Researchers at the Francis Crick Institute, working with UCL and Imperial College London, have discovered a new biological pathway that is a principal driver of inflammatory bowel disease (IBD) and related conditions, and which can be targeted using existing drugs.
About 5% of the world’s population, and one in ten people in the UK1, are currently affected by an autoimmune disease, such as IBD, the umbrella term for Crohn’s disease and ulcerative colitis. These diseases are also becoming more common, with over half a million people living with IBD in the UK as of 2022, nearly double the 300,000 previously estimated2.
Despite increasing prevalence, current treatments do not work in every patient and attempts to develop new drugs often fail due to our incomplete understanding of what causes IBD.
In research published in Nature, scientists at the Crick journeyed into a ‘gene desert’ — an area of DNA that doesn’t code for proteins — which has previously been linked to IBD and several other autoimmune diseases3.
They found that this gene desert contains an ‘enhancer’, a section of DNA that is like a volume dial for nearby genes, able to crank up the amount of proteins they make. The team discovered that this particular enhancer was only active in macrophages, a type of immune cell known to be important in IBD, and boosted a gene called ETS2, with higher levels correlating with a higher risk of disease.
Using genetic editing, the scientists showed that ETS2 was essential for almost all inflammatory functions in macrophages, including several that directly contribute to tissue damage in IBD. Strikingly, simply increasing the amount of ETS2 in resting macrophages turned them into inflammatory cells that closely resembled those from IBD patients.
The team also discovered that many other genes previously linked to IBD are part of the ETS2 pathway, providing further evidence that it is a major cause of IBD.

ETS2 as a treatment target
Specific drugs that block ETS2 don’t exist, so the team searched for drugs that might indirectly reduce its activity. They found that MEK inhibitors, drugs already prescribed for other non-inflammatory conditions, were predicted to switch off the inflammatory effects of ETS2.
The researchers then put this to the test, and discovered that these drugs not only reduced inflammation in macrophages, but also in gut samples from patients with IBD.
As MEK inhibitors can have side effects in other organs, the researchers are now working with LifeArc to find ways to deliver MEK inhibitors directly to macrophages.
James Lee, Group Leader of the Genetic Mechanisms of Disease Laboratory at the Crick, and Consultant Gastroenterologist at the Royal Free Hospital and UCL, who led the research, said: “IBD usually develops in young people and can cause severe symptoms that disrupt education, relationships, family life and employment. Better treatments are urgently needed.
“Using genetics as a starting point, we’ve uncovered a pathway that appears to play a major role in IBD and other inflammatory diseases. Excitingly, we’ve shown that this can be targeted therapeutically, and we’re now working on how to ensure this approach is safe and effective for treating people in the future.”
Christina Stankey, PhD student at the Crick, and first author along with Christophe Bourges and Lea-Maxie Haag, said: “IBD and other autoimmune conditions are really complex, with multiple genetic and environmental risk factors, so to find one of the central pathways, and show how this can be switched off with an existing drug, is a massive step forwards.”

Volunteer participants from the NIHR BioResource, with and without IBD, provided blood samples that contributed to this research. The research was funded by Crohn’s and Colitis UK, the Wellcome Trust, MRC and Cancer Research UK, and the researchers worked with collaborators across the UK and Europe.
Ruth Wakeman, Director of Services, Advocacy and Evidence at Crohn’s & Colitis UK said: “Every year, more than 25,000 people are told that they have Inflammatory Bowel Disease. Crohn’s and Colitis are complex, lifelong conditions for which there is no cure, but research like this is helping us to answer some of the big questions about what causes them. The more we can understand about Inflammatory Bowel Disease, the more likely we are to be able to help patients live well with these conditions. This research is a really exciting step towards the possibility of a world free from Crohn’s and Colitis one day.”
Lauren Golightly is 27 years old and was diagnosed with Crohn’s Disease in 2018 after experiencing stomach cramps, blood in her poo and irregular bowel habits.
She said: “Crohn’s has had a huge impact on my life. I’ve had a rocky road since diagnosis, with many hospital admissions, several different medications and even surgery to have a temporary stoma bag. One of the hardest things about having Inflammatory Bowel Disease ( IBD) is the uncertainty around it. I still experience flare-ups and can still spend quite a bit of time in hospital. Learning about this research is so exciting and encouraging. I am hopeful this could potentially make a difference for myself and so many other hundreds of thousands of people living with IBD.”

Bacteria, parasites, viruses — the immune system tackles them all. At the front line of the human immune response are cells called macrophages, which are responsible for correctly identifying intruders and then directing how the entire immune system responds. Researchers at the Salk Institute have now discovered a molecular mechanism that helps macrophages mount a coordinated response tailored to a specific immune challenge.
Activating macrophages requires the work of three versions of a protein complex called SWI/SNF: cBAF, ncBAF, and PBAF. Scientists already knew these variants had slightly different structures, but the new findings reveal that these differences have real functional consequences. Salk researchers discovered that each variant plays a distinct role in initiating macrophages’ responses to intruders and, consequently, how the immune system regulates inflammation.
By delineating these SWI/SNF variants, the team has revealed new immune system mechanisms that could be targeted with therapeutics to regulate inflammation associated with conditions like sepsis, cytokine storm, COVID-19, and many more.
The findings were published in Immunity on June 5, 2024.
“Macrophages are our first line of defense and the recruiters for adaptive immune cells, so understanding how they work is key to understanding our immune response,” says Diana Hargreaves, senior author and associate professor at Salk. “If we can figure out how macrophages tailor their responses to a given immune signal, we’ll have a better idea of how we can therapeutically target them to create desirable immune system behaviors.”
Macrophages are the first to sense an intruder in the body, so it is their responsibility to accurately identify the intruder and instruct the rest of the immune system’s response. To ensure that the correct response is mounted, macrophages require very specific internal signaling.
Each macrophage contains a set of identity-forming instructions encoded in strands of DNA, which are wrapped around protein complexes called histones and then wound into a 3D structure called chromatin. Changes to histones and chromatin impact the identity of a cell, since their modifications can expose or conceal stretches of DNA responsible for the cell’s behavior.

The SWI/SNF protein complex was already known to carry out such changes, but it was unclear whether each of the three variants did so in a unique way or led to distinct macrophage behavior. To learn more about the SWI/SNF variants, the researchers observed how macrophages in mice responded to bacterial infection and paid close attention to differences among cBAF, ncBAF, and PBAF activity.
“We found the SWI/SNF variants each serve a unique, important purpose in reorganizing chromatin across the genome and enabling macrophage inflammatory responses,” says first author Jingwen Liao, a graduate student in Hargreaves’ lab. “This is a major leap in our understanding of how immune systems respond with such a high level of specificity.”
When confronted with a bacterial threat, each of the three SWI/SNF variants regulated distinct portions of the macrophages’ DNA, producing distinct cellular responses. cBAF remodeled chromatin to promote inflammation, while ncBAF modified histones to stimulate an antiviral response. PBAF also modified histones, but the result of those modifications was less clear than cBAF or ncBAF.
The three acted distinctly and cooperatively to coordinate a complicated immune response that calls on the rest of the immune system to effectively and efficiently rid the body of threats.
“Chronic inflammation is a major cause of mortality across many diseases,” says Hargreaves. “When patients succumb to COVID, for example, that’s often a product of inflammation. This makes our findings really exciting, because we’ve found a new way to potentially toggle the immune system’s inflammatory pathways to improve outcomes in patients with chronic inflammation.”

UCSF Study finds that changes in daily salt intake may explain eczema flares.
A high sodium diet may increase the risk of eczema, according to researchers at UC San Francisco (UCSF), who found that eating just one extra gram of sodium per day increases the likelihood of flares by 22%.
Eczema, also known as atopic dermatitis, is a chronic disease that causes dry, itchy skin. It’s one of the most common skin conditions, affecting more than 31 million people in the U.S., and one in 10 people will develop it at some point.
It has become increasingly common in recent years, especially in industrialized countries, implicating environmental and lifestyle factors like diet.
Sodium, which most people consume in the form of salt, increases the risk of hypertension and heart disease. And scientists recently discovered that sodium is stored in the skin, where it may play a role in the inflammation in eczema.
Limiting dietary sodium could be an easy way for eczema patients to manage their disease.
“Most Americans eat too much salt and can safely reduce their intake to recommended levels,” said Katrina Abuabara, MD, associate professor of dermatology at UCSF and corresponding author of the study, which appears June 5, 2024, in JAMA Dermatology.

“Eczema flares can be difficult for patients to cope with,” said Abuabara, who is also associate adjunct professor of epidemiology at the UC Berkeley School of Public Health, “especially when they are unable to anticipate them and don’t have recommendations on what they can do to avoid them.”
For their cross-sectional study, the researchers analyzed data from more than 215,000 people between 30 and 70 years old from the UK Biobank, which includes urine samples and electronic medical records.
They could tell how much sodium each person was eating from urine samples; and they could see whether people had a diagnosis of atopic dermatitis, as well as the severity, from prescription codes.
They found that each additional gram of sodium excreted in urine over 24 hours was associated with 11% higher odds of an eczema diagnosis; 16% higher odds of having an active case; and 11% higher odds of increased severity.
Then, they looked at 13,000 U.S. adults in the National Health and Nutrition Examination Survey and found that eating just one additional gram a day of sodium — about half a teaspoon of table salt — was associated with 22% higher odds that someone would have an active case of eczema.

One in six patients in primary care reported cannabis use, with 35% of those using at levels indicating moderate- to high-risk for cannabis use disorder, new UCLA research finds.
The findings, to be published June 5 in JAMA Network Open, suggest that most patients reported using cannabis for symptom management, despite identifying as recreational users, indicating the need for routine cannabis screening. Currently few healthcare systems offer this screening in primary care settings.
“Patients may not tell their primary care providers about their cannabis use, and their doctors may not ask about it,” said lead author Dr. Lillian Gelberg, professor of family medicine at the David Geffen School of Medicine at UCLA and of health policy and management at the UCLA Fielding School of Public Health “Not asking patients about their cannabis use results in a missed opportunity for opening up doctor-patient communication regarding use of cannabis generally and for management of their symptoms. ”
Thirty-eight states, three US territories and the District of Columbia allow cannabis for medical use, and 24 of these states also permit recreational use. Stigma over cannabis use has fallen likely due to these legal moves. While there has been an increased perception that its use is risk free, cannabis potency has increased.
The U.S. Preventive Services Task Force recommended in 2020 that primary care physicians screen their adult patients for use of cannabis and other substances. The following year the investigators implemented the UCLA universal electronic health record-based, self-administered survey on cannabis use and medical cannabis use. Patients complete this survey as pre-visit screening prior to their primary care visits as sent to them via the Epic patient portal.
The researchers used patients’ de-identified electronic health records at UCLA collected from January 2021 to May 2023 to determine the prevalence, correlates and reasons for current cannabis use. The UCLA Health system is one of the few to ask patients to voluntarily complete cannabis use surveys during pre-appointment check-ins. The survey used the WHO Alcohol Substance Involvement Screening Test (ASSIST) to assess cannabis use.
Nearly 176,000 patients completed surveys. Of those, nearly 30,000 (17%) reported cannabis use among whom 35% had results suggesting moderate- to high-risk for a cannabis use disorder, defined as a score of 8 or higher on the screening survey. Among users, 40% used cannabis once or twice in the previous three months, 17% used monthly, 25% used weekly and 19% used it daily or almost daily.

Other findings included: Cannabis use was lowest among people living in the most disadvantaged neighborhoods (14%), yet the risk for disordered use was highest among this group Inhaled modes of cannabis use were as common as ingestion (65.0% and 64.7%), including 29% who vaped 47% used cannabis for medical reasons 76% used it to manage symptoms such as mental health symptoms or stress (56%), sleep (56%), and pain (37%). Further, most patients who reported using cannabis only for recreational reasons had also used it at some point to manage a symptom.The study has some limitations. The findings are based on patients’ self-reported use and though cannabis is legal in California, some patients may still have been reluctant to disclose using it. Much of the data were from screenings taken during the COVID-19 lockdown, during which cannabis use may have been higher than it might have been otherwise. In addition, the findings may not be applicable to other health systems, particularly in states where cannabis use is still illegal.
However, “given the high rates of cannabis use and medical cannabis use that we found in this large urban healthcare system, it is essential that healthcare systems implement routine screening of all primary care patients,” the researchers write. “Integrating screening efforts to include information regarding cannabis use for symptom management could help enhance the identification and documentation of medical cannabis usage, particularly in the healthcare context.”
Study co-authors are Dana Beck, PhD, MSN; Julia Koerber, MPH; Whitney N. Akabike, PMP, MSPH; Lawrence Dardick, MD; Clara Lin, MD; Steve Shoptaw, PhD; and Marjan Javanbakht, MPH, PhD.
The study was funded by the University of California Tobacco-Related Disease Research Program (grant #T29IR0277) and the National Institutes of Health National Center for Advancing Translational Science (NCATS) UCLA CTSI (grant #UL1TR001881).

Dr. Raffaele Teperino, head of the “Environmental Epigenetics” research group at Helmholtz Munich, along with his research team, has examined the impact of paternal diet on children’s health — specifically, the influence of diet before conception. The researchers focused on special small RNA molecules in sperm, known as mitochondrial tRNA fragments (mt-tsRNAs, see background). These RNAs play a key role in the inheritance of health traits by regulating gene expression.
For their study, the researchers used data from the LIFE Child cohort, which includes information from over 3,000 families. The analyses showed that the father’s body weight influences the weight of the children and their susceptibility to metabolic diseases. This influence exists independently from other factors such as the mother’s weight, the parental genetics, or environmental conditions.
The Father’s Diet Influences the Children
To verify the results of their analysis, the research team subsequently conducted experiments with mice. These mice were fed a high-fat diet, meaning food with a higher fat content than a normal diet. This had effects on the reproductive organs of the animals, including the epididymis. The epididymis is the area in the male reproductive system where freshly formed sperm mature. “Our study shows that sperm exposed to a high-fat diet in the mouse epididymis led to offspring with an increased tendency to metabolic diseases,” says Raffaele Teperino.
To deepen the findings, the research team conducted additional studies in the laboratory. They created embryos through in-vitro fertilization (fertilization “in a test tube”). When Teperino’s team used sperm from mice that had been exposed to a high-fat diet, they found mt-tsRNAs from these sperm in early embryos, significantly influencing gene expression. This, in turn, affects the development and health of the offspring.
“Our hypothesis that acquired phenotypes over the course of life, such as diabetes and obesity, are transmitted via epigenetic mechanisms across generations, is reinforced by this study. Here, epigenetics serves as a molecular link between the environment and the genome, even across generational boundaries. This occurs not only through the maternal line but, as our research results indicate, also through the paternal line,” explains Prof. Martin Hrabě de Angelis, co-author of this study and Research Director at Helmholtz Munich.
Preventive Health Care for Men Wishing to Become Fathers
The findings from the researchers at Helmholtz Munich underline the role of paternal health before conception — and offer new approaches to preventive health care: “Our results suggest that preventive health care for men wishing to become fathers should receive more attention and that programs should be developed for this purpose, especially with regard to diet,” says Teperino. “This can reduce the risk of diseases like obesity and diabetes in children.”
Background: The Indirect Influence of Fathers
Mitochondria are often referred to as the powerhouses of the cell. They have their own DNA, independent of the DNA in the cell nucleus. This mitochondrial DNA (mt-DNA) produces proteins in the mitochondria via the intermediate mt-RNA and is typically inherited from mothers to offspring. Previously, it was assumed that fathers had no part in the genetic makeup of their offspring’s mitochondria. However, recent studies like this one now show that sperm carry fragments of mt-RNA (“mt-tsRNA”) into the egg during fertilization. The mt-tsRNAs play a role in epigenetics, regulating gene expression in the early embryo: they can indirectly influence the development and health of the offspring by modifying the activity of certain genes in the mitochondria. Thus, fathers have an important, albeit indirect, influence on the genetic imprinting of mitochondria and thereby on the energy metabolism of their children.

Antibiotic treatment prior to surgical repair of a pediatric elbow fracture does not reduce the risk for post-operative infection, according to new findings from a team of researchers and surgeons from the University of Missouri School of Medicine.
A humerus bone fracture near the elbow is a common injury among children who fall. The typical surgical approach for repairing pediatric elbow fractures is a procedure called closed reduction percutaneous pinning (CRPP). It involves inserting pins or wires through the skin to promote stability and healing of the bone. CRPP is a minimally invasive, safe and effective procedure, but post-operative infections can occur in a small number of cases. As a result, some physicians will pre-treat the patient with antibiotics hoping to prevent infections from occurring after surgery.
In a recent randomized trial, MU researchers tested whether preoperative, preventative treatment with antibiotics resulted in lower rates of infection following CRPP. What they found was that it didn’t matter whether the patient was treated with prophylactic antibiotics or not when it came to rates of post-operative infection.
Sumit Gupta, MD, division chief, Pediatric Orthopaedics and associate professor of orthopaedic surgery at the School of Medicine helped lead the study, which involved 160 patients randomly assigned to either receive pre-surgical antibiotics or a placebo. His team found that the infection rate in those treated with the placebo was only 0.1% higher than in the treatment group. In both groups the infection rate was very low; only 1.2% to 1.3% respectively.
“The evidence suggests there is no need for pre-surgical antibiotic treatment in these types of cases,” said Gupta. “As antimicrobial resistance continues to rise, the importance of antibiotic stewardship is essential to preserving the efficacy and benefits of these lifesaving drugs.”
The current clinical practice guidelines developed by a joint panel from the American Society of Health-System Pharmacists, the Infectious Diseases Society of America, the Surgical Infection Society, and the Society for Healthcare Epidemiology of America acknowledged that the need for pre-surgical antibiotics is not well established.
“The results of our study provide important data that can be used in the development of new, evidence-based guidelines to aid surgeons in their appropriate use of antibiotics,” said Daniel Hoernschemeyer, MD, medical director of Pediatric Procedural Services and associate professor of clinical orthopaedic surgery at the School of Medicine. “It is increasing clear that we should only be using antibiotics to treat infections that are actually occurring.”
“Effect of Antibiotic Prophylaxis on Infection Rates in Pediatric Supracondylar Humerus Fractures Treated with Closed Reduction and Percutaneous Pinning: A Prospective Double-Blinded Randomized Controlled Trial” was recently published in the Journal of the American Academy of Orthopaedic Surgeons. In addition to Gupta and Hoernschemeyer, the research team from the University of Missouri included Emily Leary, PhD, director of orthopaedic biostatistics in the Department of Orthopaedic Surgery; Ennio Rizzo Esposito, MD, Rachel Phillips, MD, and Pierre-Emmanuel Schwab, MD, also of the Department of Orthopaedic Surgery.

The panel endorsed targeting a variant of the coronavirus that is now receding, though some officials suggested aiming at newer versions of the virus that have emerged in recent weeks.A committee of advisers to the Food and Drug Administration voted on Wednesday to update the formula for the Covid vaccine ahead of an anticipated fall immunization campaign, now an annual step to try to offer better protection against versions of the virus in circulation.The unanimous vote by the 16 advisers recommends a formula aimed at combating the variant JN.1, which dominated infections in the United States in February, or a version of it. In recent weeks, JN.1 has been overtaken by descendants known as KP.2 and KP.3.In the coming weeks, the F.D.A. is expected to formally recommend a variant target for vaccine makers for the next round of shots in the late summer or early fall. Any decision involves some educated guesswork, given that any new vaccine formula won’t be available until months after a variant becomes dominant.“It’s becoming clear that the ideal timing for a vaccine composition decision remains elusive,” said Jerry Weir, an official with the F.D.A.’s vaccine division.Dr. Peter Marks, who oversees that division, urged the committee to consider encouraging the mRNA vaccine makers to focus on the latest versions of the virus in broader circulation.“We always say we shouldn’t be chasing strains, but we’re paying an incredibly high premium for mRNA vaccines to be able to have the freshest vaccines,” he said, referring to the technology used by Moderna and Pfizer. He compared the choice of a vaccine to selecting fresher milk at the grocery store.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

New research from the University of Illinois Urbana-Champaign has linked multiple types of per- and polyfluoroalkyl substances (PFAS, also known as “forever chemicals”) with increased risk of cardiovascular diseases in postmenopausal women. Specifically, the study reveals how PFAS chemicals interact with pro-inflammatory pathways in older women, providing potential explanations for the increased risk.
“Previous research suggests PFAS exposures may play a role in the development of cardiovascular disease during the menopause transition, but the biological mechanisms were not well understood,” said lead study author Alicia Arredondo Eve, a postdoctoral researcher in the Department of Food Science and Human Nutrition (FSHN) in the College of Agricultural, Consumer and Environmental Sciences (ACES) at Illinois. “We focused on specific PFAS chemicals as well as the cardiovascular diseases that are more common in older women.”
It’s difficult to escape PFAS. The man-made chemicals coat nonstick pans, waterproof clothing, food wrappers, receipts, and many more items we come in contact with daily, not to mention being present in much of our water supply. Some forms — and there are thousands of chemical variants — could persist in the environment for hundreds or thousands of years, hence their “forever chemicals” moniker.
Not surprisingly, studies suggest nearly all Americans carry PFAS in their blood and other bodily tissues. But premenopausal women are a little better off. Thanks to childbirth, breastfeeding, and their monthly menstrual cycle, premenopausal women expel more PFAS than men and postmenopausal women. After menstruation stops, PFAS accumulates and can cause problems.
Scientists are still piecing together exactly what PFAS chemicals do in the body, but they appear to disrupt hormone signaling, interfering with normal reproductive and cardiovascular function. Most PFAS studies have focused on men or women during their reproductive years, but Arredondo Eve and co-author Zeynep Madak-Erdogan say postmenopausal women experience unique cardiovascular issues.
Motivated to fill the knowledge gap, the researchers analyzed data and samples from 70 postmenopausal women in Turkey. About a third of the women had been diagnosed with coronary artery disease, the world’s leading form of heart disease. Another third had coronary microvascular disease, which is common in postmenopausal women. The remaining third had no sign of heart disease.
All of the samples were tested for the presence and levels of two long-chain “legacy” PFAS (no longer manufactured in the U.S.) — PFOS and PFOA — and a newer short-chain PFAS chemical known as PFBS. Next, the researchers used complex machine-learning techniques to analyze the relationships between the PFAS and various blood metabolites and proteins.

“When you have multiple factors and you want to focus on one or two, machine learning techniques are very efficient in reducing that number,” said Madak-Erdogan, an associate professor in FSHN. “We found PFOS was closely associated with coronary artery disease, while PFOA was more predictive of coronary microvascular disease.”
Further, the two chemicals interacted with proteins and pathways associated with inflammation. Chronic inflammation, triggered by stress, poor diet, infections, or other causes, is a risk factor for both coronary artery and coronary microvascular disease. While interactions with inflammatory pathways weren’t a surprise given the diseases in question, an unexpected pattern emerged.
“The PFAS we studied affected the abundance of circulating pro-inflammatory factors differently. We did not expect that,” Arredondo Eve said. “PFOA and PFOS aren’t that different in terms of their chemical structure. Our results show you can’t lump all PFAS together.”
Higher levels of PFOA, which predicted coronary microvascular disease, were associated with higher levels of amino acids isoleucine and leucine and higher levels of pro-inflammatory cytokines. On the flipside, higher PFOS, related to coronary artery disease, was associated with lower isoleucine and leucine levels.
In addition to these opposing effects on metabolites, each PFAS was associated with a distinct set of pro-inflammatory proteins. The researchers say further preclinical research is needed to understand the mechanistic basis of these differences.
Ultimately, the study corroborates earlier research linking exposure to PFAS with cardiovascular disease in postmenopausal women, providing hints at how the chemicals interact with pro-inflammatory processes in the body. Unfortunately, the authors say there’s not much women can do to get rid of PFAS after they get into the body. Instead, they caution women to avoid prolonged exposure by choosing PFAS-free clothing, cookware, and other materials.
“We need more education as to how we can reduce our exposure to PFAS,” Madak-Erdogan said. “There also needs to be more action to regulate and mitigate these chemicals getting into the environment.”
The team plans to continue studying the effects of PFAS on women’s health.

Huge die-offs of elephant seals occurred after the virus gained nearly 20 troublesome new mutations, scientists found.Elephant seals in South America died in massive numbers because the bird flu virus acquired mutations that allowed it to spread among mammals, according to a new study.The research offers the first genetic and epidemiological evidence of bird flu virus transmission among mammals. And the findings hold a warning: The virus, called H5N1, may similarly transform to cause large-scale infections in other mammalian species, including people.The bird flu virus is responsible for an ongoing outbreak in dairy cows in the United States. Since March, it has been detected in cows in nine states, and in wastewater from several others.The virus may already be spreading from cow to cow, too, but federal officials have said that the more likely explanation for the outbreak is that it is spreading through contaminated milk.H5N1 is also presumed to have spread among mink on a fur farm in Spain. But the new study is the first to pull together different streams of evidence that substantiate transmission from mammal to mammal.The study was posted online on Saturday and has not been peer reviewed. But genetic analysis of the virus, and the scale and timing of infections in sea mammals in South America, all suggest that the animals acquired the virus from one another, not from infected birds, the researchers said.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

15 hours agoAurelia Foster