Cells frequently encounter conditions that can damage them or even lead to cell death. To keep functioning, they must rapidly adjust which genes are active so they can protect themselves. Cancer cells face even more intense challenges because the environment around a tumor is often harsh and unstable. Despite this, they manage to flourish by activating gene programs that support larger tumor growth and the ability to spread to new areas of the body.
Until now, it was unclear how cancer cells transform stressful surroundings into an advantage. Researchers at Rockefeller suspected the answer would come from understanding how the cell’s transcription machinery detects these conditions and shifts its activity. Their work has now identified a molecular switch inside breast cancer cells that redirects gene activity toward stress tolerance and tumor expansion.
The study, reported in Nature Chemical Biology, points to a possible new therapeutic target.
“This previously unknown transcription-level mechanism helps the cancer cells survive stressful conditions, so targeting it could disrupt a key survival mechanism that some cancers rely on,” says first author Ran Lin, a research associate from the Laboratory of Biochemistry and Molecular Biology at The Rockefeller University. “It’s another example of how basic research can open promising therapeutic avenues.”
“We found that this molecular switch is mediated by a generic transcription complex normally required for all protein-coding genes,” says Robert Roeder, head of the lab. “But what was most unexpected is that its individual subunits can be repurposed for several physiological functions — including a function that allows cancer cells to survive and grow in high-stress environments.”
Key Transcription Players and the Role of MED1
RNA polymerase II, also called Pol II, is the enzyme responsible for transcribing protein-coding genes in eukaryotic cells. Roeder originally discovered Pol II, and it often works together with the Mediator complex, a large coactivator made up of 30 subunits, to initiate the first steps of transcription. Additional adjustments to the resulting RNA can occur through post-transcriptional modifications, which further influence gene expression.

One important Mediator subunit is MED1. It is required for Pol II transcription in many cell types, including estrogen receptor-positive breast cancer (ER+ BC), which is one of the most common breast cancer categories.
Roeder’s lab previously showed that interactions between estrogen receptors and MED1 strongly activate gene expression in ER+ BC. In some cases, this interaction can even reduce the effectiveness of cancer drugs. These earlier findings led Lin to question whether MED1 might also support cancer cell survival when the cells are under stress.
Investigating MED1 and Acetylation
Lin began by examining whether MED1 undergoes acetylation. Acetylation involves the addition of an acetyl group to a protein, and this chemical modification can alter how proteins function. Scientists are increasingly recognizing the impact of acetylation on tumor growth, cancer spread, and treatment resistance.
Once Lin confirmed that MED1 is acetylated, he investigated how this modification affects its activity during stressful conditions. The researchers exposed cells to several types of stress, including hypoxia (lack of oxygen), oxidative stress, and heat stress.
Stress Response Through Deacetylation
The team discovered that during stress, a protein known as SIRT1 removes acetyl groups from MED1. This process, referred to as “deacetylation,” allows MED1 to partner more effectively with Pol II, boosting the potential for activating protective genes.

To further test this mechanism, the researchers engineered a version of MED1 missing six specific acetylation sites, which made it incapable of being acetylated. They then placed this modified protein into ER+ breast cancer cells where the natural MED1 had been removed using CRISPR.
The results were clear: whether MED1 was deacetylated due to stressful conditions or because it simply could not be acetylated, the outcome was the same. Breast cancer cells containing deacetylated MED1 produced tumors that grew more quickly and showed higher resistance to stress.
A Regulatory Switch Linked to Tumor Growth
“Our work reveals that the acetylation and deacetylation of MED1 act as a regulatory switch that helps cancer cells reprogram transcription in response to stress, supporting both survival and growth,” Lin says. “In cancer — particularly in ER+ breast cancer — this pathway may be co-opted or intensified to support abnormal growth and survival. We hope these insights will inform future drug development, especially for breast cancers and possibly other malignancies that rely on stress-induced gene reprogramming.”
“This MED1 regulatory pathway appears to be part of a wider paradigm in which acetylation regulates transcription factors,” Roeder adds. “Our earlier work on p53 helped establish that principle. Continuing to probe these basic mechanisms is what allows us to identify pathways that may eventually be leveraged for therapeutic purposes.”

In today’s world, many people are paying closer attention to their health and daily routines, with fitness habits and calorie-tracking apps becoming increasingly common. As part of this trend, more individuals are trying to include nutrient-dense foods such as fruits and vegetables in their diets. However, these foods can sometimes contain polycyclic aromatic hydrocarbons (PAHs) (hydrophobic organic compounds comprising multiple fused aromatic rings) and related substances. This contamination can occur through environmental exposure or through cooking methods such as heating, smoking, grilling, roasting, and frying. Some PAHs are known to be carcinogenic, creating potential health concerns.
Given these risks, accurately extracting and identifying PAHs in food is extremely important. Traditional extraction approaches, including solid-phase, liquid-liquid, and accelerated solvent extraction, are effective but often slow, labor intensive, and less environmentally friendly. To address these challenges, researchers have turned to the QuEChERS (Quick, Easy, Cheap, Effective, Rugged, and Safe) method, a technique designed to simplify and speed up the extraction of organic compounds. This approach shortens processing time, increases accuracy and recovery, and streamlines sample preparation, contributing to safer and more efficient PAH analysis.
SeoulTech Researchers Apply QuEChERS to Eight PAHs
A recent investigation by a team from the Department of Food Science and Biotechnology at Seoul National University of Science and Technology, led by Professor Joon-Goo Lee, applied the QuEChERS method to measure eight PAHs (Benzo[a]anthracene, Chrysene, Benzo[b]fluoranthene, Benzo[k]fluoranthene, Benzo[a]pyrene, Indeno[1,2,3-cd]pyrene, Dibenz[a,h]anthracene, and Benzo[g,h,i]perylene) in food. The study was published in Food Science and Biotechnology.
To perform the analysis, the researchers used acetonitrile to extract PAHs before purifying the samples with several combinations of sorbents. Using multiple food matrices, they confirmed that the QuEChERS method produced highly consistent results. Calibration curves for all eight PAHs showed exceptional linearity, with the R2 value surpassing 0.99.
Gas chromatography‒mass spectrometry testing revealed detection limits ranging from 0.006 to 0.035 µg/kg and quantification limits between 0.019 and 0.133 µg/kg. Recovery rates were equally strong, ranging from 86.3 to 109.6% at 5 µg/kg, 87.7 to 100.1% at 10 µg/kg, and 89.6 to 102.9% at 20 µg/kg, with precision values between 0.4 and 6.9% across all tested food matrices.
Prof. Lee explains, “This method not only simplifies the analytical process but also demonstrates high efficiency in detection compared to conventional methods. It can be applied to a wide range of food matrices.”
Practical Applications and Public Health Benefits

In food-related industries, this method could support more effective safety inspections and improve overall quality control. It may also lower operational costs and enhance worker safety.
“Our research can improve public health by providing safe food. It also reduces the use and emission of hazardous chemicals in laboratory testing,” concludes Prof. Lee.
Overall, the study demonstrates that the PAH analysis technique built on the QuEChERS approach is rapid, accurate, and environmentally sustainable.

The British Medical Association has announced a fresh round of strikes in England in the long-running pay dispute.Resident doctors will stage a five-day walkout from 17 December.This will be the 14th strike by the doctors’ union since March 2023 and is expected to cause significant disruption, particularly in hospitals.Resident doctors represent nearly half the medical workforce and range from doctors fresh out of university through to those with up to a decade of experience.They will walk out of both emergency and routine care, with senior doctors brought in to provide cover.

35 minutes agoShareSaveSimon Jack

Researchers at Johns Hopkins Medicine report that they have successfully used a “zap-and-freeze” method to capture rapid communication between brain cells in living tissue from both mice and humans. The approach allowed them to observe interactions that normally happen too quickly to track.
According to the team, the findings, published Nov. 24 in Neuron and supported by the National Institutes of Health, may help uncover the underlying biological causes of nonheritable forms of Parkinson’s disease.
Sporadic Parkinson’s cases represent the majority of diagnoses, the Parkinson’s Foundation notes. These cases involve disruptions in the synapse, the tiny site where one neuron passes a signal to another. Because this junction is so small and its activity unfolds rapidly, it has long been challenging to study in detail, says Shigeki Watanabe, Ph.D., an associate professor of cell biology at Johns Hopkins Medicine and the senior author of the study.
“We hope this new technique of visualizing synaptic membrane dynamics in live brain tissue samples can help us understand similarities and differences in nonheritable and heritable forms of the condition,” Watanabe says. He adds that the technique could eventually guide the development of therapies for this neurodegenerative disorder.
How Healthy Synapses Move Messages
In a healthy brain, synaptic vesicles act as tiny packages that carry chemical messages from one neuron to the next. This exchange is essential for learning, memory formation and the processing of information. Understanding how vesicles behave under normal conditions is key to identifying where communication begins to fail in neurological diseases, Watanabe says.
Watanabe previously helped design the zap-and-freeze approach to visualize fast changes in synaptic membranes (these results were published in 2020 in Nature Neuroscience). The method uses a brief electrical stimulus to activate brain tissue, followed immediately by rapid freezing. This preserves the exact positions of cellular structures for later viewing with electron microscopy.

In earlier work published in Nature Neuroscience this year, Watanabe applied the method to genetically engineered mice to investigate the role of a protein called intersectin. The study demonstrated how intersectin helps maintain synaptic vesicles in a specific location until they are ready to be released and activate a neighboring neuron.
Testing the Technique in Human Brain Tissue
For the latest study, the team examined samples from normal mice and compared them with living cortical brain tissue obtained, with permission, from six people undergoing epilepsy surgery at The Johns Hopkins Hospital. These surgeries were necessary to remove hippocampal lesions.
Collaborating with Jens Eilers and Kristina Lippmann of Leipzig University in Germany, the researchers first confirmed that zap-and-freeze worked reliably in mouse tissue by observing calcium signaling, which is the trigger that prompts neurons to release neurotransmitters.
They then used the technique to stimulate mouse neurons and captured the moment when synaptic vesicles fused with the cell membrane and released their chemical messengers. The researchers also documented how the cells retrieved and recycled vesicles afterward, a process known as endocytosis.
When the team applied zap-and-freeze to the human tissue samples, they found the same vesicle recycling steps occurring in human neurons.

Key Protein Found in Both Mouse and Human Brains
In both species, the researchers identified the presence of Dynamin1xA, a protein required for ultrafast synaptic membrane recycling, at the locations where endocytosis is believed to take place. This similarity suggests that the mechanisms observed in mice accurately reflect those in humans.
“Our findings indicate that the molecular mechanism of ultrafast endocytosis is conserved between mice and human brain tissues,” Watanabe says. He notes that this strengthens the value of using mouse models to study human brain biology.
Looking ahead, Watanabe hopes to apply the zap-and-freeze method to brain tissue collected, with permission, from individuals with Parkinson’s disease who are undergoing deep brain stimulation procedures. The goal is to observe how vesicle dynamics may differ in affected neurons.
Funding for the study was provided by the National Institutes of Health (U19 AG072643, 1DP2 NS111133-01, 1R01 NS105810-01A1, R35 NS132153, S10RR026445), Howard Hughes Medical Institute, Kazato Foundation, American Lebanese Syrian Associated Charities, Marine Biological Laboratory, Leipzig University, Roland Ernst Stiftung, Johns Hopkins Medicine, Chan Zuckerberg Initiative, Brain Research Foundation, Helis Foundation, Robert J Kleberg Jr and Helen C Kleberg Foundation, McKnight Foundation, Esther A. & Joseph Klingenstein Fund, and the Vallee Foundation.
Contributors to the research included Chelsy Eddings, Minghua Fan, Yuuta Imoto, Kie Itoh, Xiomara McDonald, William Anderson, Paul Worley and David Nauen from Johns Hopkins, along with Jens Eilers and Kristina Lippmann from Leipzig University.

14 minutes agoShareSaveMichelle RobertsDigital health editorShareSaveGetty ImagesFewer than one in 10 people who could benefit from obesity jabs like Wegovy are able to get them, warns the World Health Organization as it releases its first guidance on the drugs.With more than one billion people worldwide now obese, it is calling for more widespread and fairer access to GLP-1 medication. According to projections, more than two billion will be obese by 2030 unless action is taken. High costs, limited production capacity, and supply-chain constraints are major barriers to universal access to the injections that can help people shift significant weight, says WHO. It has already added them to its “essential” medicines list that countries are advised to provide. WHO director-general Tedros Adhanom Ghebreyesus said: “Our new guidance recognises that obesity is a chronic disease that can be treated with comprehensive and lifelong care.”While medication alone won’t solve this global health crisis, GLP-1 therapies can help millions overcome obesity and reduce its associated harms.”WHO says these drugs, sometime called skinny jabs, represent a new chapter in the gradual conceptual shift in how society approaches obesity, from a “lifestyle condition” to a complex, preventable, and treatable chronic disease.It says the drugs can be taken long-term – for six months or more – but must be prescribed along with advice on diet and exercise, so that people can keep the weight off. Too few people around the world can access them, says WHO. “Our greatest concern is equitable access,” said Tedros. Skinny jab shortageEven under the current best projected scenario, the production of GLP-1 therapies could only cover around 100 million people – less than 10% of those who need them, according to the WHO.The guideline calls on countries and companies to expand access, through strategies such as voluntary licensing – where a pharmaceutical company grants permission for others to make affordable non-brand versions of its patented drug.A patent on semaglutide – the core ingredient of Novo Nordisk’s Wegovy – is due to expire in several countries in 2026, meaning other drug-makers will soon be free to produce and sell cheap versions in places like India, Canada, China, Brazil and Turkey. WHO says countries must also create healthier environments to promote good health and prevent obesity.How obesity jabs workGLP-1 drugs mimick a natural hormone to slow digestion, curb appetite and increase feelings of fullness so people eat less.In the UK, the injections are prescription only medicines, which means they can only be prescribed by a healthcare professional for a person who clinically needs it.Some are available on the NHS, but more are sold privately. There is a black market and to be safe people should avoid buying from unregulated sellers such as beauty salons or via social media. People typically start to lose weight within a few weeks of starting on the weekly injections.Research suggests people may put most of the weight back on within a year of stopping the medication though, as their normal food cravings return.Being overweight or obese increases your risk for developing health problems, such as diabetes, heart disease, stroke, and certain cancers.Obesity affects people in every country and was associated with 3.7 million deaths worldwide in 2024, according to the WHO.

Despite major progress in medicine, infections caused by viruses and bacteria continue to rank among the leading causes of death worldwide. This has raised new scientific interest in understanding whether certain nutrients might influence the body’s defense system. A team led by Ina Bergheim from the Department of Nutritional Sciences at the University of Vienna has shown for the first time that monocytes, a group of important immune cells found in the bloodstream, react more intensely to bacterial toxins after people consume fructose — and this reaction is harmful rather than protective. The researchers found that levels of receptors that recognize bacterial toxins rose, making the body more prone to inflammation. The results were published in Redox Biology.
To investigate this effect, the researchers carried out two randomized studies involving healthy adults. They compared the immune response after drinking beverages sweetened with fructose to the response after drinking glucose-sweetened beverages. The team also examined isolated monocytes and used cell culture tests to explore the underlying biological mechanisms in greater detail.
Fructose Increases Toxin-Sensing Receptors in Immune Cells
Their findings showed that fructose intake, unlike glucose, led to higher concentrations of Toll-like receptor 2 in monocytes. Toll-like receptor 2 plays a key role in controlling how the immune system reacts. The rise in this receptor was linked to greater sensitivity to lipoteichoic acid, a bacterial toxin. “The concentration of receptors for such toxins in the body increased, which means that the inflammatory response increased,” explains study leader Ina Bergheim from the University of Vienna. The researchers also reported increased release of pro-inflammatory messengers, including interleukin-6, interleukin-1β and tumor necrosis factor-alpha.
“These findings make an important contribution to understanding how individual food components and fructose in particular can influence the immune system,” says Bergheim. “They indicate that even short-term, high fructose consumption in healthy people can influence the immune system and increase inflammation.”
Broader Health Implications of High Fructose Intake
According to the researchers, future work should examine how long-term, elevated fructose consumption may affect immune function and infection risk, especially in people who already face health challenges such as type II diabetes mellitus or fatty liver disease, which is associated with metabolic dysfunction. “Sugar, especially the fructose in sugary drinks and sweets, has long been suspected of increasing the risk of developing metabolic diseases — this needs to be investigated,” says Bergheim.

Soybean oil is the most commonly used cooking oil in the United States and appears in a wide range of processed foods. Research is now shedding light on how this highly consumed ingredient contributes to obesity in mice.
In a University of California, Riverside experiment, most mice fed a high-fat diet rich in soybean oil put on substantial weight. A separate group of genetically engineered mice did not, even though their diets were the same. These modified mice produced a slightly altered version of a liver protein that affects hundreds of genes involved in fat metabolism. The altered protein also changes how the body handles linoleic acid, one of the primary components of soybean oil.
“This may be the first step toward understanding why some people gain weight more easily than others on a diet high in soybean oil,” said Sonia Deol, a UCR biomedical scientist and corresponding author of the study published in the Journal of Lipid Research.
How Differences in Liver Proteins May Influence Metabolism
Humans produce both versions of the liver protein HNF4α, but the alternative form generally appears only in special situations, including chronic illness or metabolic stress from fasting or alcoholic fatty liver. Variations in this protein, along with individual differences in age, sex, genetics, and medications, may help explain why some people are more vulnerable to the metabolic impact of soybean oil.
The new findings expand on previous UCR research linking soybean oil to weight gain. “We’ve known since our 2015 study that soybean oil is more obesogenic than coconut oil,” said Frances Sladek, a UCR professor of cell biology. “But now we have the clearest evidence yet that it’s not the oil itself, or even linoleic acid. It’s what the fat turns into inside the body.”
Oxylipins and the Body’s Response to Linoleic Acid
Inside the body, linoleic acid is broken down into compounds known as oxylipins. Too much linoleic acid can result in elevated oxylipin levels, which are tied to inflammation and fat buildup.

The genetically engineered, or transgenic, mice produced far fewer oxylipins and had healthier liver tissue despite consuming the same soybean oil-rich diet as normal mice. They also showed better mitochondrial function, which may contribute to their resistance to weight gain.
Researchers identified specific oxylipins created from linoleic acid and alpha-linolenic acid, another fatty acid found in soybean oil. These molecules were required for weight gain in regular mice.
Why Oxylipins Alone Do Not Explain Obesity Risk
Transgenic mice on a low-fat diet still had elevated oxylipins but did not become obese. This suggests that oxylipins do not cause weight gain by themselves and that other metabolic conditions must also be involved.
Additional analysis showed that these altered mice had far lower levels of two enzyme families that convert linoleic acid into oxylipins. These enzymes operate similarly in all mammals, including humans, and their levels vary based on genetics, diet, and other biological factors.
The researchers also reported that only oxylipins in liver tissue, not those circulating in the blood, correlated with body weight. This indicates that standard blood tests may not reliably show early metabolic changes driven by diet.

Rising Soybean Oil Intake and Potential Health Impacts
Soybean oil consumption in the U.S. has increased dramatically over the past century, rising from about 2% of total calories to nearly 10% today. Although soybeans provide plant-based protein and the oil contains no cholesterol, excessive intake of linoleic acid from sources including ultra-processed foods may be contributing to chronic metabolic problems.
The UCR team also found that mice consuming soybean oil had higher cholesterol levels, despite the oil itself containing no cholesterol.
Exploring Other High-Linoleic Oils
Researchers are now examining how oxylipins lead to weight gain and whether similar reactions occur with other oils high in linoleic acid, including corn, sunflower, and safflower oils.
“Soybean oil isn’t inherently evil,” Sladek said. “But the quantities in which we consume it is triggering pathways our bodies didn’t evolve to handle.”
While human trials are not currently planned, the scientists hope their work will inform future studies and guide nutrition-related policy.
“It took 100 years from the first observed link between chewing tobacco and cancer to get warning labels on cigarettes,” Sladek said. “We hope it won’t take that long for society to recognize the link between excessive soybean oil consumption and negative health effects.”

Sunlight plays an important role in human health because it helps the body synthesize essential nutrients such as vitamin D. At the same time, spending too long in the sun can greatly increase the likelihood of developing skin cancer.
In a new study in Nature Communications, scientists at the University of Chicago report how long-term exposure to ultraviolet (UV) radiation can set off inflammatory reactions in skin cells by breaking down a key protein called YTHDF2. This protein acts like a gatekeeper that helps stop normal skin cells from turning cancerous. The researchers showed that YTHDF2 is central to controlling RNA metabolism so that cells remain healthy, and their work points to possible new strategies for preventing and treating skin cancer.
UV Radiation, Inflammation, and Rising Skin Cancer Cases
Every year, almost 5.4 million people in the United States receive a skin cancer diagnosis, and more than 90% of these cases are linked to excessive UV exposure. UV radiation can injure DNA and generate oxidative stress in skin cells, which in turn triggers inflammation that causes the familiar redness, pain, and blistering of sunburn.
“We’re interested in understanding how inflammation caused by UV exposure contributes to the development of skin cancer,” said Yu-Ying He, PhD, Professor of Medicine in the Section of Dermatology at the University of Chicago.
RNA, or ribonucleic acid, is a crucial molecule that helps translate genetic information into proteins. One important group of RNA molecules, known as non-coding RNAs, regulates gene activity without making proteins. These non-coding RNAs usually carry out their functions either in the nucleus, where the cell’s DNA is located, or in the cytoplasm, where most cellular processes occur.
How YTHDF2 Helps Protect Skin Cells
He’s laboratory focuses on how environmental stressors, including UV radiation and arsenic in drinking water, disrupt molecular pathways and damage cellular systems in ways that promote cancer. In their experiments, the team screened multiple enzymes and discovered that UV exposure significantly lowers the amount of YTHDF2 in cells. YTHDF2 is a “reader” protein that specifically recognizes RNA sequences tagged with a chemical modification called N6-methyladenosine (m6A).

“When we removed YTHDF2 from skin cells, we saw that UV-triggered inflammation was much worse,” He said. “This suggests that the YTHDF2 protein plays a key role in suppressing inflammatory responses.”
Inflammation is vital for defending the body against infections, but if it is not carefully controlled, it can drive serious diseases, including cancer. The detailed molecular mechanisms that keep this response in check after UV damage, however, are still not fully understood.
Non-Coding RNA, Immune Sensors, and UV Stress
Using multi-omics approaches and additional cell-based tests, the researchers showed that YTHDF2 binds to a particular non-coding RNA called U6, which carries an m6A modification and is categorized as a small nuclear RNA (snRNA). Under UV stress, cancer cells accumulated higher levels of U6 snRNA, and these modified RNAs were found to interact with toll-like receptor 3 (TLR3), an immune sensor known to trigger inflammatory pathways associated with cancer.
Unexpectedly, these interactions took place inside structures called endosomes, cellular compartments that usually help recycle materials rather than host U6 snRNA.
“We spent a lot of time figuring out how these non-coding RNAs get to the endosome, since that’s not where they usually reside,” He explained. “For the first time, we showed that a protein called SDT2 transports U6 into the endosome, and YTHDF2 travels with it.”
A Cellular Surveillance System Against Excessive Inflammation

Once YTHDF2 and m6A-modified U6 RNA reach the endosome, YTHDF2 prevents the RNA from activating TLR3. When YTHDF2 is missing, such as after UV-induced damage, U6 RNA can bind freely to TLR3 and set off harmful inflammatory responses.
“Our study uncovers a new layer of biological regulation, a surveillance system through YTHDF2 that helps protect the body from excessive inflammation and inflammatory damage,” He said.
This newly described pathway suggests potential strategies for preventing or treating UV-induced skin cancer by targeting the interactions between RNA and proteins that control inflammation.
The study, “YTHDF2 regulates self non-coding RNA metabolism to control inflammation and tumorigenesis,” was supported by grants from the National Institutes of Health, the University of Chicago Medicine Comprehensive Cancer Center, the ChicAgo Center for Health and EnvironmenT (CACHET), and the University of Chicago Friends of Dermatology Endowment Fund.
Additional authors include Seungwon Yang, Yan-Hong Cui, Haixia Li, Jiangbo Wei, Gayoung Park, Ming Sun, Michelle Verghese, Emma Wilkinson, Teresa Nam, Linnea Louise Lungstrom, Xiaolong Cui, Tae Young Ryu, Jing Chen, Marc Bissonnette, and Chuan He from the University of Chicago

Belgian researchers from VIB and Ghent University (UGent), working with partners in Denmark, have found strong evidence that infection with respiratory syncytial virus (RSV) early in infancy sharply raises the likelihood of developing childhood asthma. The effect is especially pronounced in children who have a family history of allergies or asthma.
The findings, published on November 28 in Science Immunology, indicate that protecting newborns from RSV could meaningfully lower asthma rates later in life.
Understanding early asthma risks
Across Europe, 5-15% of children live with asthma, a long-term condition that can affect day-to-day well-being, place a heavy strain on families, and carry significant costs for society. Because of this, discovering effective ways to reduce asthma risk before symptoms begin has become a major health priority.
“Childhood asthma is a complex disease with many contributing factors,” explains Prof. Bart Lambrecht (VIB-UGent Center for Inflammation Research), senior author of the study. “We found that early-life RSV infection and genetic allergy risk interact in a very specific way that pushes the immune system toward asthma. The encouraging news is that this process can be prevented.”
How RSV and inherited allergy risk work together
To explore this relationship, the team combined nationwide health registry information from all Danish children and their parents with controlled laboratory studies. This approach revealed how an early viral infection can magnify the impact of inherited allergy risk.

The researchers found that infants who suffer severe RSV infections in their first months of life are more likely to develop immune responses that overreact to common allergens, including house dust mites. This tendency becomes even stronger when asthma or allergy runs in the family, since allergen-specific antibodies passed from parents to their newborns increase sensitivity further.
Evidence that prevention could change long-term outcomes
A key part of the work showed that protecting newborns from RSV in experimental models prevented these immune system shifts altogether. As a result, asthma did not develop.
“With RSV prevention now becoming widely accessible, we have an opportunity to improve long-term respiratory health, not just prevent RSV hospitalizations,” says Prof. Hamida Hammad (VIB-UGent), co-senior author. “This is not just a laboratory insight. It’s a message that should help parents choose RSV prevention with confidence.”
Maternal vaccination during the third trimester of pregnancy and passive immunization of newborns using long-acting antibodies are being rolled out in many countries. However, uptake has been uneven, even though these tools are highly effective at preventing RSV hospitalizations.
“This is a moment where policy, science, and pediatricians can come together,” Lambrecht adds. “If preventing RSV infection also reduces asthma risk, the benefits for families and health systems could be enormous.”
This work was supported by the European Research Council, the University of Ghent, and Research Foundation — Flanders (FWO).