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Hematopoietic stem cells (HSCs) have the capacity to both self-renew and differentiate into all mature blood cell types, making them promising treatments for a variety of diseases. However, the mechanisms involved in engraftment — when the cells start to grow and make healthy blood cells after being transplanted into a patient — are poorly understood. A recent study led by researchers at Massachusetts General Hospital (MGH) and Boston University School of Medicine has revealed the unique signature of genes expressed by HSCs capable of undergoing this process. The findings, which are published in Nature Communications, could enable scientists to expand these cells outside of the body or to convert other types of stem cells into cells that can repopulate the blood system.
In adults, HSCs are found in the bone marrow and bloodstream, but before birth, they can be found to a greater extent in the liver, where they multiply, or proliferate, into additional HSCs at a very high rate. Moreover, research in animals has shown that HSCs in the fetal liver are more capable of engraftment than HSCs from bone marrow.
To understand what allows fetal liver HSCs to have these superior proliferation and engraftment characteristics, investigators examined the gene expression patterns that are unique to these highly potent stem cells. They combined this examination with a variety of experimental methods to characterize the protein expression and functionality of those same cells.
“This in-depth analysis revealed that these stem cells express a protein on their surface called CD201 that correlates very closely with this engraftment potential and can be used to isolate functional stem cells away from other cell types,” says co-senior author Alejandro B. Balazs, PhD, a principal investigator at the Ragon Institute of MGH, MIT and Harvard. “This will help us improve the process of bone marrow and stem cell transplantation by allowing us to purify these cells.”
The enhanced understanding of the genes involved will also help scientists propagate HSCs with high engraftment potential in the lab and manipulate them to more efficiently fight blood cell-related diseases such as sickle cell anemia, HIV and certain types of cancer. “Altogether, this work has resulted in a detailed blueprint of the most potent blood stem cells and will lead to a better understanding of why these cells have such an extraordinary regenerative capacity. Such insights will allow us to create safer and more efficient therapies for patients suffering from blood disorders,” says lead author Kim Vanuytsel, PhD, a research assistant professor of medicine at Boston University School of Medicine.
Co-senior author George J. Murphy, PhD, an associate professor of medicine at Boston University School of Medicine and co-founder of the BU and BMC Center for Regenerative Medicine (CReM), adds that the team’s openly shared resource, which has been made available in an interactive format at https://engraftable-hsc.cells.ucsc.edu, will enable new biological insights into engraftment potential and stimulate a broad range of future studies. “This important work would not have been possible without the potent, collegial collaborations that took place between Boston area institutions. This project is also a shining example of ‘open source biology’ at work where the freely shared information and insights can be harnessed by all for future discovery,” he says.
Co-authors include Carlos Villacorta-Martin, Jonathan Lindstrom-Vautrin, Zhe Wang, Wilfredo F. Garcia-Beltran, Vladimir Vrbanac, Dylan Parsons, Evan C. Lam, Taylor M. Matte, Todd W. Dowrey, Sara S. Kumar, Mengze Li, Feiya Wang, Anthony K. Yeung, Gustavo Mostoslavsky, Ruben Dries, Joshua D. Campbell, and Anna C. Belkina.
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Materials provided by Massachusetts General Hospital. Note: Content may be edited for style and length.

Using data from 10 states, a study from the U.S. Centers for Disease Control and Prevention (CDC) is one of the first real-world studies to show that two doses of an mRNA vaccine provide protection against COVID-19 associated emergency department and urgent care visits among children ages 5 to 11.
The study also found that two doses of an mRNA vaccine provide protection against COVID-19 associated emergency department and urgent care visits as well as very high protection against hospitalization among adolescents aged 12 to 17.
“A positive pattern, similar to what we have reported in adults is emerging,” said study co-author Shaun Grannis, M.D., M.S., vice president for data and analytics at Regenstrief Institute and professor of family medicine at Indiana University School of Medicine. “Prevention of emergency department and urgent care visits shows that the vaccines are thwarting moderate COVID-19 in both children and adolescents; prevention of hospitalizations in 12- to-17-year-olds indicates vaccine effectiveness against more serious disease in this age group, which we hope to also see in 5-to-11-year-olds when there is sufficient data.
“We now have compelling evidence that vaccines and, for 16- and 17-year-olds, boosters, provide important protection for both children and adolescents — data-driven information that parents should take into consideration when making decisions for their family,” said Dr. Grannis.
The study was conducted by the CDC’s VISION Network which includes, in addition to the Regenstrief Institute (Indiana), Baylor Scott & White Health (Texas), Columbia University Irving Medical Center (New York), HealthPartners (Minnesota and Wisconsin), Intermountain Healthcare (Utah), Kaiser Permanente Northern California (California), Kaiser Permanente Northwest (Oregon and Washington) and University of Colorado (Colorado).
“Effectiveness of COVID-19 Pfizer-BioNTech BNT162b2 mRNA Vaccination in Preventing COVID-19-associated Emergency Department and Urgent Care Encounters and Hospitalizations Among Non-Immunocompromised Children and Adolescents Aged 5-17 Years — VISION Network, Ten States, April 2021-January 2022” is published in the CDC’s Morbidity and Mortality Weekly Report.
Regenstrief Institute authors of the study, in addition to Dr. Grannis, are William F. Fadel, PhD and Brian E. Dixon, PhD, MPA, Regenstrief and IU Richard M. Fairbanks School of Public Health; Nimish Ramesh Valvi, DrPH, MBBS, a Regenstrief fellow; and Peter J. Embi, M.D., M.S., former Regenstrief president, and a current affiliate scientist.
All authors on this paper are Nicola P. Klein, M.D., Kaiser Permanente Vaccine Study Center, Kaiser Permanente Northern California Division of Research; Melissa Stockwell, M.D., Division of Child and Adolescent Health, Department of Pediatrics, Columbia University Vagelos College of Physicians and Surgeons, Department of Population and Family Health, Columbia University Mailman School of Public Health, New York-Presbyterian Hospital; Maria Demarco, PhD, Westat; Manjusha Gaglani, MBBS, Baylor Scott & White Health, Texas A&M University College of Medicine; Anupam B. Kharbanda, M.D., Children’s Minnesota; Stephanie A. Irving, MHS, Center for Health Research, Kaiser Permanente Northwest; Suchitra Rao, MBBS, School of Medicine, University of Colorado Anschutz Medical Campus; Shaun J. Grannis, M.D., Center for Biomedical Informatics, Regenstrief Institute, Indiana University School of Medicine; Kristin Dascomb, M.D., Division of Infectious Diseases and Clinical Epidemiology, Intermountain Healthcare; Kempapura Murthy, MBBS, Baylor Scott & White Health; Elizabeth A. Rowley, DrPH, Westat; Alexandra F. Dalton, PhD, Centers for Disease Control and Prevention COVID-19 Response Team; Malini B. DeSilva, M.D., HealthPartners Institute; Brian E. Dixon, PhD, Center for Biomedical Informatics, Regenstrief Institute, Fairbanks School of Public Health, Indiana University; Karthik Natarajan, PhD, New York-Presbyterian Hospital, Department of Biomedical Informatics, Columbia University Irving Medical Center; Edward Stenehjem, M.D., Division of Infectious Diseases and Clinical Epidemiology, Intermountain Healthcare; Allison L. Naleway, PhD, Center for Health Research, Kaiser Permanente Northwest; Ned Lewis, MPH, Kaiser Permanente Vaccine Study Center, Kaiser Permanente Northern California Division of Research; Toan C. Ong, PhD, Children’s Minnesota; Palak Patel, MBBS, Centers for Disease Control and Prevention COVID-19 Response Team; Deepika Konatham, Baylor Scott & White Health; Peter J. Embi, M.D., Indiana University School of Medicine, Regenstrief Institute, Vanderbilt University Medical Center; Sarah E. Reese, PhD, Westat; Jungmi Han, Department of Biomedical Informatics, Columbia University Irving Medical Center; Nancy Grisel, MPP, Division of Infectious Diseases and Clinical Epidemiology, Intermountain Healthcare; Kristin Goddard, MPH, Kaiser Permanente Vaccine Study Center, Kaiser Permanente Northern California Division of Research; Michelle A. Barron, M.D., School of Medicine, University of Colorado Anschutz Medical Campus; Monica Dickerson, Centers for Disease Control and Prevention COVID-19 Response Team; I-Chia Liao, MPH, Baylor Scott & White Health; William F. Fadel, PhD, Center for Biomedical Informatics, Regenstrief Institute, Fairbanks School of Public Health, Indiana University; Duck-Hye Yang, PhD, Westat; Julie Arndorfer, MPH, Division of Infectious Diseases and Clinical Epidemiology, Intermountain Healthcare; Bruce Fireman, Kaiser Permanente Vaccine Study Center, Kaiser Permanente Northern California Division of Research; Eric P. Griggs, MPH, Centers for Disease Control and Prevention COVID-19 Response Team; Nimish R. Valvi, DrPH, Center for Biomedical Informatics, Regenstrief Institute; Carly Hallowell, MPH, Westat; Ousseny Zerbo, PhD, Kaiser Permanente Vaccine Study Center, Kaiser Permanente Northern California Division of Research; Sue Reynolds, PhD, Centers for Disease Control and Prevention COVID-19 Response Team; Jill Ferdinands, PhD, Centers for Disease Control and Prevention COVID-19 Response Team; Mehiret H. Wondimu, MPH, Centers for Disease Control and Prevention COVID-19 Response Team; Jeremiah Williams, MPH, Centers for Disease Control and Prevention COVID-19 Response Team; Catherine H. Bozio, PhD, Centers for Disease Control and Prevention COVID-19 Response Team; Ruth Link-Gelles, PhD, Centers for Disease Control and Prevention COVID-19 Response Team; Eduardo Azziz-Baumgartner, M.D., Centers for Disease Control and Prevention COVID-19 Response Team; Stephanie J. Schrag, DPhil, Centers for Disease Control and Prevention COVID-19 Response Team; Mark G. Thompson, PhD, Centers for Disease Control and Prevention COVID-19 Response Team; Jennifer R. Verani, M.D., Centers for Disease Control and Prevention COVID-19 Response Team.

Exploring how brain areas communicate with each other is the focus of a long-standing research collaboration between Carnegie Mellon University, Albert Einstein College of Medicine, and Champalimaud Research. The cross-continental team is simultaneously recording populations of neurons across multiple brain areas in the visual system and utilizing novel statistical methods to observe neural activity patterns being conveyed between the areas. Their latest findings reveal that feedforward and feedback signaling involve different neural activity patterns, lending fresh understanding into how the brain processes visual information.
A myriad of brain functions, such as seeing, hearing, and making decisions, require multiple brain areas to communicate with one another. Researchers have previously studied pairs of neurons or some aggregate metric of neuronal activity across areas to assess how information is taken in, processed, and then acted upon in everyday life. Few groups have studied, in such detail, populations of neurons together to see what type of activity patterns are being communicated across brain areas.
“The idea of this study was to investigate how information flows across two areas in the visual cortex, V1 and V2,” says João D. Semedo, first author of the work published in Nature Communications and former electrical and computer engineering Ph.D. student. “We had strong reasons to believe that the areas communicated with one another, based on anatomy, but tracking the flow of signals between areas has proven to be really difficult.”
Semedo continues, “Using pioneering technology from Dr. Kohn’s lab, we have been able to record multiple brain areas at the same time, and within each of those brain areas, record many neurons. It is the activity of a group of neurons together that tells us what is specifically going on. Then, we applied statistical methods in a creative way to pull out signals that haven’t been extracted before.”
In their analysis, the group identified directed interactions between brain areas and confirmed that patterns of activity in feedforward interactions (from V1 to V2), differed from patterns of activity in feedback interactions (from V2 to V1). Weekly meetings and a tight-knit, teamwork-driven approach has enabled the collaborators to stay connected on all aspects of the work and contributed to their success.
“Understanding what is communicated from one brain area to another is tough to disentangle, because signals are flowing in all directions, all the time,” explains Adam Kohn, professor of neuroscience at the Albert Einstein College of Medicine. “The thing that is most exciting to me about this work is the perspectives it opens for the future. If we can pinpoint the activity patterns that are involved in different signaling directions, it will be a big step forward in understanding how the brain works.”
More broadly, these methods could be applied to investigate the flow of communication in other areas of the brain, outside of the visual system.
“Studies like these increase our basic scientific understanding of how the brain works,” says Byron Yu, professor of biomedical engineering and electrical and computer engineering. “Many brain disorders involve a breakdown of communication between brain areas. This pioneering work could lead to novel treatments for such disorders, and even help us develop new methods to aid brain development and ways to learn.”
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Materials provided by College of Engineering, Carnegie Mellon University. Original written by Sara Vaccar. Note: Content may be edited for style and length.

Clues to the mechanism of yeast infections, which present risks to both humans and crops, have been identified in research co-led at the University of Strathclyde.
The study has focused on a family of proteins, known as Mep-Amt-Rh, which enable them to transport ammonium, a significant compound involved in growth and differentiation of yeasts.
Three proteins of the family are found in baker’s yeast but only one of these, Mep2, is capable of triggering filamentation, the process of cell growth which can lead to infection by pathogenic fungi.
The research has discovered that variations in Mep-Amt-Rh proteins affect the specificity and the type of mechanism for transporting ammonium. When two mechanisms co-exist within Mep2, they disrupt the signalling function which brings about filamentation and impede its progress.
The research could improve understanding of yeast infection in both humans and crop plants, enabling better defence against its effects.
The collaborative research was led by Dr Arnaud Javelle at Strathclyde, Professor Anna Maria Marini and Professor Mélanie Boeckstaens at the Université Libre de Bruxelles and Professor Ulrich Zachariae at the University of Dundee. It has been published in the journal mBio.

A study led by the Barcelona Institute for Global Health (ISGlobal), a centre supported by the “la Caixa” Foundation, has analysed, for the first time, the relationship between exposure to different green spaces and oxidative stress in children. The study concluded that greater exposure to vegetation is associated with lower levels of oxidative stress and that this association is observed regardless of the children’s physical activity.
Oxygen is essential for numerous biochemical reactions that keep us alive, but its oxidation process generates harmful reactive substances that the body cannot always neutralise quickly or which cause damage that the body is unable to repair. This results in what is known as oxidative stress, which causes ageing or even illness.
To date, various studies have shown that having green spaces in the vicinity of one’s home has a positive effect on health, especially because greenness improves mental health and encourages physical exercise, thereby reducing the risk of overweight or obesity. But less attention has been paid to the direct effects of vegetation on biological processes, such as inflammation and oxidative stress. This is particularly important for understanding the role that green spaces can play in respiratory and allergic diseases.
Study Analysed Over 300 Italian Children
In order to determine whether green spaces might be associated with lower levels of oxidative stress in children, and also whether physical activity plays a role in this possible association, the researchers analysed 323 healthy children aged 8-11 years from five primary schools in Asti, a small city in north-western Italy.
Parents completed a questionnaire on how often their children engaged in physical activity. Oxidative stress was quantified in urine by measuring the concentration of the compound isoprostane. Residential and school greenness were defined according to the Normalised Difference Vegetation Index (NDVI) and vegetated portion was also estimated. Multisite exposures were obtained accounting for NDVI around the children’s homes and schools, weighted for the time spent in each location.
Possible Explanations
Several biological mechanisms could explain this direct link between green space and oxidative stress in children. Firstly, “increased exposure to these areas may contribute to children’s immune development by bringing them into contact with organisms that tend to colonise natural environments,” commented last author Judith Garcia-Aymerich, researcher and head of the Non-Communicable Diseases and Environment Programme at ISGlobal. Secondly, contact with green spaces can increase vitamin D synthesis due to ultraviolet radiation from sunlight. Vitamin D acts as an antioxidant that prevents the negative effects of oxidative stress and inflammation. Finally, vegetation improves air quality in urban areas.
No Effect Found for Physical Activity
Although proximity to green space has been associated with increased physical activity, which in turn affects oxidative stress, the study found no evidence that exercise was involved in the association between green space and oxidative stress.
Garcia-Aymerich concluded: “The short- and long-term health effects of excess oxidative stress are unknown, so we need to conduct further research and support city and public-health strategies that favour greenness.”
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Materials provided by Barcelona Institute for Global Health (ISGlobal). Note: Content may be edited for style and length.

People suffering from COVID-19 could have several different SARS-CoV-2 variants hidden away from the immune system in different parts of the body, finds new research published in Nature Communications by an international research team. The study’s authors say that this may make complete clearance of the virus from the body of an infected person, by their own antibodies, or by therapeutic antibody treatments, much more difficult.
COVID-19 continues to sweep the globe causing hospitalisations and deaths, damaging communities and economies worldwide. Successive variants of concern (VoC), replaced the original virus from Wuhan, increasingly escaping immune protection offered by vaccination or antibody treatments.
In new research, comprising two studies published in parallel in Nature Communications, an international team led by Professor Imre Berger at the University of Bristol and Professor Joachim Spatz at the Max Planck Institute for Medical Research in Heidelberg , both Directors of the Max Planck Bristol Centre of Minimal Biology, show how the virus can evolve distinctly in different cell types, and adapt its immunity, in the same infected host.
The team sought to investigate the function of a tailor-made pocket in the SARS-CoV-2 spike protein in the infection cycle of the virus. The pocket, discovered by the Bristol team in an earlier breakthrough, played an essential role in viral infectivity.
“An incessant series of variants have completely replaced the original virus by now, with Omicron and Omicron 2 dominating worldwide.” said Professor Imre Berger. “We analysed an early variant discovered in Bristol, BrisDelta. It had changed its shape from the original virus, but the pocket we had discovered was there, unaltered.” Intriguingly, BrisDelta, presents as a small subpopulation in the samples taken from patients, but appears to infect certain cell-types better than the virus that dominated the first wave of infections.
Dr Kapil Gupta, lead author of the BrisDelta study, explains: “Our results showed that one can have several different virus variants in one’s body. Some of these variants may use kidney or spleen cells as their niche to hide, while the body is busy defending against the dominant virus type. This could make it difficult for the infected patients to get rid of SARS-CoV-2 entirely.”
The team applied cutting-edge synthetic biology techniques, state-of-the-art imaging and cloud computing to decipher viral mechanisms at work. To understand the function of the pocket, the scientists built synthetic SARS-CoV-2 virions in the test tube, that are mimics of the virus but have a major advantage in that they are safe, as they do not multiply in human cells.
Using these artificial virions, they were able to study the exact mechanism of the pocket in viral infection. They demonstrated that upon binding of a fatty acid, the spike protein decorating the virions changed their shape. This switching ‘shape’ mechanism effectively cloaks the virus from the immune system.
Dr Oskar Staufer, lead author of this study and joint member of the Max Planck Institute in Heidelberg and the Max Planck Centre in Bristol, explains: “By ‘ducking down’ of the spike protein upon binding of inflammatory fatty acids, the virus becomes less visible to the immune system. This could be a mechanism to avoid detection by the host and a strong immune response for a longer period of time and increase total infection efficiency.”
“It appears that this pocket, specifically built to recognise these fatty acids, gives SARS-CoV-2 an advantage inside the body of infected people, allowing it to multiply so fast. This could explain why it is there, in all variants, including Omicron” added Professor Berger. “Intriguingly, the same feature also provides us with a unique opportunity to defeat the virus, exactly because it is so conserved — with a tailormade antiviral molecule that blocks the pocket.” Halo Therapeutics, a recent University of Bristol spin-out founded by the authors, pursues exactly this approach to develop pocket-binding pan-coronavirus antivirals.
The team included experts from Bristol UNCOVER Group, the Max Planck Institute for Medical Research in Heidelberg, Germany, Bristol University spin-out Halo Therapeutics Ltd and further collaborators in UK and in Germany. The studies were supported by funds from the Max Planck Gesellschaft, the Wellcome Trust and the European Research Council, with additional support from Oracle for Research for high-performance cloud computing resources. The authors are grateful for the generous support by the Elizabeth Blackwell Institute of the University of Bristol.

Multiple myeloma is a cancer which affects ‘plasma cells’, a type of immune cell found in the bone marrow. This cancer can weaken the immune system, cause kidney damage, and weaken bones, which may lead to fractures. Average survival rates have improved considerably thanks to new treatment options. These include lenalidomide and pomalidomide, drugs which are often successful in forcing the cancer into remission. In nearly all cases, however, the cancer will become increasingly less susceptible to these drugs, meaning it develops drug resistance. When cancer growth eventually resumes despite treatment, the patient’s prognosis is poor.
Using latest improvements for a method known as proteomics, an interdisciplinary team of researchers in Berlin was able to decode a previously unknown mechanism which can cause this type of relapse. “We were able to show that production of CDK6, a cell division-promoting cell cycle regulator, is particularly high once the cancer has become resistant to treatment,” explains one of the study’s two co-leads, Prof. Dr. Jan Krönke of the Department of Hematology, Oncology and Cancer Immunology on Campus Benjamin Franklin. “Based on our data, we believe that CDK6 inhibition could represent a new treatment approach in relapsed multiple myeloma.”
Despite extensive DNA sequencing studies, treatment resistance in multiple myeloma has only rarely been linked to changes at the genetic level, such as gene mutations or gene deletions. “This suggests that the changes taking place within the cancer cell which would explain this relapse must take place at a different level,” says the study’s second co-lead, Dr. Philipp Mertins, an MDC researcher who heads the Proteomics Platform at both the MDC and the BIH. He continues: “The cancer cells’ growth potential may also be subject to various means of control at the protein level. Here, we observed this type of effect in relation to the protein CDK6.” The researchers employed cutting-edge mass spectrometry technology in order to establish whether changes at the protein level are responsible for the cancer becoming resistant to treatment. Using both pre- and post-relapse samples from patients with multiple myeloma, the researchers were able to quantify more than 6,000 different proteins.
Comparing cancer cells collected before and after relapse, the researchers found that a range of proteins were present at either higher or lower concentrations post-relapse. Using statistical and bioninformatics analyses, the researchers were able to trace the majority of these effects back to a single protein: cyclin-dependent kinase 6, or CDK6, an enzyme which controls the cell’s entry into the cell division phase of the cell cycle.
As a first step, the researchers used cell cultures to demonstrate that CDK6 plays a key role in the development of treatment resistance in multiple myeloma. “When we artificially increased the amount of CDK6 present inside cultured myeloma cells, they lost their susceptibility to the drugs lenalidomide and pomalidomide,” explains the study’s first author, Dora Ng, a researcher at the Department of Hematology, Oncology and Cancer Immunology on Campus Benjamin Franklin. She adds: “However, when we also added a CDK6 inhibitor, the drugs became effective again and the cancer cells died. This shows that CDK6 inhibition enables at least a partial reversal of the myeloma cells’ treatment resistance.”
The researchers were then able to confirm this effect in an animal model, where the combination of pomalidomide with a CDK6 inhibitor significantly improved the odds of survival. “These data suggest that patients with treatment-resistant multiple myeloma may also benefit from the addition of CDK6 inhibitors,” says Prof. Krönke, a researcher at the German Cancer Consortium’s (DKTK) translational research center in Berlin, who is being funded via the DFG’s Emmy Noether Program. “Further studies will be needed in order to test this hypothesis. One advantage is that some CDK6 inhibitors have already been authorized for use in the treatment of breast cancer.”
The study’s second first author, Dr. Evelyn Ramberger, was responsible for performing the project’s protein analyses. A postdoc at Charité and the MDC/BIH Proteomics Platform, she is convinced that the technology holds enormous benefits for the field of cancer research: “We want to continue pursuing this new approach of using modern, comprehensive protein analyses to study cancer tissues — both in multiple myeloma and other cancers. We hope this will unveil further treatment targets and biomarkers for use in personalized cancer medicine,” she says.
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The prompt for the study came from MS patients: “We hear again and again from sufferers that they feel worse when they consume milk, cottage cheese or yogurt,” explains Stefanie Kürten from the Institute of Anatomy at University Hospital Bonn. “We are interested in the cause of this correlation.”
The professor of neuroanatomy is an expert on multiple sclerosis. She began the study in 2018 at the University of Erlangen-Nuremberg. A year and a half ago, she moved to Bonn, where she continued the work together with her research group. “We injected mice with different proteins from cow’s milk,” she says. “We wanted to find out if there was a constituent that they were responding to with symptoms of disease.”
And the researchers did indeed find what they were looking for: When they administered the cow’s milk constituent casein together with an effect enhancer to the animals, the mice went on to develop neurological disorders. Electron microscopy showed damage to the insulating layer around the nerve fibers, the myelin. The fat-like substance prevents short circuits and additionally significantly accelerates stimulus conduction.
Perforated myelin layer
In multiple sclerosis, the body’s immune system destroys the myelin sheath. The consequences range from paresthesia and vision problems to movement disorders. In extreme cases, patients need a wheelchair. The insulating sheath was also massively perforated in the mice — apparently triggered by casein administration. “We suspected that the reason was a misdirected immune response, similar to that seen in MS patients,” explains Rittika Chunder, who is a postdoctoral fellow in Prof. Kürten’s research group. “The body’s defenses actually attack the casein, but in the process they also destroy proteins involved in the formation of myelin.”
Such cross-reactivity can occur when two molecules are very similar, at least in parts. The immune system then in a sense mistakes them for each other. “We compared casein to different molecules that are important for myelin production,” Chunder says. “In the process, we came across a protein called MAG. It looks markedly similar to casein in some respects — so much so that antibodies to casein were also active against MAG in the lab animals.”
This means that in the casein-treated mice, the body’s own defenses were also directed against MAG, destabilizing the myelin. But to what extent can the results be transferred to people with MS? To answer this question, the researchers added casein antibodies from mice to human brain tissue. These did indeed accumulate in the cells responsible for myelin production in the brain.
Self-test for antibodies against casein
Certain white blood cells, the B cells, are responsible for antibody production. The study found that the B cells in the blood of people with MS respond particularly strongly to casein. Presumably, the affected individuals developed an allergy to casein at some point as a result of consuming milk. Now, as soon as they consume fresh dairy products, the immune system produces masses of casein antibodies. Due to cross-reactivity with MAG, these also damage the myelin sheath around the nerve fibers.
However, this only affects MS patients who are allergic to cow’s milk casein. “We are currently developing a self-test with which affected individuals can check whether they carry corresponding antibodies,” says Kürten, who is also a member of the Cluster of Excellence ImmunoSensation2. “At least this subgroup should refrain from consuming milk, yogurt, or cottage cheese.”
It is possible that cow’s milk also increases the risk of developing MS in healthy individuals. Because casein can also trigger allergies in them — which is probably not even that rare. Once such an immune response exists, cross-reactivity with myelin can in theory occur. However, this does not mean that hypersensitivity to casein necessarily leads to the development of multiple sclerosis, the professor emphasizes. This would presumably require other risk factors. This connection is nevertheless worrying, Kürten says: “Studies indicate that MS rates are elevated in populations where a lot of cow’s milk is consumed.”
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A new study using serum from human blood samples suggests neutralizing antibody levels produced by two-dose mRNA vaccines against the original and early variants of the SARS-CoV-2 virus wane substantially over time, and offer essentially no protection against the omicron variant.
The same Ohio State University lab found in a previous study, posted on the preprint server bioRxiv, that a third COVID-19 mRNA vaccine booster shot did produce effective levels of neutralizing antibodies against omicron. This study has not yet been peer-reviewed.
“Our new work shows that two doses of mRNA vaccine do not offer protection against omicron, and even having a breakthrough infection on top of vaccine does not help much. But our earlier study showed that the booster can really rescue the shortcomings of the two doses,” said Shan-Lu Liu, the senior author of both studies and a virology professor in the Department of Veterinary Biosciences at Ohio State.
The new research is published online as a First Release paper in the journal Science Translational Medicine.
The researchers examined antibodies in serum samples from 48 health care professionals with experimental versions of the parent virus and the alpha, beta, delta and omicron variants. Serum samples were collected pre-vaccination, three to four weeks after a first vaccine dose, three to four weeks after a second vaccine dose and six months after the second vaccine.
“There was a substantial increase in neutralizing antibodies after the second dose against every variant except the omicron variant,” said first study author John Evans, a PhD student in Ohio State’s Molecular, Cellular and Developmental Biology Program who works in Liu’s lab. “From the second dose to six months later, there was an at least five-fold drop in immunity, even against the parent virus.”
Neutralizing antibodies that block viral particles’ entry into host cells are considered the gold standard of protection against COVID-19 infection.

Like many other viruses, COVID-19 is transmitted primarily via particles carried in the air. An infected person breathes out particles containing the virus into the air, which can then be inhaled by another person, who then becomes infected.
Masks are widely considered an important first-line defense against airborne transmission of the disease, as is supported by a preponderance of evidence. Fueled by the omicron variant, the latest wave of the pandemic prompted public health officials to recommend more protective face coverings because not all masks are created equal.
In Physics of Fluids, by AIP Publishing, researchers from England, Germany, and Francefocus their expertise — and their microscopes — on examining the efficacy of particle filtration by woven fabric, which, unlike material used in standard air filters and masks, consists of fibers twisted together into yarns. There are, therefore, two lengthscales: the diameters of the fiber and the yarn.
Using 3D imagery produced by confocal microscopy to see the air flow channels, the scientists simulate the airflow through these channels and calculate filtration efficiency for particles a micrometer and larger in diameter. The study concludes for particles in this size range, the filtration efficiency is low.
“Masks are air filters, and woven fabrics, such as cotton, make for good jeans, shirts, and other apparel, but they are lousy air filters,” said co-author Richard Sear, from the University of Surrey. “So, use woven fabric for clothing, and N95s or FFP2s or KF94s for masks.”
Indeed, the flow simulations suggest when a person breathes through cloth, most of the air flows through the gaps between the yarns in the woven fabric, bringing with it with more than 90% of the particles.
“In other words, these relatively large gaps are responsible for cloth being a bad material to make air filters from,” said Sear. “In contrast, the filtering layer of an N95 mask is made from much smaller, 5-micrometer fibers with gaps that are 10 times smaller, making it much better for filtering nasty particles from the air, such as those containing virus.”
While earlier research revealed similar findings, this study represents the first to simulate particles going directly through the gaps in woven fabric.
Sear added good masks should feature the “two Fs: good filtration and good fit.”
“Surgical masks fit badly, so a lot of air goes unfiltered past the edges of the mask by the cheeks and nose,” said Sear.
The article “Modelling the filtration efficiency of a woven fabric: The role of multiple lengthscales” is authored by Ioatzin Rios de Anda, Jake W. Wilkins, Joshua F. Robinson, C. Patrick Royall, and Richard P. Sear. The article will appear in Physics of Fluids on March 1, 2022.
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Materials provided by American Institute of Physics. Note: Content may be edited for style and length.