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New research from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, in collaboration with the Karolinska Institute and Orebro University, has found that ‘young relative age’ — being young in a school class — puts a child at a long-term disadvantage compared to their older peers. Researchers are now calling for greater flexibility about school starting age.
The study, published today in the Journal of the American Academy of Child and Adolescent Psychiatry (JAACAP), looked at data from 300,000 individuals from the Swedish National Registers. The researchers found those youngest in a class were more likely to experience low educational achievement, substance misuse disorder, and depression in later life. However, younger children with ADHD appeared less at risk of depression.
Previous studies have pointed to evidence that immaturity relative to peers can contribute to an increased likelihood of being diagnosed with ADHD. Typically, a comparison is made as to whether a child shows ADHD symptoms to a significantly greater degree than to others in their year group, but this doesn’t always take in to account the potentially significant age gap between the youngest and oldest members of an age group.
Senior author Professor Jonna Kuntsi from King’s IoPPN said “The difference between the youngest and oldest member of a class can be up to 11 months. In the early stages of childhood, this is a significant difference in terms of maturity, behaviour and cognitive abilities.
“Behavioural characteristics that are normal in younger children are in some cases being compared to much older individuals, and we can see from the data that there are very real and long-term consequences to being the youngest in a class year.”
The investigators note that the negative effects of young relative age is much less common in countries like Denmark, possibly due to the more flexible approach to school starting age there. Young children that might not be ready to start school have the opportunity to start school later, and as such are at less risk of experiencing negative side effects seen in other countries. It is a practice that the researchers say could be emulated elsewhere.
Professor Kuntsi has previously called for greater focus to be placed on the relative age of students in relation to difficulties with reading, spelling or arithmetic skills which aren’t as a result of low cognitive ability. A recent large register study in Finland found that the relative age effect emerges also for specific learning disorders which Professor Kuntsi says is likely due to the same referral bias as those referred for ADHD assessment.
She cites a need for a cross-country review into approaches that best ensure children’s future outcomes are fully independent of their relative age at the start of school: “Being the youngest child in a classroom can have complex developmental consequences, and can place them at a disadvantage at the earliest stages of their academic life. If we are to overcome this, there needs to be a greater understanding from decision makers, teachers, and clinicians so that all children have an equal chance to succeed later in life.”
King’s IoPPN, in partnership with the South London and Maudsley NHS Foundation Trust and the Maudsley Charity, are in the process of opening a world leading centre for children and young people mental health. The Pears Maudsley Centre for Children and Young People is expected to open in 2023 and will bring together researchers and clinicians to help find solutions that will transform the landscape for children’s mental health.
This study was possible thanks to funding from funding from the European Commission’s Horizon 2020 research and innovation programme under grant agreement No 667302, and the from the Swedish Council for Health, Working Life and Welfare.
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The discovery that the anaesthetic ketamine can help people with severe depression has raised hopes of finding new treatment options for the disease. Researchers at Karolinska Institutet in Sweden have now identified novel mechanistic insights how the drug exerts its antidepressant effect. The findings have been published in the journal Molecular Psychiatry.
According to the World Health Organization, depression is a leading cause of disability worldwide and the disease affects more than 360 million people every year.
The risk of suffering is affected by both genetics and environmental factors. The most commonly prescribed antidepressants, such as SSRIs, affect nerve signalling via monoamines in the brain. However, it can take a long time for these drugs to help, and over 30 percent of sufferers experience no relief at all.
The need for new types of antidepressants with faster action and wider effect is therefore considerable. An important breakthrough is the anaesthetic ketamine, which has been registered for some years in the form of a nasal spray for the treatment of intractable depression.
Unlike classic antidepressants, ketamine affects the nerve signalling that occurs via the glutamate system, but it is unclear exactly how the antidepressant effect is mediated. When the medicine has an effect, it relieves depressive symptoms and suicidal thoughts very quickly.
However, ketamine can cause unwanted side effects such as hallucinations and delusions and there may be a risk of abuse so alternative medicines are needed. The researchers want to better understand how ketamine works in order to find substances that can have the same rapid effect but without the side effects.

Eradicating COVID-19 across the globe is theoretically more feasible than for polio but much less so than it was for smallpox, according to an analysis by New Zealand researchers.
The researchers, writing in the international journal BMJ Global Health, ranked the feasibility of eradicating the three diseases based on technical, socio-political and economic factors.
Smallpox, which was declared eradicated in 1980, had the highest average score for eradication feasibility. It had an average score of 2.7 on a three-point scale across 17 variables. In comparison COVID-19 had an average score of 1.6 and polio an average of 1.5.
Professor Nick Wilson from the University of Otago, Wellington, says their analysis puts eradicating COVID-19 into the realms of possibility in terms of technical feasibility.
He says the combination of vaccination programmes, public health measures and the global interest in combating the disease all contribute to making eradication possible.
“Elimination of COVID-19 at the country level has been achieved and sustained for long periods in various parts of the Asia Pacific region, which suggests that global eradication is possible.”
Vaccination programmes have been responsible for the global eradication of smallpox and two of the three serotypes of poliovirus. Some other diseases are close to being eradicated without the use of vaccines, with China recently becoming the 40th country to be certified malaria-free.

Researchers from King’s College London have created a novel interactive VR system to be used by patients when undertaking an MRI.
In a new paper published in Scientific Reports, the researchers say they hope this advancement will make it easier for those who find having a MRI scan challenging such as children, people with cognitive difficulties or those who suffer from claustrophobia or anxiety.
In normal circumstances, MRI scans fail in up to 50 percent of children under 5 years of age, which means that hospitals often rely on sedative medication or even anesthesia to get children successfully scanned.
These measures are time consuming and expensive and have their own associated risks. From a neuroscience point of view, it also means that MRI based studies of brain function are generally only ever studied in these vulnerable populations during an artificial induced sleep state so may not be representative of how the brain works in normal circumstances.
Lead researcher Dr Kun Qian from the School of Biomedical Engineering & Imaging Sciences at King’s College London said having an MRI scan can be quite an alien experience as it involves going into a narrow tunnel, with loud and often strange noises in the background, all while having to stay as still as possible.
“We were keen to find other ways of enabling children and vulnerable people to have an MRI scan,” Dr Qian said.

Mount Sinai researchers have found an important clue to a rare but serious aftereffect of COVID-19 in children, known as multisystem inflammatory syndrome in children or MIS-C.
The researchers reported that RNA sequencing of blood samples from the Mount Sinai COVID-19 Biobank led to the discovery that specific infection-fighting cells of the immune system are downregulated in children with MIS-C, and that this is associated with a sustained inflammatory response, a hallmark of infection with SARS-CoV-2, the virus that causes COVID-19. The study was published in Nature Communications on August 11.
MIS-C is characterized by fever, pain, and inflammation of multiple organs including the heart, lungs, kidneys, skin, eyes, or gastrointestinal tract. More than 2,600 cases of MIS-C have been reported in the United States since the COVID-19 pandemic began. While an autoimmune condition has been suggested as an underlying cause, specific genes, pathways, and cell types remain unknown. Through Mount Sinai’s extensive gene-expression study, the researchers have taken a significant step in providing the field with new exploratory pathways involving complex networks and subnetworks of genes they constructed from pediatric cases of MIS-C and COVID-19 from the Mount Sinai COVID-19 Biobank.
One of the more significant of these gene networks implicated the suppression of two types of immune cells: natural killer (NK) cells and CD8+ T cells. Previous research has shown that when CD8+ T cells are persistently exposed to pathogens, they enter a state of “exhaustion,” resulting in a loss of their effectiveness and ability to proliferate. The researchers in the new study specifically pointed to the CD8+ T cells being in this exhausted state, thus potentially weakening the inflammatory immune response. An increase in NK cells is also associated with exhausted CD8+ T cells.
“Our study implicated T cell exhaustion in MIS-C patients as one of the potential drivers of this disease, suggesting that an increase in both NK cells and circulating exhausted CD8+ T cells may improve inflammatory disease symptoms,” says lead co-author Noam Beckmann, PhD, Assistant Professor of Genetics and Genomic Sciences, and member of the Mount Sinai Clinical Intelligence Center (MSCIC), at the Icahn School of Medicine at Mount Sinai. “Additionally, we found nine key regulators of this network known to have associations with NK cell and exhausted CD8+ T cell functionality.”
Dr. Beckmann adds that one of those regulators, TBX21, is a promising therapeutic target because it serves as a master coordinator of the transition of CD8+ T cells from effective to exhausted.
Mount Sinai’s work on MIS-C represents the first gene-expression study from the hospital’s COVID-19 Biobank. Created through the work of a volunteer team of more than 100 nurses, doctors, and researchers, the repository serves as the backbone of Mount Sinai’s rapidly expanding COVID-19 research. The team has collected blood samples from several hundred COVID-19 patients (including “longitudinal” or multiple samples from the same person) admitted to Mount Sinai hospitals which, in turn, have generated a diverse set of molecular data yielding invaluable insights into better understanding and new therapeutic approaches to the disease.

For the first time, researchers have developed a successful approach for identifying proteins inside different types of neurons in the brain of a living animal.
Led by Northwestern University and the University of Pittsburgh, the new study offers a giant step toward understanding the brain’s millions of distinct proteins. As the building blocks of all cells including neurons, proteins hold the keys to better understanding complex brain diseases such as Parkinson’s and Alzheimer’s, which can lead to the development of new treatments.
The study will be published on Aug. 11 in the journal Nature Communications.
In the new study, researchers designed a virus to send an enzyme to a precise location in the brain of a living mouse. Derived from soybeans, the enzyme genetically tags its neighboring proteins in a predetermined location. After validating the technique by imaging the brain with fluorescence and electron microscopy, the researchers found their technique took a snapshot of the entire set of proteins (or proteome) inside living neurons, which can then be analyzed postmortem with mass spectroscopy.
“Similar work has been done before in cellular cultures. But cells in a dish do not work the same way they do in a brain, and they don’t have the same proteins in the same places doing the same things,” said Northwestern’s Yevgenia Kozorovitskiy, senior author of the study. “It’s a lot more challenging to do this work in the complex tissue of a mouse brain. Now we can take that proteomics prowess and put it into more realistic neural circuits with excellent genetic traction.”
By chemically tagging proteins and their neighbors, researchers can now see how proteins work within a specific, controlled area and how they work with one another in a proteome. Along with the virus carrying the soybean enzyme, the researchers also used their virus to carry a separate green fluorescent protein.

Her eye chart tests showed improvement. It took a radical experiment to find out why her reality wasn’t matching up.The burning started as soon as the 59-year-old woman put the drops into her eye. She blinked to try to rinse away the medication with her tears. She leaned forward to the mirror. Her left eye was red and angry-looking. She’d been using these eye drops for nearly a year to treat her newly diagnosed glaucoma, adding artificial tears for the dry eyes that appeared a few months later. And while she’d had plenty of problems with her eyes since all this started, this fiery pain was new. The vision in her left eye had been bad for a few years by then, but with an operation nearly two years earlier to remove an abnormal membrane on her retina and more recent cataract surgery, she had hoped she would have her old vision back by now. She was a physician-researcher and spent much of her time reading and writing, so her vision was very important to her livelihood. But despite the efforts of her eye doctors — and at this point she had many — she still couldn’t see well. It was when she was getting ready for the cataract surgery that the patient learned she had glaucoma. After her initial exam, her new eye surgeon told her that the pressure inside her left eye was abnormally high, and she was already showing signs of damage from it. He wanted her to see one of his colleagues, Dr. Amanda Bicket, a glaucoma specialist who was then at the Wilmer Eye Institute at Johns Hopkins. A quick phone call later, she had an appointment to see the doctor that day. It was urgent that this be evaluated and treated before her upcoming surgery. Drops, Drops and More DropsWhat we call glaucoma is really a group of diseases in which the optic nerve — the tissue that transmits what the eye sees to the brain — is damaged, usually by increased pressure within the eye. It is the second most common cause of blindness in the world, and surgery can be a trigger in those who are prone to the disease. The good news is that there are effective, sight-sparing treatments. The first are medications that reduce the intraocular pressure (IOP) by either slowing the production of the fluid in the eye or increasing the drainage of that fluid out of the eye. In cases like this patient’s where there is already damage to the nerve, a tiny tube must be inserted into the front of the eye to allow the excess fluid to drain and bring the pressure even lower. Bicket started the patient on the pressure-lowering drops that day, and three days later, she had her cataract extracted and the pressure-reducing tube inserted. The day after these surgeries, she came back to Bicket’s office to have the bandage removed and her vision checked. It was bad: She could just barely make out the E at the top of the eye chart. That put her vision at 20/200, which means that at 20 feet she could see only what normally sighted people saw when they were standing 200 feet away from the chart. For context, if both of her eyes were persistently 20/200, she would be considered legally blind.Photo illustration by Ina JangBicket reassured the worried patient. It’s going to get better, she told her. And it did, slowly. Over the following weeks, her visual acuity was measured at 20/150, then 20/100, 20/80 and finally 20/50. Bicket was pleased. Everything was going as she expected. The patient wasn’t so sure. It was good to hear that her vision was improving on the tests, but she still felt that she couldn’t see worth a darn. Moreover, her eyes were dry, and her eyelids sometimes scratched as if they were dusted with a layer of sand. So in addition to the drops to lower her pressure and the ocular antibiotic and steroids she sometimes had to use, she started using artificial tears for the dryness. With all these medications, she could end up putting drops in her eyes a dozen times a day. Worst of all, she was now intensely sensitive to light. Her computer screen was like an interrogation beam. She turned off all the lights in her office and wore a broad-brimmed hat and post-surgical wraparound sunglasses to shield her eyes from the relentless light, both indoors and out. She had to stop driving; the sunlight on even the cloudiest day forced her to close her eyes. Everyday tasks — at work and at home — became difficult, sometimes impossible. A Risky ExperimentAfter months of this, the woman could feel her life getting smaller and smaller. She wondered if she was going to have to apply for disability. Finally she mentioned this to Bicket. The doctor was shocked. Her vision was so much better, Bicket countered. “Well, my vision may be better, but I still can’t see,” the patient replied. Bicket referred her to a low-vision clinic. The optometrist there recommended glasses with special glare-reducing lenses. They didn’t do much. Then came the day she put in the first of her two glaucoma drops, and her eyes began to burn. She immediately sent an email to Bicket, telling the doctor that she was going to stop that medication and just use the others. Maybe it was this medicine that was causing the photophobia, the eye dryness and now the burning. “I’m fine with any short-term IOP-drop experiment you’d like to run,” Bicket wrote back. But the symptoms the patient was having didn’t match the usual side-effect profile of any of the medications she was using. There was another possibility, Bicket added: Maybe it’s not any single drop, but all of them. They all contain a preservative called benzalkonium chloride (BAK). “If that is what you don’t tolerate,” Bicket wrote, “stopping one agent vs. another won’t help.” The patient decided to stop them all, she wrote to Bicket. It was a risky action, because the drops were important for keeping her pressure down and avoiding further damage. But the pain and light sensitivity were unbearable. The Lag Between Test and RealityThree days later, the patient had her answer. Her eyes felt so much better without the drops. The gritty feeling when she blinked was gone. So was the photophobia. It had to be the BAK. The patient turned to PubMed to read up on it. There was a lot there. Preservatives were essential to prevent the growth of bacteria in bottles of medications that contained more than a single dose, and BAK was the most commonly used preservative in both over-the-counter and prescription eye drops. The patient’s discomfort, she discovered, was not due to an allergy to the preservative but rather was a response to the way BAK works. This compound kills germs by dissolving the layer of lipids that make up their outer protective coat. Here’s the problem: Eyes are kept from drying out by a similar protective coat — of tears. Tears are composed of a thin sheet of liquid from the lacrimal (tear) gland, which is in turn covered by a layer of oil made by the meibomian glands. BAK breaks down this outer protective lipid layer, exposing the salty fluid to the air. In many of those who have dry eyes, the unprotected fluid evaporates, and the patient’s eyes become even dryer. Eye-drop users who make enough tears won’t be affected, but many do not. Aging will also reduce this protective layer, putting older users of medications containing BAK at higher risk of drying eyes. The dryness can eventually lead to permanent damage to the cornea, the clear outermost layer of the eye. The patient immediately switched to single-dose bottles of the drops; these don’t need any preservatives at all. With that change, her eyes began to heal. It has been five years, and she still can’t see well out of the left eye, and she now has glaucoma in the right one as well. But she has figured out how to work with the vision she has, and her glaucoma is well controlled. Bicket, who is now at the University of Michigan, has been fascinated by the difference between the visual acuity measured in the office and patients’ own sense of how well they can see. Research she and colleagues published recently shows that this can lag behind the tested acuity by weeks or sometimes months. The first question anyone facing eye surgery will ask, Bicket told me, is how long will it take for them to recover enough to go back to work, or to read or drive. “The simple answer,” she says, “is we just don’t know.” But Bicket is working hard to find out.Lisa Sanders, M.D., is a contributing writer for the magazine. Her latest book is ‘‘Diagnosis: Solving the Most Baffling Medical Mysteries.’’ If you have a solved case to share with Dr. Sanders, write her at Lisa .Sandersmd@gmail.com.

SharecloseShare pageCopy linkAbout sharingimage sourceGetty ImagesFalse and misleading claims that Covid-19 vaccines harm fertility and cause miscarriages are still circulating online, against all the evidence.Doctors are extremely cautious about what they recommend during pregnancy, so the original advice was to avoid the jab. But now, so much safety data has become available that this advice has changed and the vaccine is now actively encouraged (as getting Covid itself can put a pregnancy at risk). We have looked at some of the more persistent claims – and why they are wrong.A study shows the vaccine accumulating in the ovaries – FalseThis theory comes from a misreading of a study submitted to the Japanese regulator.The study involved giving rats a much higher dose of vaccine than that given to humans (1,333 times higher). Only 0.1% of the total dose ended up in the animals’ ovaries, 48 hours after injection. Far more – 53% after one hour and 25% after 48 hours – was found at the injection site (in humans, usually the arm). The next most common place was the liver (16% after 48 hours), which helps get rid of waste products from the blood. The vaccine is delivered using a bubble of fat containing the virus’s genetic material, which kick-starts the body’s immune system.And those promoting this claim cherry-picked a figure which actually referred to the concentration of fat found in the ovaries.Fat levels in the ovaries did increase in the 48 hours after the jab, as the vaccine contents moved from the injection site around the body. But, crucially, there was no evidence it still contained the virus’s genetic material.Posts also claimed the study had been “leaked”, though it was in fact publicly available online. Monitoring data shows vaccines cause miscarriages – FalseSome posts have highlighted miscarriages reported to vaccine-monitoring schemes, including the Medicines and Healthcare products Regulatory Agency (MHRA) Yellow Card scheme in the UK and the Vaccine Adverse Event Reporting System (VAERS) in the US. Anyone can report symptoms or health conditions they experience after being vaccinated. Not everyone will choose to report, so this is a self-selecting database.There were indeed miscarriages reported in these databases – they are unfortunately common events – but this does not mean the jab caused them. A study has found data showing the miscarriage rate among vaccinated people was in line with the rate expected in the general population – 12.5%.Dr Victoria Male, a reproductive immunologist at Imperial College London, says these reporting systems are very good for spotting side-effects from the vaccine that are normally rare in the general population – that’s how a specific type of blood clot was linked in some rare cases to the AstraZeneca vaccine. If you suddenly start seeing unusual symptoms in vaccinated people, it raises a red flag. The unfounded claims about vaccines and fertilityTrue stories, fake claims about periods and the vaccine They are not so good at monitoring side-effects that are common in the population – such as changes to periods, miscarriages and heart problems. Seeing them in the data doesn’t necessarily raise these red flags because you’d expect to see them anyway, vaccine or not. It’s only if we start getting many more miscarriages than are seen in unvaccinated people that this data would prompt an investigation – and that’s not been the case.Some people have also shared graphs showing a big rise in the overall number of people reporting their experiences to these schemes compared with previous years, for other vaccines and drugs. This has been used to imply the Covid vaccine is less safe. But the rise doesn’t tell us that, what it shows is that an unprecedented proportion of the population is being vaccinated. Vaccines could attack the placenta – No evidenceA widely shared petition from Michael Yeadon, a scientific researcher who has made other misleading statements about Covid, claimed the coronavirus’s spike protein contained within the Pfizer and Moderna vaccines was similar to a protein called syncytin-1, involved in forming the placenta. He speculated that this might cause antibodies against the virus to attack a developing pregnancy, too.Some experts believe this was the origin of the whole belief that Covid vaccines might harm fertility. In fact syncytin-1 and the coronavirus’s spike protein are just about as similar as any two random proteins – if the body was that easily confused, it would risk attacking its own organs every time it caught an infection and developed antibodies.But now evidence has been gathered to help disprove his theory. US fertility doctor Randy Morris, who wanted to respond directly to the concerns he’d heard, began monitoring his patients who were undergoing IVF treatment to see whether vaccination made any difference to their chances of a successful pregnancy.Out of 143 people in Dr Morris’s study, vaccinated, unvaccinated and previously infected women were about equally likely to have a successful embryo implantation and for the pregnancy to continue to term. The study is small, but it adds to a large volume of other evidence – and were the claim true, you would expect that to show up even in a study of this size.Dr Morris pointed out that people spreading these fears had not explained why they believed antibodies produced in response to the vaccine could harm fertility but the same antibodies from a natural infection would not.The problem is, while scientists are rushing to provide evidence to reassure people, by the time they can report their findings people online have moved on to the next thing. As Dr Morris explained: “The hallmark of a conspiracy theory is as soon as it’s disproven, you move the goalpost.”Follow Rachel on Twitter

A potential new treatment for mast cell cancers reduces the number of mast cells by “mutating” the messenger RNA (mRNA) before it can deliver instructions for manufacturing the gene responsible for cell proliferation. The method, known as frameshifting, changes the pre-mRNA so that the mature mRNA is degraded and any protein produced from its instructions is altered and inert. In a mouse model, frameshifting directed at the c-KIT gene reduced mast cell tumor size and prevented infiltration into other organs.
Mast cells regulate immune responses. But too many mast cells can result in a number of diseases, the most serious of which are mast cell leukemia and mast cell sarcoma. A gene known as c-KIT produces a protein, KIT, which is associated with mast cell survival and proliferation. C-KIT mutations can increase proliferation of mast cells in multiple organs, leading to mast cell cancers.
“Current treatments for mast cell cancers target signaling from the receptor encoded by the c-KIT gene, and the efficacy of current therapies can be negatively affected by c-KIT mutations associated with disease development,” says Glenn Cruse, assistant professor of immunology at North Carolina State University and corresponding author of the research. “We are targeting the gene itself, regardless of mutation. If we target the gene that drives progression, then we can target the disease.”
Cruse and a team of researchers from NC State and the National Institutes of Health (NIH) used a technique known as exon skipping to produce the frameshift mutation.
Before a gene or protein is produced, the pre-mRNA, which is composed of both coding and non-coding regions called exons and introns, is spliced so that introns are removed and only the exons — a gene’s “production instructions” — remain. The resulting mature mRNA then delivers its instructions and the gene or protein is produced. If something goes wrong or a mutation occurs, a stop codon — a short sequence in the mRNA — stops production of the faulty protein by causing that strand of the mRNA to be degraded or destroyed.
The researchers used this mechanism to their advantage by binding a short RNA molecule called an oligonucleotide to exon 4 within the c-KIT pre-mRNA, effectively fooling the splicing proteins into thinking the exon was an intron, and removing it. The missing, or skipped, exon creates a frameshift in the reading frame of the mRNA, causing it to be recognized as a mutant and degraded.
“We are altering the message that makes the protein — flipping an ‘on’ switch to ‘off,'” Cruse says. “If you get mRNA to produce a protein that is mutated and severely truncated, your cell will recognize that and degrade the message so that the protein isn’t produced.”
The researchers used their frameshifted c-KIT mRNA approach on mast cell leukemia cells in vitro and found that KIT protein expression, signaling and function were reduced. The cancer cells stopped proliferating and began dying within hours. In a mouse model, tumor growth and infiltration of other organs were reduced and tumor cell death increased when the frameshifted c-KIT mRNA was induced.
“The other advantage to our technique is that it solves the problem of degradation evasion,” Cruse says. “Occasionally faulty messages will evade degradation and their mutated proteins get produced anyway. But proteins produced by the frameshifted c-KIT mRNA are inert, or non-functional. So even if they get produced, they cannot cause more harm.”
The research appears in Molecular Therapy and is supported by the National Institutes of Health. NC State postdoctoral researcher Douglas Snider is first author. The technology described in the paper has been licensed by Hoth Therapeutics.
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Materials provided by North Carolina State University. Original written by Tracey Peake. Note: Content may be edited for style and length.

Researchers at Vanderbilt University Medical Center have found that people recovering from COVID-19 and those vaccinated against the causative virus, SARS-CoV-2, produce identical clones, or groups, of antibody-producing white blood cells.
Their discovery, reported this week in the journal Cell Reports, sheds light on the selection pressures driving the emergence of SARS-CoV-2 variants that have the potential to escape from naturally occurring antibodies and those induced by vaccination.
Current vaccines, including those that use genetic material, mRNA, encoding a viral protein to elicit an immune response, are largely protective against the delta variant now sweeping through unvaccinated populations around the world. Yet scientists worry other variants may emerge that are more virulent and transmissible — even among those already vaccinated.
The findings reported this week could help scientists design more effective vaccines and antibody therapies against a broader range of variants, the researchers concluded.
“We were surprised to discover that there are so many shared antibodies between individuals after SARS-CoV-2 infection, but that is a good sign,” saidthe paper’s corresponding author, James Crowe, Jr., MD, director of the Vanderbilt Vaccine Center.
“It was encouraging to find that an mRNA vaccine also induces those clones, which in part explains why these antibodies work so well in so many people,” said Crowe, who holds the Ann Scott Carell Chair and is Professor of Pediatrics and Pathology, Microbiology & Immunology at VUMC.