Category: 8. Health

A research team from Bochum and Hannover shows that the hepatitis E virus also attacks organs other than the liver.

The hepatitis E virus (HEV) causes severe liver inflammation. A research team from Ruhr University Bochum, Germany, and TWINCORE, the Centre for Experimental and Clinical Infection Research in Hannover, has now been able to prove for the first time that it can also infect kidney cells and replicate there. Antiviral drugs such as ribavirin are less effective there than in the liver. The results of the study have now been published in the journal Liver International on June 27, 2025.

Entire life cycle possible in the kidney

Hepatitis E viruses mainly infect liver cells and cause the most damage in the liver. “However, it was already known that they can go down the wrong path and infect other cells, such as nerve cells,” says last author Dr. André Gömer from the Department of Molecular and Medical Virology at Ruhr University Bochum.

The team from Bochum and Hannover has now succeeded in proving in cell culture that the viruses also infect kidney cells and can multiply with their help. “The entire replication cycle of the virus takes place in kidney cells in the same way as in liver cells,” says Gömer.

The infected kidney cells responded less well to treatment with the antiviral drug ribavirin than the liver cells. “This is probably due to the significantly different metabolic profiles of the two organs,” says Gömer. In the kidney, the virus is therefore relatively insensitive to drug treatment.

“It could be that in chronic infections, the kidney acts as a reservoir from which the viruses spread again after a supposedly successful treatment,” says Nele Meyer, a PhD student in the Translational Virology research group at TWINCORE. She and the physician Avista Wahid are the first authors of the study. Such a reservoir could also enable the viruses to adapt better to treatment.

Evolution in the organ

The team also conducted a comparative genetic analysis of hepatitis viruses from chronically infected patients using their blood plasma, stool and urine. While viruses are mainly excreted from the liver in the stool, those from the kidneys are found in the urine. ‘The viruses found in the different samples differ significantly from each other,” reports Dr Patrick Behrendt, head of the Translational Virology group at TWINCORE and also last author of the article. “This indicates that the populations have been developing independently of each other for some time and have undergone a kind of evolution in the respective organ.”

The hepatitis E virus

The hepatitis E virus (HEV) is the main cause of acute viral hepatitis. After the first documented epidemic outbreak in 1955 to 1956, more than 50 years passed before researchers began to focus intensively on the topic. Acute infections normally heal themselves in patients with an intact immune system. In patients with a reduced or suppressed immune system, such as organ transplant recipients or HIV-infected patients, HEV can become chronic. HEV is also particularly dangerous for pregnant women.

Funding

The work was supported by the German Center for Infection Research, the Volkswagen Foundation, the German Research Foundation (398066876/GRK 2485/2 and 448974291) and the Federal Ministry of Education and Research (VirBio project, funding code: 01KI2106).

In the early 2000s the U.S. Diabetes Prevention Program (DPP), a large randomized clinical trial, showed that intensive lifestyle modification was better than a medication called metformin at preventing at-risk patients from developing Type 2 diabetes.

In a newly completed follow-up study, a team of researchers including Vallabh “Raj” Shah, professor emeritus in The University of New Mexico Departments of Internal Medicine and Biochemistry & Molecular Biology at the School of Medicine, found that the health benefits from the lifestyle intervention persisted more than 20 years later.

In a paper published in The Lancet Diabetes & Endocrinology, they reported that the greatest results from both interventions were seen in the first few years of the study, and they were durable, Shah said. “The data suggests that those people who didn’t get diabetes also didn’t get diabetes after 22 years,” he said.

The DPP was launched in 1996 to compare the benefits of metformin – then newly approved by the FDA to treat Type 2 diabetes – and a lifestyle modification regimen that included exercise and a healthy diet. The study enrolled 3,234 patients with prediabetes at 30 institutions in 22 states.

The intensive lifestyle intervention reduced the development of diabetes by 24%, and metformin reduced diabetes development by 17%, according to the new study. The DPP had previously found that after the first three years of study, the lifestyle intervention of moderate weight loss and increased physical activity reduced the onset of Type 2 diabetes by 58% compared with a placebo medicine, while metformin reduced development of diabetes by 31%.

Compared with the original placebo group, the median time without diabetes was extended by three-and-a-half years in the lifestyle group and two-and-a-half years in the metformin group.

Within three years, they had to stop the study because lifestyle was better than metformin. That means lifestyle, which everybody is banking on, is more effective – that is the news.”

Vallabh “Raj” Shah, professor emeritus in The University of New Mexico

But because a wealth of health and biological data had already been collected for patients participating in the project, the DPP was repurposed into the DPP Outcomes Study (DPPOS), enabling researchers to follow their health outcomes in multiple domains over a period of decades, he said.

Shah has contributed to kidney disease research for more than three decades, conducting multiple studies at Zuni Pueblo and other American Indian communities in western New Mexico. He has also overseen the participation of the American Indian cohort enrolled in the DPPOS. Meanwhile, David Schade, MD, chief of the Division of Endocrinology in the UNM School of Medicine, recruited New Mexico participants in the study.

More recently, he said, DPPOS researchers have taken advantage of their large, well-documented cohort to repurpose the study to focus on diseases associated with aging, such as cancer and dementia, Shah said.

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On July 16, 2025, from 9:00 am to 11:00 am (Washington DC time or EDT), join us on the Transatlantic Dialogue on Climate and Health Impacts in Situations of Vulnerability, the fourth in a series of a joint initiative by WHO/Europe and the Pan American Health Organization (PAHO).

This 4th session focuses on climate change and health equity, and will provide input to develop a summary for policy-makers on advancing health equity-oriented approaches for climate action for Member States on both sides of the Atlantic.

This Dialogue aims to:

• Share knowledge on the differential impacts of climate change among population groups across countries and regions, including exposure, vulnerability and coping capacity.
• Exchange experiences on successful interventions that integrate health equity in climate action while acknowledging common and region-specific challenges.
• Foster a collaborative dialogue and stimulate further collaboration towards actionable policy recommendations and strategies that integrate a health equity lens.

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How to participate

• WHEN: Wednesday, 16 July 2025
• TIME: 9:00 a.m. (Washington, D.C., EDT), 3:00 pm (Geneve, Madrid)
• LANGUAGES: Spanish and English

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Context

Climate change has become an undeniable driver of adverse health outcomes worldwide, with evidence mounting on its multifaceted impacts. However, the burden of climate-related health risks is not evenly distributed. Populations more likely to be affected are those exposed to higher risks due to social, economic and environmental factors, including socioeconomic deprivation, geographic location and occupational exposure. 

Populations in situations of vulnerability (as well as children, pregnant women, older adults, ethnic minorities and those living in low-lying coastal or flood-prone areas) face disproportionate impacts, compounded by social determinants that limit their capacity to cope and adapt. This differential vulnerability underscores the critical importance of integrating health equity into climate and health action. Despite increasing awareness of these disparities, most climate–health initiatives have focused broadly on population-wide impacts, often neglecting the specific needs of populations and territories in situations of vulnerability. 

Therefore, there is a necessity to take an equity-based approach, ensuring that adaptation, mitigation and resilience-building efforts explicitly address social inequities, leaving no one behind.

Agenda

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A study published June 25 in the American Journal of Psychiatry provides new insights into a long-standing question in psychiatric research: What is the underlying neurobiological mechanism of psychomotor disturbance in psychiatric disorders?

This study, which explores the relationship between brain connectivity and motor function, reveals a connection between grip strength, well-being and the brain’s default mode network (DMN), offering novel insights for potential clinical applications.

Psychomotor disturbances — ranging from catatonia and psychomotor agitation to disorganized behavior and repetitive movements — are highly prevalent in psychiatric conditions. Despite their high prevalence, the neural mechanisms behind these disturbances have remained elusive.

 

“There has been an exponential increase in the interest to understand psychomotor processes in disease pathology — the fundamental nature of the motor system enhances our ability to link psychological processes to brain to symptoms, promoting clinically useful targets for intervention,” said senior author Alexandra Moussa-Tooks, PhD, an adjunct professor at Vanderbilt University School of Medicine, and co-director of the Clinical and Cognitive Neuroscience Center and head of the Motor Adaptations in Psychotic Disorders Lab at Indiana University Bloomington.

One of the main focuses of this study is the role of grip strength as a measure of both motor function and overall well-being.

“Grip strength is one measure of motor function that has been associated with all-cause mortality and overall well-being,” said first author Heather Burrell Ward, MD, assistant professor of Psychiatry and Behavioral Sciences at Vanderbilt University Medical Center. “It has been assumed that associations between grip strength and well-being are purely related to mechanical impairments reflective of overall poorer physical health.

 

“Therefore, the brain correlates of grip strength have been presumed to lie in the motor system, so previous brain analyses are frequently restricted to motor regions. However, a unifying brain circuit explanation linking grip strength and overall well-being has remained elusive until now. Ours is the first analysis to link grip strength and well-being to alterations in resting-state functional connectivity.”

This study takes a groundbreaking approach by identifying brain regions beyond the motor system that contribute to grip strength and overall health. Using data from the multisite Human Connectome Project for Early Psychosis, which involved 206 participants, including individuals with early psychosis and healthy controls, the researchers applied a data-driven, connectome-wide analysis to uncover the brain circuits associated with grip strength and well-being.

“We observed that higher grip strength was correlated with greater connectivity from multiple brain regions to the DMN,” Ward said.

Given the associations between grip strength and well-being, researchers then repeated this analysis to determine if they would identify similar brain correlates for grip strength and well-being — and they did.

“We identified significant relationships between the same brain regions and their connectivity patterns to the DMN that were related to well-being, overall function and grip strength,” Ward said. “These results have dramatic implications for treatment of psychomotor function in psychotic disorders, as they suggest a unifying role of DMN connectivity in psychomotor disturbance, overall function and well-being.”

Specifically, interventions targeting DMN connectivity could be used to treat psychomotor disturbance and well-being. Repetitive transcranial magnetic stimulation (rTMS) is one form of noninvasive brain stimulation that can be used to modulate DMN connectivity. As director of Neuromodulation Research in the Department of Psychiatry, Ward is currently leading multiple clinical trials that use rTMS to modulate DMN connectivity for people with psychosis.

“These results are exciting because they provide us with novel insights on what brain regions we should target to improve psychomotor function and overall well-being,” Ward said. “With our state-of-the art, fMRI-guided rTMS research at Vanderbilt, we can now test these interventions to develop novel and highly effective treatments for psychosis.”

To learn more, visit www.vumc.org/heatherwardlab.

 

New research from UC Davis Comprehensive Cancer Center has uncovered an evolutionary change that may explain why certain immune cells in humans are less effective at fighting solid tumors compared to non-human primates. This insight could lead to more powerful cancer treatments.

The study was published in Nature Communications. It revealed a tiny genetic difference in an immune protein called Fas Ligand (FasL) between humans and non-human primates. This genetic mutation makes the FasL protein vulnerable to being disabled by plasmin, a tumor-associated enzyme. This vulnerability seems unique to humans and is not found in non-human primates, such as chimpanzees.

The evolutionary mutation in FasL may have contributed to the larger brain size in humans. But in the context of cancer, it was an unfavorable tradeoff because the mutation gives certain tumors a way to disarm parts of our immune system.”

Jogender Tushir-Singh, senior author for the study and associate professor, Department of Medical Microbiology and Immunology

Tumor environment neutralizes key immune protein

FasL is an immune cell membrane protein that triggers a programmed cell death called apoptosis. Activated immune cells, including CAR-T cells made from a patient’s immune system, use apoptosis to kill cancer cells.

The UC Davis team discovered that in human genes, a single evolutionary amino acid change – serine instead of proline at position 153 – makes FasL more susceptible to being cut and inactivated by plasmin.

Plasmin is a protease enzyme that is often elevated in aggressive solid tumors like triple negative breast cancer, colon cancer and ovarian cancer.

This means that even when human immune cells are activated and ready to attack the tumor cells, one of their key death weapons – FasL – can be neutralized by the tumor environment, reducing the effectiveness of immunotherapies.

The findings may help explain why CAR-T and T-cell-based therapies can be effective in blood cancers but often fall short in solid tumors. Blood cancers often do not rely on plasmin to metastasize, whereas tumors like ovarian cancer rely heavily on plasmin to spread the cancer.

Plasmin inhibitors may enhance immunotherapy

Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. That finding may open new doors for improving cancer immunotherapy.

By combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL, scientists may be able to boost immune responses in patients with solid tumors.

“Humans have a significantly higher rate of cancer than chimpanzees and other primates. There is a lot that we do not know and can still learn from primates and apply to improve human cancer immunotherapies,” said Tushir-Singh. “Regardless, this is a major step toward personalizing and enhancing immunotherapy for the plasmin-positive cancers that have been difficult to treat.”

LA JOLLA, CA—A new study, published recently in Nature Communications, offers the first-ever map of which parts of Chikungunya virus trigger the strongest response from the body’s T cells. 

With this map in hand, researchers are closer to developing Chikungunya vaccines or therapies that harness T cells to strike specific targets, or “epitopes,” to halt infection. The new study also offers important clues for understanding why many people experience chronic, severe joint pain for years after clearing the virus.

“Now we can see what T cells are seeing patients with chronic disease,” says LJI Assistant Professor Daniela Weiskopf, Ph.D., senior author of the new study.

This research comes as many mosquito-borne viruses, including Chikungunya, are moving into new areas of the globe.

“Historically, Chikungunya was considered an emerging virus. Now all of Latin America has been exposed,” says Weiskopf. “These mosquitoes are traveling further north, and we need to know what’s going on with this virus before it arrives in the United States.”

T cells jump into action

Chronic Chikungunya virus disease strikes between 30 to 60 percent of those infected—usually women—and causes severe joint pain. This debilitating joint pain can last for years following the initial viral infection. 

In a study out earlier this year, Weiskopf and her colleagues showed that these patients have a population of inflammatory CD4+ T cells that closely resembles the T cell signature of rheumatoid arthritis, an autoimmune disease.

“So many people, mostly women, have chronic disease following Chikungunya virus infection,” says Weiskopf. “This has an impact on the workforce and impacts the economy. And there’s no treatment.”

Weiskopf and her colleagues are working to understand why these CD4+ T cells linger and cause problems long after a person clears the virus. For this study, they investigated whether people who develop chronic disease produce T cells that naturally target a different set of epitopes on Chikungunya virus.

Would a different “flavor” of T cells be more likely to stay in the body after infection?

Weiskopf and her team used a “peptide pool” approach to assemble a map of key T cell epitopes on Chikungunya virus. The researchers broke up the virus into very small amino acid sequences, called peptides. Then they took T cells from people with chronic Chikungunya virus disease and exposed these cells to the pool of peptides.

By stimulating the T cells, the researchers discovered exactly which parts of the virus are most likely to be recognized by T cells. These “immunodominant” regions may prove to be good targets for future Chikungunya treatments.

Rimjhim Agarwal, a UC San Diego graduate student and member of the Weiskopf Lab, spearheaded experiments to learn more about these T cells. Agarwal received funding from The Tullie and Rickey Families SPARK Awards for Innovations in Immunology to take a closer look. 

For her project, funded through the generosity of the Rosemary Kraemer Raitt Foundation Trust, Agarwal  compared CD4+ T cells from people with chronic Chikungunya virus disease to people who cleared the virus quickly with no lasting symptoms.

Agarwal found that both patient groups had T cells that targeted the same viral epitopes. People who developed chronic disease did not recognize different proteins of the virus.

Now the question is—why do these T cells stick around to cause inflammation in some but not all people? Weiskopf and Agarwal are now looking at where Chikungunya virus might hide in the body to stimulate a long-term T cell response.

The LJI team also hopes to help other laboratories shed light on how to fight the virus. “Identifying the immunodominant T cell epitopes could seed new research into Chikungunya-specific T cell responses,” says Agarwal.

Additional authors of the study, “Identification of immunogenic and cross-reactive chikungunya virus epitopes for CD4+ T cells in chronic chikungunya disease,” included Calvin Ha, Fernanda H. Côrtes, Yeji Lee, Amparo Martínez-Pérez, Rosa Isela Gálvez, Izabella N. Castillo, Elizabeth J. Phillips, Simon A. Mallal, Angel Balmaseda, Eva Harris, Claudia M. Romero-Vivas, Lakshmanane Premkumar, Andrew K. Falconar, Alba Grifoni, and Alessandro Sette.

The research was supported by LJI’s Tullie and Rickey Families SPARK Awards for Innovations in Immunology, the National Institutes of Health (grants 75N93019C00065 and 75N93024C00056), La Jolla Institute for Immunology, Kyowa Kirin, Inc. (KKNA-Kyowa Kirin North America), and ARPA-H (grant 1AY1AX000039).

DOI: 10.1038/s41467-025-60862-7

Researchers examine how the use of animal testing to identify endocrine-disrupting substances in the EU can be reduced. Although it is, in principle, possible to identify such substances without using animals, non-animal methods are still rarely applied.

A team from the MERLON research project, led by the DTU National Food Institute, has mapped the use of alternatives to animal testing – so-called New Approach Methodologies (NAMs) – in the identification of endocrine disruptors. This required a thorough review of the complex legal framework underlying the EU’s regulation of chemicals in everyday products, ranging from hair shampoo to food.

The conclusion is that alternative methods are almost never used to demonstrate the harmful effects of endocrine-disrupting substances, even though EU legislation allows for their use in this context. The research has been published in the scientific journal Regulatory Toxicology and Pharmacology.

According to the EU law, alternative methods may be used to demonstrate harmful effects of endocrine disruptors if they provide a ‘similar predictive capacity’ as animal tests. The problem is that we currently have only one alternative method that can actually be used for this purpose – namely ‘read-across’, where data from one substance is used to assess another, similar substance.”

Marie Louise Holmer, Special Consultant at the DTU National Food Institute, and one of the authors of the scientific article

“Read-across is ready to be used now, and we should apply it as broadly as possible. However, when it comes to other alternative methods, such as computer-based models and cell-based tests, substantial further development is still required.”

Better for both animals and humans

Alternative testing methods are, from an animal welfare perspective, clearly preferable. However, these methods are also much faster to carry out, which means that NAMs could significantly increase the efficiency of identifying endocrine disruptors in the EU.

“This is an area in which we are in urgent need of the support offered by digitalisation and new laboratory techniques. The WHO estimates that over 60,000 chemical substances are in global commerce. With today’s methods, we would not be able to test them all for the many harmful effects associated with endocrine disruptors – not even in 100 years,” says Marie Louise Holmer.

Endocrine disrupting substances pose risks to humans, animals and the environment, and can affect health in multiple ways. They may, for example, be carcinogenic, impair fertility, or interfere with the development of the brain and immune system. In the EU, substances can be regulated if testing confirms they are endocrinedisrupting – and such testing has so far primarily relied on animal experiments.

Animal testing has been widely debated for many years. Following a large public petition, the European Commission is developing a roadmap to outline how all animal testing for chemical safety assessments can eventually be phased out.

A balanced transition

The researchers advocate a balanced approach. They argue that there is a need both to develop and validate alternative methods and to explore how these, potentially in combination, can predict harmful effects to the same degree as animal tests. At the same time, animal testing should be refined and optimised to provide as much valuable information as possible.

“We must ensure that the alternatives are just as effective as animal testing before animal methods can be phased out completely. That is why we also emphasise the continued need for animal testing until alternatives are fully accepted and routinely implemented in chemical regulation,” says Marie Louise Holmer.

Dialogue to build common ground

One of the recommendations from the researchers is to bring together all stakeholders affected by the legislation in order to build consensus.

“We need, among other things, to determine when results from New Approach Methodologies – or combinations of New Approach Methodologies – are sufficiently robust and reliable to predict harmful effects and thus replace animal testing,” says Marie Louise Holmer.

Stakeholders could include national authorities (such as the Danish Environmental Protection Agency), relevant EU agencies, researchers, industry representatives, and NGOs.

Facts: Identifying endocrine-disrupting substances in the EU

Three criteria must be fulfilled to classify a substance as endocrine-disrupting:

1. It must cause harm (as assessed via animal tests or NAMs – the latter are currently seldom used for this purpose).
2. It must interfere with hormone systems (NAMs are already used here).
3. A link must be demonstrated between the hormonal disruption and the adverse effect.

Facts: What are NAMs?

NAMs include:

• In vitro tests – laboratory experiments carried out on cells or tissues outside a living organism.
• In silico models – computer-based models that predict the properties and effects of chemicals.
• Read-across – using data from one chemically similar substance to assess another.

Canada must address the growing crisis of communicable diseases that has occurred in tandem with a rise in misinformation that threatens our health systems, argue authors in an editorial in CMAJ (Canadian Medical Association Journal) https://www.cmaj.ca/lookup/doi/10.1503/cmaj.250916.

“A crisis of communicable diseases is unfolding in North America, just as Canada’s health systems’ responses are being hampered by the dismantling of public health and research infrastructure in the United States,” writes family physician Dr. Shannon Charlebois, medical editor, CMAJ, with coauthor Dr. Jasmine Pawa, Dalla Lana School of Public Health, University of Toronto, Ontario. “Coordinated attacks on US health institutions by the country’s executive office have drastically reduced their capacity to collect, interpret, and share data in the service of public health delivery. This coincides with a concerning spread of novel and existing communicable diseases across the continent, including in Canada.”

The spillover effect of changes in the US will likely affect Canada and other countries around the globe, as programs to track infectious diseases and address potential pandemic threats like avian flu have been cut or cancelled, and specialized staff with the capacity to rapidly develop reliable tests have been fired. Canada and other countries have relied on this work for disease surveillance and public health preparedness.

Now is the time for Canada to act on long-standing calls to strengthen health surveillance systems, improve interoperability and data exchange between electronic medical records and health systems, and better document and report rates of vaccine coverage.

The editorial outlines the threats from several infectious diseases to Canadians – information the public should be made aware of. However, “[p]eople living in Canada are vulnerable to a cross-border bleed of not only microorganisms, but also of attitudes, health misinformation, and exposure to biased US media.” write Charlebois and Pawa.

“Canada does not have control over the situation south of the border, but strengthening national capacity to manage communicable diseases by optimizing data collection and interprovincial sharing of the information required to do this is possible.”

The National Association of County and City Health Officials (NACCHO) yesterday released its 2024 Forces of Change Survey report that found that more and more local health departments are losing staff through layoffs or attrition, raising concerns about a shrinking public health safety net.

The study spotlights experiences of health departments at the county, city, and district level, including staffing and budget changes, health department governance, use of public health fellowship and training programs, the roles of public health nurses, program evaluation capacity, and activities that address the infectious disease consequences of substance use. Of 1,200 local health departments invited to complete the survey from March to June 2024, a total of 667 (56%) responded.

“The latest findings highlight critical trends and challenges faced by local health departments during a time of uncertainty in the local public health landscape,” NACCHO said in a news release.

1 in 5 local health departments note job losses

The survey found that, in 2023, 19% of local health departments reported job losses—an increase from 14% in 2021 and 17% in 2022. The rate rose to nearly 40% among large local health departments. Also, 17% of local health departments reported budget cuts during fiscal year (FY) 2024, with 23% anticipating cuts in FY2025.

The latest findings highlight critical trends and challenges faced by local health departments during a time of uncertainty in the local public health landscape.

In addition, 90% of local health departments reported that nurses are involved in health promotion and protection; 72% said they are involved in emergency preparedness, disaster recovery, and cross-sector collaboration; and 41% reported that nurses contribute to policy and advocacy work.

NACCHO also reported, “In 2024, 84% of local health departments reported having programs with an evaluation component. While most incorporated evaluation into their work, nearly 60% reported challenges due to insufficient staff time or capacity.”

NACCHO added, “Overall, few local health departments had individuals from training and fellowship programs assigned to their agency, which puts future workforce development at risk.” NACCHO represents more than 3,300 local health departments.