Too much fat can increase the risk of diabetes, heart disease, and other health problems. Yet the opposite can also be dangerous. In rare genetic and autoimmune conditions such as familial partial lipodystrophy type 2 (FPLD2), abnormal fat loss and uneven fat distribution can also lead to diabetes and other metabolic diseases.

A Longstanding Fat Loss Mystery

Elif Oral, M.D., a clinician and Professor in the Division of Metabolism, Endocrinology and Diabetes, has spent much of her career trying to understand this apparent contradiction. Her goal has been to uncover why pathological fat loss damages metabolism and to improve treatment options for people with lipodystrophy syndromes.

Working with patients who have FPLD2, Oral joined Ormond MacDougald, Ph.D., Professor of Molecular & Integrative Physiology, graduate student researcher Jessica Maung, Ph.D., and a broader collaborative team to investigate what happens inside diseased fat tissue.

“A simple explanation is that all of the fat cells (adipocytes) have really catastrophic things happening in them,” said Maung.

To study the process, the researchers developed a mouse model in which they could switch off the lamin A/C gene specifically in adipocytes. This is the same gene that is mutated in people with FPLD2.

Fat Cells Lose Their Normal Functions

The researchers examined both the animal models and tissue donated by patients. They found major changes in gene activity that prevented fat cells from properly processing and storing lipids.

At the same time, the adipocytes and the immune cells within the fat tissue shifted into a pro-inflammatory state. The mitochondria inside the fat cells also stopped functioning normally. Mitochondria help generate energy for cells, so their failure can have widespread effects on cell health.

Said Maung, “All of these effects come together to create this perfect environment for the tissue to be really unhealthy and eventually disappear.”

Why Healthy Fat Protects Metabolism

When healthy adipose tissue is lost, the body can no longer manage lipids or release metabolic hormones in the usual way. This breakdown can contribute to serious conditions, including diabetes and fatty liver disease.

“This is really underscoring the importance of healthy fats in keeping metabolism intact and functional,” said Oral. “People think of Type 2 diabetes as a disease of beta cells, but it’s actually a disease of fat cells, too.”

Beta cells are the insulin-producing cells in the pancreas. Although they play a central role in diabetes, the new findings show that fat cells are also deeply involved in maintaining normal blood sugar control and metabolic health.

New Targets for Future Treatments

The researchers hope their findings will point to new therapeutic targets. One possibility is to protect adipose tissue before it deteriorates, preventing fat cells from disappearing and reducing the metabolic damage caused by the disease.

The work also highlights the importance of close collaboration between laboratory scientists, clinicians, and patients.

“I think this work is an outstanding example of a collaboration between a translational clinical researcher and a basic science physiologist,” said MacDougald. “We also can’t overstate the importance of the patient population and their involvement in developing therapies and their dedication to understanding their disease.”

Additional authors include Rebecca L. Schill, Akira Nishii, Maria Foss de Freitas, Bonje N. Obua, Marcus Nygård, Maria D. Mendez-Casillas, Isabel D.K. Hermsmeyer, Donatella Gilio, Ozge Besci, Yang Chen, Brian Desrosiers, Rose E. Adler, Anabela D. Gomes, Merve Celik Guler, Hiroyuki Mori, Romina M. Uranga, Ziru Li, Hadla Hariri, Liping Zhang, Anderson de Paula Souza, Keegan S. Hoose, Kenneth T. Lewis, Taryn A. Hetrick, Paul Cederna, Carey N. Lumeng, Susanne Mandrup.

Using donated brain tissue from older adults with and without cognitive decline, along with samples from cognitively healthy centenarians, the team uncovered distinct cellular programs and immune cell states linked to both disease progression and resistance. The findings, published in Nature Medicine, point to changes in microglia, the brain’s resident immune cells, as a potentially important focus for future Alzheimer’s treatments.

“This has been an exciting journey with many partners. The study, entirely based on human donor material, provides insight into one type of resilience mechanism in the progression of AD to dementia,” says Prof. Bart De Strooper (VIB-KU Leuven Center for Neuroscience, KU Leuven), ERC grantee and one of the co-senior authors of the study.

Why Alzheimer’s Pathology Does Not Always Cause Dementia

Alzheimer’s disease affects more than 55 million people worldwide. It is commonly associated with the buildup of amyloid-β plaques and tau tangles in the brain. However, these biological signs do not always match a person’s mental condition.

Some people accumulate substantial amounts of plaques and tangles yet remain cognitively healthy. This has led scientists to focus more closely on how brain cells react to these abnormal proteins, rather than simply measuring how much pathology is present.

Microglia appear to be especially important. These immune cells help monitor and protect the brain, but their behavior can change dramatically as Alzheimer’s advances. By understanding those changes, researchers may be able to explain why some people remain resilient and identify new ways to prevent cognitive decline.

The new findings suggest that people can resist Alzheimer’s related damage through more than one biological pathway. By comparing brain tissue from people with dementia, people without dementia, and cognitively healthy centenarians (people over the age of 100 years), the researchers identified different microglial responses associated with protection from the disease’s effects.

“Understanding better how the brain resists the disease will provide new avenues towards therapies to prevent neurodegeneration and dementia,” adds Prof. Mark Fiers (VIB-KU Leuven), co-senior author of the study.

Mapping a Critical Alzheimer’s Transition

To investigate how resilience develops, the team combined two advanced methods that examine tissue at the level of individual cells (spatial transcriptomics and single-cell sequencing).

These technologies allowed the researchers to identify six distinct tissue domains that appeared to represent different stages of Alzheimer’s progression. One especially important transition separated regions dominated by amyloid-β plaques from those associated with tau pathology and neurodegeneration.

That shift was accompanied by a major change in the behavior of microglia.

During the earlier stages of the disease process, microglia entered an inflammatory state linked to amyloid plaques. At a later stage, they moved into a different antigen-presenting state that appeared at the same time as tau pathology.

Antigen presentation is a process in which immune cells display molecular material to help coordinate an immune response. In this case, the change may mark a biological turning point that helps determine whether Alzheimer’s pathology continues toward brain cell damage and dementia.

Two Biological Paths to Alzheimer’s Resilience

The researchers also found that resilience did not look the same in every person.

Octogenarians who had developed amyloid plaques but remained free of dementia showed the early microglial response. However, their microglia did not move into the later immune state associated with disease progression.

Centenarians followed a different route. Their brains activated the later microglial program, but this response occurred largely without being tied to tau accumulation.

In other words, a cellular state that was associated with neurodegeneration in some people appeared to be separated from damaging effects in others. This suggests that resilience is not simply a matter of avoiding Alzheimer’s pathology. It may also depend on how the brain controls, redirects, or adapts its response to that pathology.

A New Direction for Alzheimer’s Treatment

The results could support the development of more precise Alzheimer’s therapies.

Instead of focusing only on removing amyloid plaques, future treatments might aim to preserve beneficial early microglial activity or influence the transition between different microglial states. Molecules involved in these shifts could become valuable therapeutic targets.

Timing may also be critical. Treatments could be most effective before the brain reaches the point where inflammatory activity becomes connected to tau pathology, neurodegeneration, and cognitive decline.

“These findings open new opportunities to target microglial states — especially pathways such as TREM2 — and extend resilience rather than simply focusing on plaque removal. We are excited to continue this journey and understand the causal role of microglial transitions leading to the identification of novel therapeutic approaches to delay or prevent disease progression,” concludes Niels Plath, CSO of Muna Therapeutics.

The Backrooms are an internet-created fictional setting imagined as an infinite network of empty, fluorescent-lit rooms. The concept centers on the idea of accidentally slipping out of normal reality and becoming trapped in this monotonous, labyrinthine environment with no clear exit.

Since first emerging online in 2019 on the online bulletin board 4chan, the Backrooms phenomenon has expanded across Reddit, TikTok, YouTube and gaming platforms, where users collectively map, narrate and extend its mythology. Common to much of the user-generated content are eerie images and haunting stories of mysterious, yellow wallpapered corridors and empty office-like spaces that exist outside of, or beyond, reality itself.

Much of the interest on the internet circulates around filmmaker Kane Parsons’ viral “found footage” videos on YouTube. Parsons took the phenomenon from low resolution static images into immersive cinematic exploration, helping to establish Backrooms as one of social media’s most recognizable horror environments. With Parsons now adapting the Backrooms for a feature-length horror thriller, the strange fictive world is rapidly entering mainstream discourse.

At first glance, the Backrooms may resemble just another accelerated urban legend (also known as “creepypasta”) such as Slenderman or The Russian Sleep Experiment. But our research suggests something more significant is occurring in terms of changing consumer interest in spaces related to horror or trauma, their mediation, and new ways of experiencing them.

Behind the yellow wallpaper

The Backrooms began with a single unsettling image posted anonymously online: a claustrophobic warren of tawdrily yellow, windowless rooms with aged carpets and harsh overhead fluorescent lights.

Intrigued by the vague mixture of menace and nostalgia that the image evoked, internet users began sharing stories and speculating that the Backrooms is a hidden dimension into which people might accidentally find themselves.

With commercial tourism, social media and vlogging much of today’s world feels overexposed and overexplained, with seemingly every destination photographed, every experience reviewed and all hidden gems channeled into content. The mystery of the Backrooms felt different.

Today, the r/backrooms subreddit contains hundreds of thousands of members, while Backrooms content across TikTok and Instagram continues to attract enormous engagement. Content tagged #backrooms on TikTok exceeds half a million posts, while Instagram fan pages such as @xbackroom, which have hundreds of thousands of followers, further extend the mythology through images, edits and speculative storytelling. Users create maps, fictional diary entries, survival guides, found-footage videos and first-person explorations that collectively expand the world.

This is one reason the Backrooms feel different from traditional horror films or ghost stories. Rather than passively consuming a finished narrative, audiences actively participate in constructing and navigating the environment itself.

Folklore scholar Michael Kinsella has described this kind of online activity as a form of “online legend-tripping” where audiences become contributors, collaborators and world-builders rather than simply spectators.

The horror of familiar places

Dark tourism research reveals that people are drawn to places associated with death, disaster, tragedy and the uncanny, whether former prisons, abandoned sites, or locations connected to unsettling historical events. These locations often involve an encounter with atmospheres that feel emotionally, symbolically or existentially charged.

The Backrooms extend this logic into new and participatory territory. Unlike virtual dark tourism that allows for “armchair travel” to real-world dark heritage sites, there is no physical location anchoring the Backrooms nor any historical tragedy to commemorate. Instead, the Backrooms provide a collectively imagined and online environment of unease, abandonment and liminality.

Interest in the Backrooms persists precisely because they lack a fixed mythology, geographical reality, or narrative history, allowing users to construct meaning around places that, nonetheless, feel uncannily familiar. With their dated decor, hotel-like hallways, overhead ceiling tiles and abandoned office spaces, the Backrooms resemble the overlooked non-places of modern life – spaces many people recognize but rarely notice.

In this sense, the Backrooms reveal how digital culture is beginning to reshape experiences traditionally associated with tourism, allowing for the mundane to become menacing.

The Backrooms operate less like a story people receive and more like a world they enter. Across YouTube videos, video games, VR experiences and TikTok edits, audiences are located inside the environment itself blurring the boundaries between storytelling, role-playing, tourism and online participation.

This boundary-crossing may help explain why the phenomenon resonates so strongly at this cultural moment. The internet is no longer just a network of information or communication platforms; it is gradually evolving into a landscape people emotionally navigate and fully inhabit.

The Backrooms points toward a future where collectively imagined digital worlds function as meaningful cultural environments in their own right: places people travel to, explore, emotionally invest in and repeatedly return to, despite never physically existing at all.

This means that when a telescope captures the light from a distant galaxy, the image does not reveal where that galaxy is today. It shows the galaxy as it appeared when the light began its journey. To estimate its present distance, astronomers must use a cosmological model that accounts for how the universe has expanded over time.

The leading model used today is called LCDM. It includes dark matter (different episode) and dark energy (different episode). The strengths and limitations of LCDM are worth discussing separately (different episode), but alternative models do not significantly change the overall picture described here.

The Edge of the Observable Universe

The universe is about 13.77 billion years old, but the most distant regions we can observe are now roughly 45 billion light-years away. Space expanded during the entire time that their light was traveling toward us.

This boundary is known as the particle horizon, the cosmological horizon, or the comoving horizon, depending on how stylish you feel in the moment. It defines the outer edge of our observable bubble and marks the greatest distance we can see today.

At first, the numbers seem contradictory. How can the observable universe extend 45 billion light years when the universe is only 13.77 billion years old? The answer is that the universe can expand faster than light.

Why Faster Than Light Expansion Is Allowed

This does not violate the laws of physics. The speed of light limits how quickly objects can move through space in a local region. An observer will never see a nearby rocket ship pass by faster than light.

Cosmic expansion is different. Faraway galaxies are not necessarily speeding through space in the usual sense. Instead, the space between us and those galaxies is growing. Special relativity does not place the same restriction on how quickly large distances can increase across the universe.

Astronomers can estimate how quickly a galaxy is receding by measuring its redshift. As a galaxy moves away, its light is stretched toward redder wavelengths in the electromagnetic spectrum. Edwin Hubble used this effect to uncover evidence that the universe is expanding.

In an expanding universe, more distant galaxies generally recede more quickly because a greater amount of space lies between them and us. More space means more distance that can expand.

The point at which galaxies begin receding faster than light is called the Hubble distance. It lies about 13.77 billion light-years away.

Why We Can Still See Faster Moving Galaxies

We can observe galaxies beyond the Hubble distance because the light reaching us today was emitted long ago, when those galaxies were much closer. We may also eventually receive light from some galaxies located even farther away, provided that the light began traveling toward us when the galaxies were nearer.

However, there is an ultimate limit called the cosmological event horizon (which is ever so slightly different from the black hole event horizon). It is currently about 17 billion light years away.

Any light emitted RIGHT NOW from beyond that boundary will NEVER reach us, ever, no matter how long we wait. The expansion of space will prevent it from crossing the growing distance.

Dark Energy and the Vanishing Universe

The accelerating expansion driven by dark energy makes this separation even more extreme. The cosmological event horizon will continue to expand in the future, but it will eventually approach a maximum distance of about 60 billion light years.

Even then, observers will not be able to see everything within that distance. Light from the most remote galaxies will become stretched to such enormous wavelengths that it will effectively disappear from view.

In about 100 billion years, every galaxy beyond the Local Group of galaxies will fade from sight, forever. Future observers will live in a universe that appears far smaller and emptier than the one we can see today.

In mice, the medications reduced hedonic feeding, which means eating for enjoyment rather than because the body needs energy. The drugs appeared to do this by changing activity in a reward circuit located deep inside the brain.

This newly mapped pathway is separate from the appetite-control systems previously linked to drugs such as semaglutide. Researchers say it may also offer clues about whether GLP-1 medications could eventually be used to address other problems involving reward and craving, including substance use disorder.

Oral Alternatives to Injectable GLP-1 Drugs

The University of Virginia team studied small-molecule GLP-1 receptor agonists. These compounds differ from larger peptide medications such as semaglutide, which is used in well-known drugs including Ozempic, Wegovy, and Rybelsus.

The researchers focused on orforglipron, a Food and Drug Administration (FDA)-approved oral medication, as well as the experimental small-molecule drug danuglipron. Oral compounds of this kind can be taken as pills and may cost less to manufacture than injectable GLP-1 drugs.

“As the accessibility of these medications continues to rise and patient uptake increases, it’s crucial that we understand the neural mechanisms underlying the effects we’re seeing,” said Lorenzo Leggio, M.D., Ph.D., Clinical Director of NIH’s National Institute on Drug Abuse (NIDA).

How Semaglutide and Other GLP-1 Drugs Affect Hunger

Scientists have already studied the effects of larger peptide GLP-1 drugs, such as semaglutide, extensively. Research has shown that these medications reduce hunger-driven eating by acting on networks in the hypothalamus and hindbrain.

Much less was known about what small-molecule oral GLP-1 drugs do after they enter the brain.

To investigate, the researchers used gene-editing techniques to modify GLP-1 receptors in mice, making the receptors more similar to those found in humans.

A Surprising Signal Deep in the Brain

The team gave the mice either orforglipron or danuglipron and then examined which parts of the brain became active.

As expected, the drugs affected regions already associated with appetite regulation. However, they also activated the central amygdala, an area involved in desire and reward.

This region lies deeper in the brain than scientists had previously thought GLP-1 drugs could reach directly.

Additional experiments showed that activation of the central amygdala reduced dopamine release in important parts of the brain’s reward system while the mice were eating for pleasure.

Turning Down the Reward of Food

“We’ve known that GLP-1 drugs suppress feeding behavior driven by energy demand. Now it seems oral small-molecule GLP-1s also dial back eating for pleasure by engaging a brain reward circuit,” said co-corresponding author Ali Guler, Ph.D, a professor of biology at the University of Virginia.

The findings suggest that oral GLP-1 drugs may influence more than physical hunger. They may also weaken the pleasurable reward signals that make certain foods especially tempting.

Researchers now want to determine whether these next-generation medications can reduce cravings for substances other than food. Follow-up studies will specifically examine their possible effects on substance use disorder.

Funding and Regulatory Details

NIH supported this research through the National Institute of Neurological Disorders and Stroke (NINDS) grants R01NS111220, R01NS122834, and R01NS120702, the National Institute of General Medical Sciences (NIGMS) grant R35GM140854, the National Heart, Blood, and Lung Institute (NHLBI) grant R01HL153916, and the National Cancer Institute (NCI) grant P30CA044579.

This study was not completed as a clinical trial associated with an application and has not been assessed by FDA for product approval for stated indications.

Researchers at the University of Nottingham led the INSPIRE clinical trial, which tested inulin, a natural dietary fiber found in chicory root, Jerusalem artichokes, and other vegetables. Taking inulin each day significantly reduced pain among participants with OA.

Published in the journal Nutrients, the findings indicate that supporting gut health could provide a new way to manage a widespread and disabling condition that commonly affects older adults.

A Simpler Approach to Knee Osteoarthritis

Hundreds of millions of people worldwide live with knee OA, which is a major cause of chronic pain and disability, especially later in life. Treatment often involves pain medication, which can produce side effects, or exercise programs that some patients find difficult to continue over time.

“This study raises the exciting possibility that a simple dietary change — adding a fiber supplement to your breakfast or yogurt — could meaningfully reduce pain and improve physical function,” said Dr. Afroditi Kouraki, lead author of the study from the School of Medicine at the University of Nottingham.

How Prebiotic Fiber May Influence Pain

The gut microbiome consists of trillions of bacteria that live in the digestive system and affect many aspects of health, including the way the body experiences pain. Inulin is a prebiotic, which means it provides nourishment for beneficial gut bacteria.

When these bacteria consume inulin, they produce short-chain fatty acids (SCFAs). One of the most important is butyrate, a compound that can affect inflammation and the biological pathways involved in pain throughout the body.

Participants who received inulin had higher levels of both butyrate and glucagon-like peptide-1 (GLP-1) — a gut hormone associated with pain regulation and muscle health. Increased GLP-1 levels were also linked to better grip strength, suggesting a possible connection between gut health and muscle function that researchers believe deserves further study.

Inulin and Physiotherapy Reduced Pain

The six-week randomized controlled trial included 117 adults with knee OA. Participants were divided into four groups that received inulin alone, digital physiotherapy-supported exercise (PSE) alone, both treatments together, or a placebo.

Inulin and physiotherapy each reduced knee pain independently. However, only the inulin group experienced improved grip strength and lower pain sensitivity. These measurements can reflect how the nervous system detects and processes painful signals.

The inulin group also had a much lower dropout rate. Only 3.6% of participants taking the supplement left the study, compared with 21% of those in the physiotherapy group. The difference suggests that adding a supplement to a daily routine may be easier for many patients to maintain than following an exercise program.

Dr. Kouraki said: “Our findings suggest that targeting gut health with a prebiotic supplement is a safe, well-tolerated, and effective way to reduce pain in people with knee osteoarthritis. The very low dropout rate compared to the exercise group is also encouraging from a public health perspective — people were able to fit this supplement easily into their daily lives.”

A Possible Gut-Muscle-Pain Connection

Senior author Professor Ana Valdes from the School of Medicine added: “The link we observed between GLP-1 and grip strength is particularly intriguing and points to a broader gut-muscle-pain axis that warrants further investigation. This could have implications not just for osteoarthritis, but for understanding how gut health influences ageing and physical resilience more broadly.”

Professor Lucy Donaldson, Director of Research at Arthritis UK said: “The pain of arthritis can severely impact quality of life. Our recent lived experience survey showed that six in ten people are living in pain most or all of the time due to their arthritis.

“Researchers are starting to explore the role of the gut microbiome in our experience of pain. This exciting preliminary research highlights how diet and physiotherapy can act in different ways to have benefits for people with arthritis. We know a variety and balance of healthy foods, including fiber, and regular physical activity matter, and we’re glad to be supporting research that explores how they work to help people with arthritis.”

Researchers led by Professor Ryuichi Tatsumi of Kyushu University’s Faculty of Agriculture have identified a molecule that could protect and enhance an important signal involved in muscle repair. The results were published on July 24, 2026, in Scientific Reports.

How the Body Activates Muscle Repair

The research focuses on hepatocyte growth factor, or HGF, a protein that helps initiate the repair of skeletal muscle. Under normal conditions, HGF remains inactive within the structural network surrounding muscle fibers.

When muscle tissue is injured or exposed to mechanical stimulation, HGF is released. It then attaches to c met receptors on satellite cells, the stem cells responsible for maintaining and repairing skeletal muscle. This signal brings the cells out of their inactive state, allowing them to multiply, mature, and help rebuild damaged muscle fibers.

Aging can disrupt this repair system. Previous research from the team found that HGF can undergo a chemical modification known as nitration. During this process, a nitro group is added to two locations on the protein, Y198 and Y250. These sites are located in the same region HGF uses to connect with c met.

After nitration occurs, HGF can no longer attach effectively to the receptor. The researchers compare the damaged protein to a rusted key that no longer fits its lock. This loss of function may be one of the underlying causes of muscle wasting and reduced regeneration in older adults.

“HGF is not necessarily missing as we age,” explains Tatsumi. “Rather, it can be chemically altered after it is made. That led us to wonder whether a compound with strong antioxidant capacity might protect HGF, either by preventing nitration or by compensating for the functional loss it causes.”

Testing Sulfur Based Antioxidants

The scientists investigated two compounds with strong antioxidant properties: glutathione trisulfide (GSSSG) and lipoic acid trisulfide (LASSS). Both are trisulfides, a class of molecules containing three sulfur atoms connected in sequence.

These compounds have attracted growing interest in pharmaceutical research because of their distinctive sulfur chemistry and their ability to participate in redox reactions.

Early experiments showed that both GSSSG and LASSS reduced nitration at the Y198 and Y250 sites on HGF. However, neither compound fully restored the protein’s ability to bind to its receptor.

The researchers then increased the molar ratio of HGF to trisulfide, moving from 1:4000 to 1:8000.

LASSS Creates a Stronger HGF Signal

The higher concentration produced an unexpected result. When HGF was mixed with LASSS, its ability to bind to c met rose to more than twice that of untreated HGF. The protein also became more resistant to the loss of function caused by nitration, particularly at Y198.

This improvement was seen only with LASSS. GSSSG did not produce the same effect.

“This exceeded our expectations,” comments Tatsumi. “We knew trisulfides had diverse biological functions, but we never expected that simply mixing HGF with LASSS would produce such a striking effect.

“What this tells us is that LASSS does more than simply neutralize reactive molecules. It may interact directly with HGF and induce a subtle structural change, creating an enhanced ‘Super HGF’ form that binds c-met more strongly and resists nitration.”

The findings suggest that LASSS may directly alter the structure of HGF in a beneficial way. Rather than acting only as an antioxidant, the compound may create a more active form of the protein that connects more strongly with its receptor while resisting chemical damage.

Promising Results in a Mouse Model

To determine whether the protective effect could also occur in living tissue, the team tested LASSS in mice with muscle atrophy caused by tail suspension.

Mice treated with LASSS before the procedure had significantly lower levels of nitration than untreated mice. Once again, GSSSG did not provide measurable protection. These results indicate that the beneficial effects of LASSS are not limited to laboratory experiments involving isolated proteins.

However, additional studies involving aging animals will be required to determine whether LASSS is safe and effective in vivo.

A Possible Strategy for Preserving Muscle

The discovery could support the development of new approaches for maintaining muscle repair during aging, extended bed rest, and other conditions that involve long periods of inactivity.

The researchers believe the effects of LASSS on HGF may apply across multiple species, including humans and companion animals such as cats and dogs. In the future, the approach could potentially help people maintain strength, independence, quality of life, and a longer healthy lifespan as they grow older.

The findings, published in Nature Microbiology, come from scientists at the Center for Translational Antiviral Research (CTAR). Their work focused on canine distemper virus, which produces a disease in ferrets that closely resembles measles.

Antiviral Blocks Two Routes of Transmission

The researchers tested a recently developed drug candidate called GHP-88310 (described in Science Advances). The medication is a broad-spectrum inhibitor of the viral polymerase, an enzyme the virus needs in order to reproduce.

The team examined whether prophylactic (shortly before or after exposure) use of the drug could prevent transmission through direct contact or shared air. GHP-88310 successfully blocked both forms of spread. When the drug was used to treat animals that were already infected, it also reduced the length of time they remained capable of transmitting the virus.

“Silencing measles outbreaks quickly is essential to reestablish control over the virus,” said senior author Richard Plemper, a Regents’ Professor and director of the CTAR. “This study follows our recent development of the drug candidate GHP-88310. It demonstrates that the drug is suitable to augment traditional ring vaccination against measles.”

Measles Outbreaks Return Across North America

Measles has reemerged in the United States since 2025, causing thousands of infections across several states, hundreds of hospitalizations and three confirmed deaths. Canada and Mexico have also experienced major outbreaks involving multiple deaths, raising concerns about whether North America can maintain its measles elimination status.

“We were very excited to see that GHP-88310 given by mouth completely prevented airborne transmission in our ferret model of measles,” said first author Carolin Lieber, a senior postdoctoral fellow in the Plemper lab. “This finding is unprecedented for a viral polymerase inhibitor and demonstrates the extraordinary antiviral potency of this drug.”

Tests Mimicked Homes and Classrooms

To model realistic transmission conditions, the researchers created a controlled system in which infected and uninfected animals either came into direct physical contact or shared the same airspace without touching.

“We designed the study to recapitulate viral spread between people with direct contact, for instance in a household, and between more distant social contacts, for example in classrooms or other indoor settings that bring people into proximity without direct interaction,” said Plemper. “In addition to this prophylactic benefit, GHP-88310 used therapeutically shortened the duration of disease in our model. If equally applicable to human hosts, it may shorten the severe social and economic burden of prolonged quarantine of patients and further aid outbreak management.”

Drug Candidate Moves Toward Clinical Testing

The researchers are now preparing GHP-88310 for formal clinical trials.

Other contributors to the study included Josef Wolf, Claire Ruckel and Lauren Harrison of the Center for Translational Antiviral Research in the Institute for Biomedical Sciences at Georgia State.

The research was supported by the National Institute of Allergy and Infectious Diseases (NIAID) of the National Institutes of Health (NIH).