Health sector cautiously welcomes NHS AI rollout
New Lung Model Reveals RSV Immune Response, Points to Better Treatments
Researchers at University College London (UCL) Great Ormond Street Hospital for Children (GOSH) have built a new lab model of infant lungs to show why respiratory syncytial virus (RSV) makes infants so much sicker than adults, and to allow them to test new treatments. The miniature model of a baby’s airways was created using pediatric airway cells, blood vessel cells, and neutrophils (a type of white blood cell that acts as the immune system’s primary response to infection).
Studies using the new model suggest that future therapies for RSV should target both the virus and its immune response to ensure babies get the best possible outcomes. Research lead Claire Smith, PhD, at UCL Great Ormond Street Institute of Child Health, said, “This model allows us to watch early immune responses unfold and study them in a human setting that reflects the infant airway. That’s something animal models often struggle to capture, especially when it comes to age-specific effects.”
Senior and corresponding author Smith and colleagues reported on their findings in Nature Communications in a paper titled “Neutrophil myeloperoxidase as a functional biomarker for RSV severity: implications for in vitro therapeutic screening.” In their report they concluded, “These findings identify neutrophil–epithelial interactions as a useful target for intervention and support the use of physiologically relevant human models to accelerate the development of therapies that limit immunopathology while preserving antiviral defense.”
RSV is the biggest cause of severe respiratory tract infections in infants and young children, resulting in over three million hospital admissions worldwide every year. RSV infection causes wheezing and breathing difficulties, and in the worst cases infants end up in intensive care. Despite this, treatment options for severe RSV disease remain extremely limited. “The lack of accessible, effective therapies highlights the need for continued advancements in RSV treatment and prevention,” the authors wrote.
During RSV infection neutrophils are rapidly mobilized to the lungs and play a key role in virus-targeting host defenses, the investigators continued. However, excessive neutrophil infiltration and activation can also contribute to airway inflammation, epithelial damage, and disease severity. “Understanding neutrophil behavior and activation during RSV infection, including during their migration across the airway epithelial barrier, is crucial for developing therapeutic strategies to mitigate pathological inflammation without compromising the antiviral response,” they suggested.
For their reported study the team aimed to create an in vitro model that recapitulates key clinical outcomes of infants with RSV bronchiolitis. To do this they established an air-liquid interface (ALI) system that incorporated pediatric airway epithelial cells, endothelial cells, and neutrophils from adults, to mirror the blood-airway barrier. “Differentiated airway epithelial cells (AECs) cultured at the air–liquid interface (ALI) provide a physiologically relevant platform to study neutrophil migration and the effect of antiviral treatments on this process,” they note. To compare with an adult response to RSV, the research team also made a model of an adult’s airways.
When the models were infected with RSV, the team found that the pediatric airway cells attracted far more white blood cells than did the adult airway cells. This influx can block an infant’s small airways and make it harder for them to breathe.
Neutrophils normally circulate in the blood but enter lung tissue in response to infection. In the baby airway model, researchers found that the neutrophils that entered the lung tissue were more activated and triggered a stronger inflammatory reaction than in the adult model. This effect was dependent on the immune cells physically moving through the infected tissue, not just responding to chemical signals released by it, making this type of model essential for study.
The results suggest that it is the infant airway itself, not just the virus, that ramps up the immune response and causes damage to the lungs. First author Machaela Palor, PhD, at UCL Great Ormond Street Institute of Child Health, said: “These findings help explain why RSV is often much more severe in infants than in adults. The pediatric airway actively shapes how immune cells behave during the infection.”
The researchers tested two antiviral drugs (remdesivir and RSV604). they found that both stopped the virus from multiplying, but only RSV604 also calmed the overactive immune response, reducing levels of a key inflammatory protein myeloperoxidase (MPO) released by white blood cells—high levels of which are linked to more severe RSV disease in babies. Remdesivir had no effect on this, suggesting that not all antivirals are equal when it comes to protecting the infant airway from immune-driven damage. “While both drugs reduced viral load, only RSV604 attenuated MPO expression,” the team stated.
The findings suggest that treating severe RSV in babies may require more than just stopping the virus—it may also be important to calm an overactive immune response. “This model suggests that MPO could be useful as a readout of therapeutic efficacy,” the team stated. “Targeting neutrophil-driven inflammatory pathways may be critical for reducing pathology in infant RSV infection.”
The researchers hope their findings and the new approach to research on RSV will accelerate the development of treatments better tailored to infants. “Our model gives us a way to assess both sides of the problem at once,” Smith said. “We can not only ask whether the drug stops the virus but also whether it helps control immune response in the infant airway. “This work reinforces the idea that age matters in respiratory infection. Understanding how infant airways shape immune responses will be key to designing safer and more effective RSV treatments.”
The post New Lung Model Reveals RSV Immune Response, Points to Better Treatments appeared first on GEN – Genetic Engineering and Biotechnology News.
STAT+: All eyes on data on Biogen’s tau therapy
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Lots happening in London these days, my colleague Andrew Joseph reports: At a pancreatic cancer meeting, researchers were buzzing about the implications of daraxonrasib, and at a major Alzheimer’s meeting, tau therapies are taking center stage.
Back here in the U.S., HHS has begun to craft national guidance on safely tapering SSRIs, and the FDA just cleared Sanofi’s wearable injector for a myeloma drug.
More than 5,000 NHS Scotland data breaches since 2023
Genetic Map Opens Door to Development of New Therapies to Reverse Bone Loss
An international team of scientists report that they have successfully mapped the cells and genes that regulate bone formation and loss and discovered the critical role that blood vessel cells play in bone health. By combining genomic sequencing with data from half a million individuals, the research team identified hundreds of previously unknown genes that govern bone health and revealed cells surrounding blood vessels as one of the drivers of bone repair.
The study “Multiscale analysis and functional validation of the cellular and genetic determinants of skeletal disease” is published in Nature Genetics. The team says its findings fundamentally enhance our understanding of skeletal disease. It is hoped the discovery will enable the development of new therapies to rebuild lost bone, offering hope to almost half of all individuals over 50 living with rare and common skeletal conditions such as osteoporosis, osteoarthritis and osteogenesis imperfecta, as well as those with rare bone disorders and cancers that spread to bone.
“Most people don’t realize that bones are constantly changing; the human body replaces its skeleton every 10 years or so,” said Peter Croucher, PhD, professor at the Garvan Institute of Medical Research in Australia. “This is a hugely important process, but until now we’ve had a limited understanding of the cells and mechanisms that control this turnover of bone. “Most of the drugs now available focus only on halting bone disease, rather than rebuilding lost bone, which is really important for reversing damage.”
Detailed map of cells and genes that regulate bone health
The team used single-cell RNA sequencing to measure which genes are switched on within individual cells found in bone, focusing on the interface between the hard bone and bone marrow which is the key site for the formation and breakdown of bone.
The Institute’s Ryan Chai, PhD, pointed out that the team’s analysis found 34 different groups of cells and defined the genes that are active in each of these cell types. “To our surprise, more than half of the genes identified have never before been shown to play a role in maintaining bone health, which is a significant finding,” he added.
![Ryan Chai, PhD, and Peter Croucher, PhD, from the Garvan Institute of Medical Research. [Garvan Institute]](https://www.genengnews.com/wp-content/uploads/2026/07/Low-Res_141A8709_Peter_C_Ryan_C-300x200.jpg)
The team used its map to identify cells involved in rare and common skeletal diseases, including osteogenesis imperfecta and osteoporosis. For the latter, the researchers analyzed the UK Biobank, one of the world’s biggest and most comprehensive collections of biological samples.
By analyzing genetic and bone density data from half a million people participating in the UK Biobank, the team was able to pinpoint exactly which cells drive skeletal disease, according to John Kemp, PhD, associate professor from Mater Research.
“These include cells known to regulate bone formation and bone loss, as well as blood vessel cells that, until now, have had underappreciated roles in bone health,” he said.
Croucher explained that the research uncovered new therapeutic opportunities against not only bone disease, but also cancer. “Bone is the main hiding place for dormant cancer cells and a common site of relapse, so identifying the cells and genes that drive bone turnover also opens new opportunities to prevent cancer metastasis,” he said.
The team is now further investigating the roles of newly discovered bone-regulating cells and genes in the hope of developing new medicines against these targets. Its data has been made accessible to medical researchers worldwide through an open access platform.
The post Genetic Map Opens Door to Development of New Therapies to Reverse Bone Loss appeared first on GEN – Genetic Engineering and Biotechnology News.
STAT+: A breakthrough in pancreatic cancer has experts excited — and braced for what’s to come
LONDON — When researchers started planning a pancreatic cancer conference here, the aim was to simply offer a counterpart to a regular U.S. meeting, where international scientists and doctors could discuss the latest developments in the specialty.
Then came the biggest shake-up in pancreatic cancer care in decades.
“It’s one of those moments,” Talia Golan, an oncologist at Israel’s Sheba Medical Center, said on a panel that conference organizers hastily added to the schedule centered on a new pancreatic cancer drug. She likened the medicine’s recent clinical trial performance to other milestones in cancer treatment such as the arrival of the first checkpoint inhibitors.
More than half of patients report easy GP access through NHS App
STAT+: Tau in the spotlight at Alzheimer’s conference
This is the web edition of STAT’s AAIC in 30 newsletter. Sign up to get it in your inbox here.
Welcome to the first edition of our pop-up newsletter from AAIC. I’m STAT’s London-based reporter, and I’ll be here with you over the next couple days. I hope those of you in town can find time to escape the abyss of the conference center and enjoy London, because this city in the summer is something special. Maybe you’re ahead of the curve and took in England’s win last night. In which case, maybe you’re joining me in needing to pound the coffee. Any thoughts, questions, or hot takes on Zverev v. Sinner, I’m at Andrew.Joseph@statnews.com.
One other note before we get going: STAT has put together a special report on dementia diagnostics, treatments, and care. We also have a special conference discount on offer, so head here and use the code “AAIC” to download the report for only $5. With the exchange rate, that’s less than the cost of this morning’s flat white.

