregulated macrophage-fibroblast niche can be driven by Crohn’s disease-associated mutations in the gene NOD2.
These findings are reported on the 20th anniversary of the discovery by Judy H. Cho, MD, Dean of Translational Genetics and Director of The Charles Bronfman Institute for Personalized Medicine at the Icahn School of Medicine at Mount Sinai, her colleagues, and others that genetic variants that cause the protein produced by NOD2 to lose function are associated with increased risk for Crohn’s disease. NOD2 recognizes bacterial components, and the intestinal immune system is exposed to high bacterial concentrations in both healthy and diseased states. However, the reasons why mutations in NOD2 cause increased risk for Crohn’s disease and why some patients do not respond to anti-TNF medications remained incompletely defined until now. Patients carrying NOD2 mutations have increased activated fibroblast and macrophage gene expression, and in particular, elevated gp130-related gene expression. Given this finding, the researchers believe that blocking the protein gp130 may help patients who are nonresponsive to the treatment of anti-TNF medications.
“Our work defines a completely new mechanism whereby NOD2 mutations confer risk, namely through altered differentiation of newly recruited blood monocytes over time,” says Dr. Cho. “It sharpens current research efforts involved in serial tissue and blood analyses to define how non-response or loss-of-response to anti-TNF therapies may be improved.”
Shikha Nayar, the study’s first author and a PhD candidate in Dr. Cho’s lab at Icahn Mount Sinai, said the findings could provide a more custom-made approach to future patient care. “We’ve developed novel in vivo and in vitro models to define mechanisms and timing of disease progression,” she says. “These studies may help tailor treatments more effectively for Crohn’s disease patients carrying NOD2 mutations and elevated signatures we have described.”
The Department of Pediatric Gastroenterology at Emory University contributed to the study. This work was also supported by National Institutes of Health (NIH) grants R01 DK106593, R01 DK123758-01, U01 DK062422 (to J.H.C.).
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Harvard University researchers have identified the biological mechanism of how chronic stress impairs hair follicle stem cells, confirming long-standing observations that stress might lead to hair loss.
In a mouse study published in the journal Nature, the researchers found that a major stress hormone causes hair follicle stem cells to stay in an extended resting phase, without regenerating the hair follicle and hair. The researchers identified the specific cell type and molecule responsible for relaying the stress signal to the stem cells, and showed that this pathway can be potentially targeted to restore hair growth.
“My lab is interested in understanding how stress affects stem cell biology and tissue biology, spurred in part by the fact that everyone has a story to share about what happens to their skin and hair when they are stressed. I realized that as a skin stem cell biologist, I could not provide a satisfying answer regarding if stress indeed has an impact — and more importantly, if yes, what are the mechanisms,” said Ya-Chieh Hsu, Ph.D., the Alvin and Esta Star Associate Professor of Stem Cell and Regenerative Biology at Harvard and senior author of the study. “The skin offers a tractable and accessible system to study this important problem in depth, and in this work, we found that stress does actually delay stem cell activation and fundamentally changes how frequently hair follicle stem cells regenerate tissues.”
The hair follicle is one of the few mammalian tissues that can undergo rounds of regeneration throughout life, and has become a paradigm that informs much of our fundamental understanding of mammalian stem cell biology. The hair follicle naturally cycles between growth and rest, a process fueled by hair follicle stem cells. During the growth phase, hair follicle stem cells become activated to regenerate the hair follicle and hair, and hairs grow longer each day. During the resting phase, the stem cells are quiescent and hairs can shed more easily. Hair loss can occur if the hairs shed and the stem cells remain quiescent without regenerating new tissue.
The researchers studied a mouse model of chronic stress and found that hair follicle stem cells stayed in a resting phase for a very long time without regenerating tissues. A major stress hormone produced by the adrenal glands, corticosterone, was upregulated by chronic stress; providing corticosterone to mice was able to reproduce the stress effect on the stem cells. The equivalent hormone in humans is cortisol, which is also upregulated under stress and is often referred to as the “stress hormone.”
“This result suggests that elevated stress hormones indeed have a negative effect on hair follicle stem cells,” Hsu said. “But the real surprise came when we took out the source of the stress hormones.”
Under normal conditions, hair follicle regeneration slows over time — the resting phase becomes longer as the animals age. But when the researchers removed the stress hormones, the stem cells’ resting phase became extremely short and the mice constantly entered the growth phase to regenerate hair follicles throughout their life, even when they were old.

SharecloseShare pageCopy linkAbout sharingimage copyrightGetty ImagesPfizer says trials of its Covid vaccine in children aged 12 to 15 show 100% efficacy and a strong immune response.Initial results from trials in 2,260 adolescents in the US also suggest the vaccine is safe with no unusual side-effects.The drug company says it will submit its data to the US and European authorities for emergency use in 12- to 15-year-olds.There are currently no plans for children to be vaccinated in the UK.Children’s risk of becoming very ill or even dying with Covid-19 is tiny, and throughout the pandemic they have very rarely needed hospital treatment.Adults – particularly those over 50 and people with serious underlying health conditions – have a much higher risk, which is why they have been vaccinated as a priority in the UK. How will we know Covid vaccines are safe?What is the risk of schools spreading coronavirus?Slight Covid uptick in secondary school children’No evidence’ schools spread lots of Covid Pfizer is one of a number of drug companies testing their Covid vaccines on children. The aim of vaccinating them – particularly older children – would be to keep schools open, reduce the spread of coronavirus in the community and protect vulnerable children with conditions which put them at increased risk.AstraZeneca announced trials of its vaccine in UK children aged six to 17 some time ago, and the first of 300 volunteers were due to be jabbed last month. The vaccine is currently only authorised for people aged 18 and over in the UK.Alongside trials in teenagers, the Pfizer-BioNTech vaccine, which is authorised for use in those aged over 16, is also being tested in children under 12, with the aim of involving babies from just six months old. The company started dosing the first healthy, young children in this trial last week.UnknownsIn the Pfizer trial in 12- to 15-year-olds, 18 cases of Covid-19 were seen in the group given a dummy vaccine and none in group given the Covid vaccine which protects against it.All participants received two doses 21 days apart, and the 18 cases were all children with symptoms. There were no tests for asymptomatic infection – children displaying no symptoms.The figures are preliminary and full data has not been released, peer-reviewed or published in a journal.Dr Peter English, former consultant in communicable disease control and past chair of the BMA public health medicine committee, said more detail was needed to properly evaluate the company’s claims.”It would be useful to know how effective the vaccine is at preventing asymptomatic infection. Young people are less likely to have severe disease; and when they are infected, they are more likely to have asymptomatic infection, allowing them to transmit the disease to others,” he said.The company’s press release also doesn’t mention the impact of variants on the trials, how cases were identified in children and whether a longer gap between doses was tested.image copyrightGetty Images’Next school year’Albert Bourla, chairman and chief executive officer of Pfizer, said the company was “encouraged” by the clinical trial data.”We plan to submit these data to FDA [US Federal Drugs Administration] as a proposed amendment to our Emergency Use Authorization in the coming weeks, and to other regulators around the world, with the hope of starting to vaccinate this age group before the start of the next school year.”Ugur Sahin, CEO and co-founder of BioNTech, said the initial results in adolescents suggested children “are particularly well protected by vaccination”.He added: “It is very important to enable them to get back to everyday school life and to meet friends and family while protecting them and their loved ones.” Moderna, the US company behind another Covid vaccine ordered by the UK, has also started testing its jab on children under 11.Related Internet LinksOxford’s Covid-19 Vaccine TrialsPfizer-BioNTech Announce Positive Topline Results of Pivotal COVID-19 Vaccine Study in Adolescents – pfpfizeruscomThe BBC is not responsible for the content of external sites.

Infected rodents pose no immediate danger to humans, but the research suggests that mutations are helping the coronavirus expand its range of potential hosts.Bats, humans, monkeys, minks, big cats and big apes — the coronavirus can make a home in many different animals. But now the list of potential hosts has expanded to include mice, according to an unnerving new study.Infected rodents pose no immediate risk to people, even in cities like London and New York, where they are ubiquitous and unwelcome occupants of subway stations, basements and backyards.Still, the finding is worrying. Along with previous work, it suggests that new mutations are giving the virus the ability to replicate in a wider array of animal species, experts said.“The virus is changing, and unfortunately it’s changing pretty fast,” said Timothy Sheahan, a virologist at the University of North Carolina at Chapel Hill, who was not involved in the new study.In the study, the researchers introduced the virus into the nasal passages of laboratory mice. The form of the virus first identified in Wuhan, China, cannot infect laboratory mice, nor can B.1.1.7, a variant that has been spreading across much of Europe, the researchers found.But B.1.351 and P1, the variants discovered in South Africa and Brazil, can replicate in rodents, said Dr. Xavier Montagutelli, a veterinarian and mouse geneticist at the Pasteur Institute in Paris, who led the study. The research, posted online earlier this month, has not yet been reviewed for publication in a scientific journal.The results indicate only that infection in mice is possible, Dr. Montagutelli said. Mice caught in the wild have not been found to be infected with the coronavirus, and so far, the virus does not seem to be able to jump from humans to mice, from mice to humans, or from mice to mice.“What our results emphasize is that it is necessary to regularly assess the range of species that the virus can infect, especially with the emergence of new variants,” Dr. Montagutelli said.The coronavirus is thought to have emerged from bats, with perhaps another animal acting as an intermediate host, and scientists worry that the virus may return to what they describe as an animal “reservoir.”Apart from potentially devastating those animal populations, a coronavirus spreading in another species may then acquire dangerous mutations, returning to humans in a form the current vaccines weren’t designed to fend off.A mink looks out from its cage at a farm in Denmark, where mink populations were hit hard by the coronavirus.Mads Claus Rasmussen/Agence France-Presse — Getty ImagesMinks are the only animals known to be able to catch the coronavirus from humans and pass it back. In early November, Denmark culled 17 million farmed mink to prevent the virus from evolving into dangerous new variants in the animals.More recently, researchers found that B.1.1.7 infections in domesticated cats and dogs can cause the pets to develop heart problems similar to those seen in people with Covid-19.To establish a successful infection, the coronavirus must bind to a protein on the surface of animal cells, gain entry into the cells, and exploit their machinery to make copies of itself. The virus must also evade the immune system’s early attempts at thwarting the infection.Given all those requirements, it is “quite extraordinary” that the coronavirus can infect so many species, said Vincent Munster, a virologist at the National Institute of Allergy and Infectious Diseases. “Typically, viruses have a more curtailed host range.”Mice are a known reservoir for hantavirus, which causes a rare and deadly disease in people. Even though the coronavirus variants don’t seem to be able to jump from mice to people, there is potential for them to spread among rodents, evolve into new variants, and then infect people again, Dr. Munster said.The variants may also threaten endangered species like black-footed ferrets. “This virus seems to be able to surprise us more than anything else, or any other previous virus,” Dr. Munster said. “We have to err on the side of caution.”Dr. Sheahan said he was more concerned about transmission to people from farm animals and pets than from mice.“You’re not catching wild mice in your house and snuggling — getting all up in their face and sharing the same airspace, like maybe with your cat or your dog,” he said. “I’d be more worried about wild or domestic animals with which we have a more intimate relationship.”But he and other experts said the results emphasized the need to closely monitor the rapid changes in the virus.“It’s like a moving target — it’s crazy,” he added. “There’s nothing we can do about it, other than try and get people vaccinated really fast.”