Category: 8. Health

Researchers at the Korea Research Institute of Standards and Science (KRISS) have created a new nanomaterial that can simultaneously detect and treat cancer using multiple approaches. In laboratory tests with mice, the gold-iron particles enabled real-time tumor imaging while delivering targeted treatment through heat, chemical reactions and immune system activation. Published in the Chemical Engineering Journal, the study indicates these multifunctional particles have the potential to locate tumors, treat them at the optimal moment and help trigger immune responses against cancer cells.

The core of the KRISS research lies in the nanodisk’s gold-iron-gold sandwich structure, where each layer serves a distinct purpose. The outer gold layers enable heat-based cancer cell destruction when activated by laser light. Meanwhile, the iron core provides magnetic guidance and triggers chemical reactions that damage tumor cells through oxidation and ferroptosis. This structural design allows the particles to deliver three complementary therapies simultaneously. The combination promises to offer a significant advance over current nanomaterials that typically offer a single treatment modality.

“Unlike conventional nanomaterials, which are composed of a single element and perform only one function, the material developed in this study utilizes the combined properties of gold and iron to perform multiple functions,” said Dr. Lee Eun Sook, in a press release.

Photo-acoustic imaging in the mouse study demonstrated that “PA imaging using AuFeAuNDs as a robust contrast agent offers precise localization of tumor tissue and guidance for PTT.” The researchers noted in the paper that “the magnetic-targeted AuFeAuNDs not only eliminate tumor cells but also initiate ICD by releasing DAMPs in tumor-bearing mice, leading to the augmentation of cytotoxic T cells.”

In turn, this imaging capability promises to enable clinicians to monitor nanoparticle accumulation in real-time and determine optimal treatment timing, assuming the research proceeds to human trials. The study showed that the particles triggered “immunogenic cell death (ICD) by releasing damage-associated molecular patterns (DAMPs), thus stimulating an anti-tumor immune response.”

The KRISS breakthrough builds on extensive global research into multifunctional cancer nanoparticles. Georgia Tech and Emory researchers recently developed Janus cellular backpacks that insert into cell membranes while carrying therapeutic payloads. Other teams have explored gold-copper sulfide hybrids that combine NIR-II imaging with chemical therapy, while multiple groups are investigating metal-organic framework platforms for combined heat and chemical treatments. Despite these varied strategies, most rely on core-shell or surface-modified designs rather than the precise trilayer architecture achieved by KRISS through nanoimprint lithography. The KRISS approach may thus offer an advantage when it comes to stability and controlled therapeutic delivery.

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Filed Under: Drug Discovery, Oncology

 

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Before Q2, HCPLive spoke with Steve Levine, MD, from Compass Pathways, for a Q1 recap and a look ahead at what was to come in psychiatry. Now that the quarter has wrapped, we’re revisiting those expectations.

Back in April, Levine highlighted 2 key studies to watch: Compass Pathways’ topline results for COMP360 psilocybin and Beckley Psychtech’s intranasal 5-MeO-DMT (BPL-003), both for TRD. Compass delivered on June 23, publishing phase 3 data from COMP005. A single 25 mg dose of COMP360 led to a significant reduction in depression severity at 6 weeks.

Beckley followed with their phase 2b data on July 1. BPL-003 met its primary and secondary endpoints, showing rapid, robust antidepressant effects after a single dose.1 Patients on 8 mg and 12 mg had meaningful symptom reduction by week 8, and most were ready for discharge within 90 minutes, fitting well within the 2-hour in-clinic model.

Along with the promising COMP360 data, this recap spotlights the unsuccessful phase 3 ARISE trial for xanomeline-trospium (Cobenfy) as an adjunctive schizophrenia treatment, an interview with John Kane, MD, on promising LB-102 data, and new podcast episodes of Medical Ethics Unpacked and the Gus Alva Perspective.

FDA Updates

FDA Officially Eliminates Clozapine REMS

On June 13, 2025, the US Food and Drug Administration (FDA) officially eliminated the clozapine REMS program to improve access to this effective treatment for schizophrenia. Although monitoring for severe neutropenia remains recommended, prescribers now have sole responsibility for determining clozapine’s use. In response, the Schizophrenia & Psychosis Action Alliance and American Association of Psychiatric Pharmacists are launching A New Era in Clozapine Management this fall to support safe, stigma-free prescribing.

What’s Moving in the Pipeline

Compass Pathways’ COMP360 Psilocybin Shows Benefit in Phase 3 TRD Trial

Compass Pathways announced positive topline results from its pivotal phase 3 COMP005 trial on June 23. A single 25 mg dose of COMP360 led to significant reductions in depression severity at 6 weeks among patients with TRD, meeting the primary endpoint. No major safety concerns were reported. The company plans to share 26-week follow-up data once its companion trial (COMP006) progresses.

Cobenfy Falls Short in Phase 3 ARISE Trial as Adjunctive Schizophrenia Therapy

In the phase 3 ARISE trial, xanomeline and trospium chloride (Cobenfy) did not achieve a statistically significant benefit as an adjunctive schizophrenia treatment. The 6-week study showed only a modest 2-point PANSS score difference versus placebo. However, subgroup analysis suggested Cobenfy may be more effective when paired with non-risperidone antipsychotics. Despite the missed endpoint, the safety profile remained favorable, and further research is encouraged.

Interview With John Kane, MD, on LB-102

LB-102 Significantly Improves Disease Severity in Acute Schizophrenia, with John Kane, MD

LB-102, a novel oral benzamide antipsychotic, demonstrated significant improvement in disease severity in the phase 2 NOVA trial. Doses of 50–100 mg led to meaningful CGI-S score reductions and positive effects on PANSS scores, with minimal weight gain and extrapyramidal symptoms. Lead investigator John Kane, MD, noted its potential to address unmet needs, particularly for negative symptoms and maintenance therapy.

Gus Alva Perspective

Launched May 16, 2025, The Gus Alva Perspective is a clinician-focused podcast hosted by psychiatrist Gus Alva, MD, medical director of ATP Research. With new episodes twice monthly, the show offers expert commentary on treatment advances and exclusive coverage leading up to the Southern California Psychiatry Meeting.

Featured Episodes:

The Gus Alva Perspective: SoCal Psych Preview—Schizophrenia Updates, with Jonathan Meyer, MD

The Gus Alva Perspective: SoCal Psych Preview—Tardive Dyskinesia, with Jonathan Meyer, MD

The Gus Alva Perspective: SoCal Psych Preview—Metabolic Revolution in Mood Disorders, with Roger McIntyre, MD

Medical Ethics Unpacked

Medical Ethics Unpacked: Shifting Vaccine Regulation and Policy, with Jason Schwartz, PhD

Jason Schwartz, PhD, of Yale, joins hosts Dominic Sisti, PhD, and Steve Levine, MD, to discuss the ethics of vaccine regulation. They examine how COVID-19 reshaped vaccine trust, amplified political divisions, and exposed vulnerabilities in public health infrastructure. The conversation addresses tensions between individual rights and collective health, misinformation’s impact, and the controversial replacement of ACIP members by HHS Secretary Robert F. Kennedy Jr.

Medical Ethics Unpacked: Unique Ethical Challenges of Psychedelic Therapies

Amy McGuire, JD, PhD, from Baylor College of Medicine, joins Sisti and Levine to explore the unique ethical issues in psychedelic therapy, particularly informed consent, cultural integration, and altered states of consciousness. The FDA’s recent rejection of MDMA-assisted therapy for PTSD has heightened debate over how to responsibly introduce these treatments into Western clinical practice.

References

atai Life Sciences and Beckley Psytech Announce Positive Topline Results from the Phase 2b Study of BPL-003 in Patients with Treatment-Resistant Depression. Beckley Psychtech. July 1, 2025. https://www.beckleypsytech.com/posts/atai-life-sciences-and-beckley-psytech-announce-positive-topline-results-from-the-phase-2b-study-of-bpl-003-in-patients-with-treatment-resistant-depression. Accessed July 1, 2025.

Scientists at the National Institutes of Health (NIH) and their colleagues at the University of California, San Diego, have found that fine-particulate air pollution, which includes pollution from vehicles and industry, was strongly associated with increased genomic changes in lung cancer tumors among people who have never smoked.

By assembling the largest-ever whole-genome analysis of lung cancer in individuals who have never smoked, researchers were able to link air pollution exposure to increased cancer-driving and cancer-promoting genetic mutations. This could potentially lead to more prevention strategies for never-smokers.

Researchers analyzed lung tumors from 871 never-smoker patients across 28 geographic locations worldwide as part of the Sherlock-Lung study They found associations between air pollution exposure and changes in the TP53 gene, and other genetic mutational signatures previously associated with tobacco smoking. They also observed a relationship between air pollution and shorter telomeres, which are sections of DNA found at the end of chromosomes. Telomeres shorten naturally with age and shorter telomeres are related to cells inability to continue to replicate. However, scientists found fine particulate air pollution was linked to premature shortening of telomeres.

Prior genomic studies of lung cancer have focused on tobacco smokers, leaving a significant gap in our understanding of how lung cancer develops in people who have never used tobacco. By beginning to uncover the mechanisms through which tissues acquire cancer-causing or cancer-promoting mutations following environmental exposures, this study helps scientists better understand the primary drivers of lung cancer in this population—which represents up to 25% of all lung cancer cases globally.

Interestingly, the researchers found that while exposure to secondhand smoke was associated with slightly higher mutation burdens and shorter telomeres, compared to tumors in patients who were not exposed, it did not lead to an increase in cancer-driving mutations or mutational signatures. This suggests that secondhand smoke may have a lower overall ability to cause genetic mutations, known as mutagenicity, compared to air pollution.

This work was led by researchers at NIH’s National Cancer Institute and the University of California, San Diego, and published in Nature on July 2, 2025.

This news release was published by the National Institutes of Health on July 2, 2025.

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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.

REGISTER HERE

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