In March 2024, dairy cows in Texas were found to be infected with highly pathogenic avian flu, or H5N1 bird flu, in the first known case of the virus spreading to cattle. Since then, H5N1 has been found in about 200 animals — and 3 people — across 12 states, according to the Centers for Disease Control and Prevention. The virus was soon detected in raw milk, leading researchers to investigate whether dairy products pose a risk to consumers.
“How far is the virus getting through?” asked Erica Spackman, Ph.D., a virologist at the U.S. Department of Agriculture (USDA) in Athens, Ga. To find out, she and her collaborators tested nearly 300 milk products from 132 processors.
The researchers found no infectious virus in the samples, Spackman and her collaborators report this week in the Journal of Virology, a journal of the American Society for Microbiology. “Milk is safe,” she said. “Just like bacterial pathogens that occur in milk, or other viruses that could occur in milk, the sanitation processes that are in place are getting rid of the pathogens.”
The milk processing pipeline includes multiple layers of protection, Spackman said. Microbiological surveillance of milk products can identify pathogens, and milk from cows with mastitis or other disease conditions does not enter the food supply. Finally, heating during the pasteurization process can destroy H5N1 and other, more common bacterial pathogens.
Bird flu primarily infects and spreads among migratory birds and can be transmitted to domestic poultry, but the virus has been detected in other animals as well. Recently, those have included cats, dogs and juvenile goats, as well as a polar bear in Alaska and elephant and fur seals in the Antarctic. However, the discovery of H5N1 on dairy farms in March was a surprise — the virus had never been found in dairy cattle before.
Soon after the discovery, diagnostic testing revealed that an infectious form of the virus was present in raw milk, suggesting the virus passes from cow to milk. That finding led the U.S. Food and Drug Administration and the USDA to investigate whether pasteurization effectively eliminated risks posed to consumers. Between April 18 and April 22, 2024, researchers used real-time PCR to analyze 297 samples of pasteurized retail milk products, including 23 types of products, collected from 17 states.
“We did a viability assay to detect live virus and went as sensitive as we could to get even the least little bit of virus, but couldn’t detect anything,” Spackman said. Using PCR, the researchers did identify viral genetic material in 20% of samples. “It looks like the virus is just totally inactivated,” she said.
Spackman said the new findings “give us reassurance that what we have been doing — pasteurization — is keeping us safe from what we don’t know about.”

The ongoing opioid epidemic in the U.S. kills tens of thousands of people every year. Naloxone, sold under the brand name Narcan, has saved countless lives by reversing opioid overdoses. But new and more powerful opioids keep appearing, and first responders are finding it increasingly difficult to revive people who overdose.
Now, researchers have found an approach that could extend naloxone’s lifesaving power, even in the face of ever-more-dangerous opioids. A team of researchers from Washington University School of Medicine in St. Louis, Stanford University and the University of Florida have identified potential drugs that make naloxone more potent and longer lasting, capable of reversing the effects of opioids in mice at low doses without worsening withdrawal symptoms. The study is published July 3 in Nature.
“Naloxone is a lifesaver, but it’s not a miracle drug; it has limitations,” said co-senior author Susruta Majumdar, PhD, a professor of anesthesiology at Washington University. “Many people who overdose on opioids need more than one dose of naloxone before they are out of danger. This study is a proof of concept that we can make naloxone work better — last longer and be more potent — by giving it in combination with a molecule that influences the responses of the opioid receptor.”
Opioids such as oxycodone and fentanyl work by slipping inside a pocket on the opioid receptor, which is found primarily on neurons in the brain. The presence of opioids activates the receptor, setting off a cascade of molecular events that temporarily alters how the brain functions: reducing the perception of pain, inducing a sense of euphoria and slowing down breathing. It is this suppression of breathing that makes opioids so deadly.
The molecular compound described in the paper is a so-called negative allosteric modulator (NAM) of the opioid receptor. Allosteric modulators are a hot area of research in pharmacology, because they offer a way to influence how the body responds to drugs by fine-tuning the activity of drug receptors rather than the drugs themselves. Co-author Vipin Rangari, PhD, a postdoctoral fellow in the Majumdar lab, did the experiments to chemically characterize the compound.
Naloxone is an opioid, but unlike other opioids, its presence in the binding pocket doesn’t activate the receptor. This unique feature gives naloxone the power to reverse overdoses by displacing problematic opioids from the pocket, thereby deactivating the opioid receptor. The problem is that naloxone wears off before other opioids do. For example, naloxone works for about two hours, while fentanyl can stay in the bloodstream for eight hours. Once naloxone falls out of the binding pocket, any fentanyl molecules that are still circulating can re-attach to and re-activate the receptor, causing the overdose symptoms to return.
The research team — led by co-senior authors Majumdar; Brian K. Kobilka, PhD, a professor of molecular and cellular physiology at Stanford University; and Jay P. McLaughlin, PhD, a professor of pharmacodynamics at the University of Florida — set out to find NAMs that strengthen naloxone by helping it stay in the binding pocket longer and suppress the activation of the opioid receptor more effectively.

To do so, they screened a library of 4.5 billion molecules in the lab in search of molecules that bound to the opioid receptor with naloxone already tucked into the receptor’s pocket. Compounds representing several molecular families passed the initial screen, with one of the most promising dubbed compound 368. Further experiments in cells revealed that, in the presence of compound 368, naloxone was 7.6 times more effective at inhibiting the activation of the opioid receptor, partly because naloxone stayed in the binding pocket at least 10 times longer.
“The compound itself doesn’t bind well without naloxone,” said Evan O’Brien, PhD, the lead author on the study and a postdoctoral scholar in Kobilka’s lab at Stanford. “We think naloxone has to bind first, and then compound 368 is able to come in and cap it in place.”
Even better, compound 368 improved naloxone’s ability to counteract opioid overdoses in mice and enabled naloxone to reverse the effects of fentanyl and morphine at 1/10th the usual doses.
However, people who overdose on opioids and are revived with naloxone can experience withdrawal symptoms such as pain, chills, vomiting and irritability. In this study, while the addition of compound 368 boosted naloxone’s potency, it did not worsen the mice’s withdrawal symptoms.
“We have a long way to go, but these results are really exciting,” McLaughlin said. “Opioid withdrawal likely won’t kill you, but they’re so severe that users often resume taking opioids within a day or two to stop the symptoms. The idea that we can rescue patients from overdose with reduced withdrawal might just help a lot of people.”
Compound 368 is just one of several molecules that show potential as NAMs of the opioid receptor. The researchers have filed a patent on the NAMs, and are working on narrowing down and characterizing the most promising candidates. Majumdar estimates that it will be 10 to 15 years before a naloxone-enhancing NAM is brought to market.
“Developing a new drug is a very long process, and in the meantime new synthetic opioids are just going to keep on coming and getting more and more potent, which means more and more deadly,” Majumdar said. “Our hope is that by developing a NAM, we can preserve naloxone’s power to serve as an antidote, no matter what kind of opioids emerge in the future.”

Dexamethasone is one of the most important drugs in the treatment of severe COVID-19, but patients respond very differently to the therapy. Researchers at the German Center for Neurodegenerative Diseases (DZNE) and Charité — Universitätsmedizin Berlin have now discovered how the cortisone compound influences the impaired inflammatory response and which patients benefit from it. Their method uses so-called single-cell analyses and raises hopes for a precise prediction tool for other therapies and diseases as well. The findings have been published in the scientific journal Cell.
It has long been puzzling why certain drugs work so well for some people and fail to work at all for others. Researchers at DZNE and Charité — Universitätsmedizin Berlin have now tested a method that allows to uncover the underlying molecular mechanisms more precisely than before. For their study, they investigated the molecular effect of dexamethasone in patients with severe COVID-19, who responded differently to treatment with the drug.
Using so-called single-cell analyses, they discovered that a certain type of immune cells is responsible for the completely contrary reactions. They also identified a way of predicting early in the treatment whether it will work for the respective person. The tested approach could also be useful in the therapy of other diseases.
Monocytes indicate course of therapy
At the beginning of the coronavirus pandemic, it became apparent that the immune system of people with a severe course of the disease often reacts excessively to the virus. They were therefore given dexamethasone, a cortisone derivative that is used to treat numerous diseases in order to influence the immune system. In many patients, treatment with dexamethasone resulted in rapid improvement. However, in other individuals, condition remained critical, sometimes even worsening and leading to death. The current study results now reveal how the drug works in those cases where the therapy is effective.
“Our data show that the life-saving effect of dexamethasone is linked to the reaction of so-called monocytes,” says Dr. Anna Aschenbrenner from DZNE, who lead the study together with Prof. Dr. Florian Kurth from Charité and other colleagues. Monocytes belong to the white blood cells and constitute a central component of the immune system. “Some of the monocytes showed a response to the treatment — but only in those individuals whose condition improved with the therapy and who ultimately survived the infection,” says Aschenbrenner. “Why the monocytes show this reaction in some patients and not in others is a mystery. However, it is also known from other diseases that dexamethasone does not work equally well in all people.”
Altered signature
Already in 2020, in one of the first studies on the immune response in people with severe COVID-19, the researchers from Bonn and Berlin found an altered, pathological monocyte “signature” — in simple terms, this is a kind of molecular fingerprint that reflects the characteristics of these immune cells. Dexamethasone treatment reversed these changes when therapy was effective, as shown in the current study. “The response of the monocytes precedes the improvement in health status by several days,” says Florian Kurth from Charité’s Department of Infectious Diseases and Critical Care Medicine. “Thus, if the immune cells respond to dexamethasone at an early stage, we can anticipate that the treatment will work. If the cells do not respond, meaning that the therapy will have no effect, we can use additional medications to help the affected individuals.” However, further research is needed before the new method can be used in clinical practice.

The researchers were able to elucidate these processes with the help of single-cell sequencing. “This method allows for the individual characterisation of every single cell. Analysing cell signatures in such detail provides insights into the organism that were not possible just a few years ago,” says Prof. Dr. Joachim Schultze, Director for Systems Medicine at DZNE and also one of the study’s lead authors. Using single-cell sequencing, the researchers studied blood samples from people who were treated with dexamethasone at Charité due to severe COVID-19 disease. Early in the pandemic, these samples had been systematically collected at various times during disease progression. Their analysis revealed that the reaction of the monocytes was an indicator of the future course of therapy.
New approach for targeted drug development
“The significance of our results goes far beyond COVID-19,” says Prof. Dr. Leif Erik Sander, also one of the study’s principal investigators. He is Director of Charité’s Department of Infectious Diseases and Critical Care Medicine and research group leader at the Berlin Institute of Health at Charité (BIH). “The combination of cleverly designed clinical trials and high-resolution molecular analysis can provide crucial insights into the working of medicines. Already in the early stages of testing new drugs, this approach could identify factors that predict response to therapy.” In the future, this could speed up drug development and enable personalised therapies.
“I assume that this approach can also be transferred to other diseases,” says Florian Kurth. “Depending on the specific disease and therapy, there will be different cells serving as indicators. As soon as they are identified using single-cell sequencing, simpler laboratory methods that are already established will be sufficient to determine the relevant cellular changes.”
In research, this approach is referred to as “companion diagnostics” — the simultaneous accompanying of a therapy with molecular analyses. Anna Aschenbrenner sees the application of the method particularly in infectious diseases: “Here, immune cells play a key role and they are easily accessible via blood samples. But there is also potential for non-infectious diseases with systemic effects, which ultimately affect the entire organism. Because diseases such as cancer or even Alzheimer’s can also be reflected in the immune cells of the blood.”

A new way to map the spread and evolution of pathogens, and their responses to vaccines and antibiotics, will provide key insights to help predict and prevent future outbreaks. The approach combines a pathogen’s genomic data with human travel patterns, taken from anonymised mobile phone data.
Researchers from the Wellcome Sanger Institute, University of the Witwatersrand and National Institute for Communicable Diseases in South Africa, the University of Cambridge, and partners across the Global Pneumococcal Sequencing project1, integrated genomic data from nearly 7,000 Streptococcus pneumoniae (pneumococcus)samples collected in South Africa with detailed human mobility data2. This enabled them to see how these bacteria, which cause pneumonia and meningitis3, move between regions and evolve over time.
The findings, published today (3 July) in Nature, suggest initial reductions in antibiotic resistance linked to the 2009 pneumococcal vaccine may be only temporary, as non-targeted strains resistant to antibiotics such as penicillin gained a 68 per cent competitive advantage.
This is the first time researchers have been able to precisely quantify the fitness — their ability to survive and reproduce — of different pneumococcal strains. The insight could inform vaccine development to target the most harmful strains, and may be applicable to other pathogens.
Many infectious diseases such as tuberculosis, HIV, and COVID-19 exist in multiple strains or variants circulating simultaneously, making them difficult to study. Pneumococcus, a bacterium that is a leading cause of pneumonia, meningitis, and sepsis worldwide4, is a prime example with over 100 types and 900 genetic strains globally. Pneumonia alone kills around 740,000 children under the age of five each year5, making it the single largest infectious cause of death in children.
Pneumococcal diversity hampers control efforts, as vaccines targeting major strains leave room for others to fill the vacant niches. How these bacteria spread, how vaccines affect their survival, and their resistance to antibiotics remains poorly understood.
In this new study, researchers analysed genome sequences from 6,910 pneumococcus samples collected in South Africa between 2000 and 2014 to track the distribution of different strains over time. They combined these data with anonymised records of human travel patterns collected by Meta2.

The team developed computational models which revealed pneumococcal strains take around 50 years to fully mix throughout South Africa’s population, largely due to localised human movement patterns.
They found that while introduction of a pneumococcal vaccine against certain types of these bacteria in 2009 reduced the number of cases caused by those types6, it also made other non-targeted strains of these bacteria gain a 68 per cent competitive advantage, with an increasing proportion of them becoming resistant to antibiotics such as penicillin. This suggests that the vaccine-linked protection against antibiotic resistance is short-lived.
Dr Sophie Belman, first author of the study, former PhD student at the Wellcome Sanger Institute and now a Schmidt Science Fellow at the Barcelona Supercomputing Centre, Spain, said: “While we found that pneumococcal bacteria generally spread slowly, the use of vaccines and antimicrobials can quickly and significantly change these dynamics. Our models could be applied to other regions and pathogens to better understand and predict pathogen spread, in the context of drug resistance and vaccine effectiveness.”
Dr Anne von Gottberg, author of the study at National Institute for Communicable Diseases, Johannesburg, South Africa, said: “Despite vaccination efforts, pneumonia remains one of the leading causes of death for children under five in South Africa. With continuous genomic surveillance and adaptable vaccination strategies to counter the remarkable adaptability of these pathogens, we may be able to better target interventions to limit the burden of disease.”
Professor Stephen Bentley, senior author of the study at the Wellcome Sanger Institute, said: “The pneumococcus’s diversity has obscured our view on how any given strain spreads from one region to the next. This integrated approach using bacterial genome and human travel data finally allows us to cut through that complexity, uncovering hidden migratory paths in high-definition for the first time. This could allow researchers to anticipate where emerging high-risk strains may take hold next, putting us a step ahead of potential outbreaks.”
Notes Partners from the Global Pneumococcal Sequencing project can be found here: https://www.pneumogen.net/gps/ The human mobility data used in this study are Meta Data for Good baseline data, released during the 2020 SARS-CoV-2 pandemic. These data rely on personal consent for location sharing, and Data for Good ensures individual privacy by preventing re-identification in aggregated datasets. For more information on pneumococcal disease, visit: https://www.cdc.gov/pneumococcal/about/index.html https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5666185/ https://www.who.int/news-room/fact-sheets/detail/pneumonia Before these vaccines, 85 per cent of pneumococcal strains were those targeted by the vaccines. By 2014, this dropped to 33.2 per cent. This change was consistent across all nine provinces in South Africa.

He found that a failed contraceptive, tamoxifen, could block the growth of cancer cells, opening up a whole new class of treatment.V. Craig Jordan, a pharmacologist whose discovery that a failed contraceptive, tamoxifen, could block the growth of breast cancer cells opened up a whole new class of drugs and helped save the lives of millions of women, died on June 9 at his home in Houston. He was 76.Balkees Abderrahman, a researcher who worked closely with Dr. Jordan and was his caregiver for several years, said the cause was renal cancer.Dr. Jordan was known as a meticulous, even obsessive researcher, a quality demonstrated in his work on tamoxifen. The drug was first synthesized in 1962, though it was discarded after not only failing to prevent conception but, in some cases, promoting it.But Dr. Jordan, then still a doctoral student at the University of Leeds in Britain, saw something that no one else did. It had long been known that estrogen promoted breast cancer growth in postmenopausal women — and he suspected that tamoxifen could help stop it.Cancer of all kinds had long been seen as an unconquerable foe, treatable only with blunt, dangerous tools like chemotherapy. But the early 1970s saw a new wave of research, fueled in part by President Richard M. Nixon’s “war on cancer” campaign, which over the next 30 years would lead to a revolution in oncology.Dr. Jordan at the MD Anderson Cancer Center at the University of Texas in 2019. As a result of his research, tamoxifen received F.D.A. approval for use in breast cancer treatment in 1999.MD Anderson Cancer CenterWe 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.

28 minutes agoGetty ImagesPeople prescribed semaglutide, sold as Ozempic and Wegovy, to lose weight, may have a higher risk of developing a serious but rare eye condition, a study suggests.

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Everyday clothing may soon be able to capture and record body movements according to new research published by the Universities of Bristol and Bath.
Harmless low voltages are passed through conductive threads which are stitched into garment seams to create electrical circuits. Their resistance changes with the movement of the wearer’s body. The work opens up new possibilities to make digital clothing which senses and captures movements much more accurately than is possible using current phones and smart watches.
The paper, presented at the Designing Interactive Systems (DIS) conference in Copenhagen today (3 July), lays the foundations for e-textile designers and clothing manufacturers to create cutting edge garments that could enhance exercise, physiotherapy and rehabilitation.
Professor Mike Fraser of the University of Bristol’s School of Computer Science commented: “We’re excited by the opportunity for clothing manufacturers to implement our designs in sleeves and other garment seams.
“We’ve shown that common overlocked seams in standard garment constructions can do a good job of sensing movement. The design avoids the need for a separate power source by pairing the seam with a charging coil, drawing the energy wirelessly from a mobile phone placed in the pocket.
“This means advanced motion sensing garments could be made without altering existing manufacturing processes.
“We have also shown that smartphone apps using advanced Artificial Intelligence (AI) techniques can use this movement data to match body movement to specific postures or gestures such as physiotherapeutic exercises.”
The team have produced a short film for the conference illustrating how the technique works.

A world-first study has found low-dose aspirin may treat flu-induced blood vessel inflammation, creating better blood flow to the placenta during pregnancy.
Animal studies examined whether the treatment for preeclampsia could be applied to flu infections — and the results, according to the research team, were very promising.
Lead researcher and RMIT Post-Doctoral Research Fellow, Dr Stella Liong, said flu infections during pregnancy can resemble preeclampsia, a pregnancy complication that causes inflammation to the aorta and blood vessels.
Low-dose aspirin is commonly taken to prevent preeclampsia, as it stops the body from creating chemicals that cause inflammation.
“When the vascular system is inflamed, it leads to poor blood flow and affects the aorta’s function,” she said.
“This is especially a problem during pregnancy where good blood flow to the placenta is crucial to the development of the fetus.”
The research, led by RMIT University in collaboration with Trinity College Dublin, Ireland Professor John O’Leary and University of South Australia Professor Doug Brooks, found fetuses and placenta from mice with influenza A were smaller than those from uninfected mice.

Markers of low oxygen to the blood and poor blood vessel development were also evident in the fetuses.
However, mice treated daily with low-dose aspirin had less inflammation and improved fetal development and offspring survival.
While the research was still awaiting human clinical trials, Liong said low-dose aspirin was already recognised as safe to take during pregnancy.
However, the research team recommended pregnant people seek medical advice before taking new medications.
Brooks said influenza A infections during pregnancy was a big concern as every pregnancy overlaps with part of a flu season.
“There are long term implications for both the mother and the fetus, and aspirin might provide a simple solution for preventing this influenza associated pathology,” Brooks said.

Why flu infection is dangerous during pregnancy
O’Leary said the research findings had huge implications for pregnancy and seasonal influenza virus infections for pregnant people.
“This study shines a light, for the first time, on the role of vascular inflammation associated with influenza virus and the potential dramatic effect of the disease-modifying drug aspirin, in low dosage, in pregnant women with co-morbid influenza,” O’Leary said.
While there weren’t many studies of the impacts of flu infections during pregnancy, project lead and RMIT Professor Stavros Selemidis said it was clear that pregnancy changed how the body responded to the virus.
Liong and Selemidis’ earlier breakthrough research found the flu virus during pregnancy could trigger a damaging hyperactive immune response, causing the virus to spread around the body from the lungs through the blood vessels.
“We used to think the flu virus just stayed in the lungs, but during pregnancy it escapes from the lungs to the rest of the body,” Selemidis said.
“This infection could set you up for cardiovascular disease later in life, but also set up cardiovascular disease in the offspring later in life.”
While vaccination was still the considered the best way to prevent flu infection during pregnancy, Selemidis pointed out vaccination rates were generally low in the pregnant population.
“Low vaccination rates aside, the flu shot may not generate the perfect immune response, especially if someone is pregnant or has an underlying medical condition,” he said.
“That’s why it’s useful to have a potential back up in low-dose aspirin to help prevent vascular dysfunction during pregnancy and improve fetal development.”