Scientists discover a completely different way to fight viruses

 

Scientists have uncovered a previously unknown way that sea anemones defend themselves against viruses, revealing that the evolution of animal immune systems may be far more diverse than previously believed. The newly identified defense relies on a protein that closely resembles one of the most important antiviral proteins in humans, yet performs the opposite function while still being essential for protecting the animal from infection. The findings suggest that evolution produced more than one successful strategy for fighting viruses across the animal kingdom.

The research, led by PhD candidate Ton Sharoni and Prof. Yehu Moran at the Hebrew University of Jerusalem in collaboration with scientists from the University of North Carolina at Charlotte, was published in Nature Ecology & Evolution. It challenges the long standing idea that animals inherited a single core antiviral system from a common ancestor and instead points to multiple evolutionary solutions for resisting viral infections.

An Ancient Animal Offers New Clues About Immunity

Viruses have threatened living organisms throughout evolutionary history. In humans and other vertebrates, one of the body's key antiviral defenses depends on a protein called MAVS. When a virus is detected, MAVS helps trigger the immune system so it can respond to the infection.

To investigate how old this defense system might be, the researchers studied sea anemones. These ancient marine animals split from the evolutionary line that eventually led to humans more than 600 million years ago. Because they are close relatives of corals and jellyfish, sea anemones provide scientists with a valuable glimpse into the early evolution of animal immunity.

During the study, the team discovered a previously unknown protein they named CARDIB (CARD Inhibitor Binding protein). At first, CARDIB looked remarkably similar to MAVS, leading researchers to believe it might perform the same antiviral role found in humans.

That assumption quickly fell apart.

"Everything about CARDIB suggested it should function like MAVS," said Prof. Yehu Moran, head of the Department of Ecology, Evolution and Behavior at the Hebrew University. "Instead, we discovered that it does the exact opposite. Rather than activating antiviral defenses, CARDIB normally suppresses them."

A Surprising Protein That Protects by Slowing the Immune System

The discovery immediately raised an important question. Why would an animal deliberately suppress its own immune response?

To find out, the researchers used CRISPR gene editing to remove the CARDIB gene from sea anemones before exposing them to viruses.

The results were unexpected. Sea anemones without CARDIB became much more susceptible to infection. Viruses multiplied more rapidly, the animals failed to properly activate their antiviral defenses, and their ability to fight infection dropped dramatically.

"The results were completely counterintuitive," said Sharoni. "Although CARDIB acts as a brake on the immune system under normal conditions, that brake turns out to be essential for mounting an effective antiviral response."

Overall, the experiments showed that sea anemones rely on an antiviral pathway that is fundamentally different from the one used by humans, even though both systems contain molecular components that look strikingly alike.

Natural Environment Confirms the Discovery

The researchers also wanted to determine whether this newly identified immune pathway mattered outside carefully controlled laboratory conditions.

To answer that question, genetically modified sea anemones were moved from laboratory aquaria into outdoor marine mesocosms supplied with natural estuarine water in South Carolina. This exposed the animals to the wide variety of viruses and microorganisms found in their normal environment.

The difference became obvious within days. Sea anemones lacking CARDIB and related antiviral genes accumulated substantially more viruses than unmodified animals. Researchers also found that one immune gene that appeared only moderately important in laboratory tests became clearly important under natural environmental conditions.

"This demonstrated that the pathway we discovered is not simply a laboratory phenomenon," said Moran. "It plays a crucial role in helping these animals cope with the viral challenges they face in nature."

Multiple Evolutionary Solutions to Fighting Viruses

The findings suggest that evolution did not settle on a single universal antiviral strategy. Instead, different groups of animals may have independently developed distinct molecular systems for detecting viruses and preventing them from spreading.

"Humans and sea anemones both need protection from viruses, but this work shows that evolution can organize those defenses in fundamentally different ways," Moran added.

The research also underscores the importance of looking beyond traditional laboratory animals. Ancient organisms such as sea anemones can preserve evolutionary innovations that would remain hidden if scientists focused only on humans, mice, and other commonly studied species.

As researchers continue exploring the remarkable diversity of life, discoveries like this are revealing that evolution has repeatedly found unexpected ways to solve some of biology's most fundamental challenges.

Journal Reference:

1. Ton Sharoni, Adrian Jaimes-Becerra, Sydney Birch, Hee-Jin Kwak, Daria Aleshkina, Magda Lewandowska, Joachim M. Surm, Hannah Justin, Reuven Aharoni, Adam M. Reitzel, Yehu Moran. An ancient anthozoan protein reveals an alternative evolutionary path of antiviral signalling. Nature Ecology, 2026; DOI: 10.1038/s41559-026-03112-3

Courtesy:

The Hebrew University of Jerusalem. "Scientists discover a completely different way to fight viruses." ScienceDaily. ScienceDaily, 30 June 2026. <www.sciencedaily.com/releases/2026/06/260630020534.htm>. 

 

 

Old muscle stem cells can act young again but there’s a catch

 

Growing older often means recovering more slowly from muscle injuries, but scientists may have uncovered an important reason why.

A new study from UCLA, conducted in mice, found that aging muscle stem cells build up high levels of a protein that slows their ability to spring into action and repair damaged tissue. At the same time, that protein appears to help the cells endure the challenging conditions found in aging muscle.

The research, published in the journal Science, suggests that some biological changes linked to aging may not simply be signs of decline. Instead, they may serve as protective adaptations that help cells survive.

"This has led us to a new way of thinking about aging," said Dr. Thomas Rando, senior author of the study and director of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

"It's counterintuitive, but the stem cells that make it through aging may actually be the least functional ones. They survive not because they're the best at their job, but because they're the best at surviving. That gives us a completely different lens for understanding why tissues decline with age."

Protein Linked to Slower Muscle Repair

The researchers, led by postdoctoral scholars Jengmin Kang and Daniel Benjamin, compared muscle stem cells taken from young and old mice. They found that levels of a protein known as NDRG1 rose dramatically with age, reaching concentrations 3.5 times higher in older cells.

NDRG1 functions like a brake inside the cell. It suppresses a signaling pathway called mTOR, which normally helps drive cell activation and growth.

To determine whether NDRG1 was contributing to slower muscle recovery, the scientists studied mice that had aged naturally to roughly the equivalent of 75 human years. When they blocked NDRG1 activity, the older muscle stem cells quickly regained youthful behavior, becoming more active and improving muscle repair after injury.

The improvement, however, came with a drawback. Without the protective effects provided by NDRG1, fewer stem cells remained alive over time. As a result, the tissue became less capable of regenerating after repeated injuries.

Survival Versus Performance

"Think of it like a marathon runner versus a sprinter," said Rando, who is also a professor of neurology at the David Geffen School of Medicine at UCLA. "The stem cells in young animals are hyper-functioning -- really good at what they do, namely sprinting, but they're not good for the long term. They can make it through the 100-yard dash, but they can't make it even halfway through the marathon. By contrast, aged stem cells are like marathon runners -- slower to respond, but better equipped for the long haul. However, what makes them so proficient over long distances is exactly what renders them poor at sprinting."

The researchers confirmed their results using several different methods. They examined muscle stem cells from both young and old mice in laboratory cultures as well as in living tissue.

Across these experiments, the pattern remained consistent. Higher levels of NDRG1 reduced the cells' ability to rapidly activate and repair muscle, while also increasing their resilience and long-term survival.

A Cellular Survivorship Bias

According to the researchers, the rise in NDRG1 may be driven by what they describe as a "cellular survivorship bias" -- stem cells with insufficient NDRG1 gradually disappear over time, leaving behind a population that survives better but functions more slowly.

"Some age-related changes that look detrimental -- like slower tissue repair -- may actually be necessary compromises that prevent something worse: the complete depletion of the stem cell pool," Rando said.

The researchers compare this phenomenon to trade-offs seen throughout nature. During difficult conditions such as drought, famine, or extreme cold, animals often shift resources toward survival mechanisms like hibernation rather than reproduction. Muscle stem cells may be doing something similar as they age, directing resources away from their reproductive role (making more cells) and toward survival.

"Species survive because they reproduce, but in times of deprivation, animals turn on their own resilience programs," Rando said. "There are a lot of examples in nature of allocating resources to survival under times of stress. It's exactly aligned with what we're seeing at the cellular level."

Implications for Future Aging Therapies

The findings could help guide future efforts to develop therapies that improve tissue repair while preserving stem cell survival. However, Rando cautions that enhancing one aspect of stem cell function may come with unintended consequences.

"There's no free lunch. We can improve the function of aged cells for a period of time, for certain tissues, but every time we do this, there's going to be a potential cost and a potential downside."

The team plans to continue studying the molecular mechanisms that determine how stem cells balance survival and performance during aging.

"This gene is almost like our doorway that we've opened into understanding what controls these trade-offs that are so critical, not only for evolution of species but also for the aging of tissues within an individual," Rando said.

Funding for the study came from the National Institutes of Health, the NOMIS Foundation, the Milky Way Research Foundation, the Hevolution Foundation, and the National Research Foundation of Korea.

Journal Reference:

1. Jengmin Kang, Daniel I. Benjamin, Qiqi Guo, Chauncey Evangelista, Soochi Kim, Marina Arjona, Pieter Both, Mingyu Chung, Ananya K. Krishnan, Gurkamal Dhaliwal, Richard Lam, Thomas A. Rando. Cellular survivorship bias as a mechanistic driver of muscle stem cell aging. Science, 2026; 391 (6784): 517 DOI: 10.1126/science.ads9175

Courtesy:
University of California - Los Angeles Health Sciences. "Old muscle stem cells can act young again but there’s a catch." ScienceDaily. ScienceDaily, 3 July 2026. <www.sciencedaily.com/releases/2026/06/260622014315.htm>.