Ton Sharoni was studying sea anemones when he stumbled onto something that shouldn't have worked. The Ph.D. candidate at the Hebrew University of Jerusalem had identified a protein in these ancient marine creatures that looked, at first glance, remarkably similar to a key component of human immunity. Everything about it suggested it should function the same way. Instead, it did the exact opposite — and that reversal turned out to be the whole point.
Sharoni and his advisor, Prof. Yehu Moran, along with collaborators at the University of North Carolina at Charlotte, have published their findings in Nature Ecology & Evolution. Their discovery challenges a long-held assumption: that the molecular machinery humans use to fight viruses traces back, in some form, to the earliest animals. What they found in sea anemones — creatures that diverged from the lineage leading to humans more than 600 million years ago — suggests evolution found more than one solution to the same problem.
The protein in question, which the team named CARDIB, resembles human MAVS, a protein that activates immune responses when viruses invade. Researchers had assumed this system was ancient, conserved across hundreds of millions of years of animal evolution. But CARDIB doesn't activate anything. It suppresses immune defenses under normal conditions. "Everything about CARDIB suggested it should function like MAVS," said Moran, who leads the Department of Ecology, Evolution and Behavior at Hebrew University. "Instead, we discovered that it does the exact opposite."
The obvious question arose: why would suppressing your own immune system be useful? The researchers used CRISPR gene editing to remove the CARDIB gene from sea anemones and exposed them to viral threats. The results were counterintuitive. Animals without CARDIB became far more vulnerable to infection. Viruses multiplied more easily, antiviral defenses failed to activate properly, and the creatures lost much of their ability to fight back.
"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," Sharoni explained.
The team wanted to confirm this wasn't just a laboratory artifact. They took genetically modified sea anemones from lab aquaria and transferred them to outdoor marine mesocosms in South Carolina filled with natural estuarine water teeming with diverse viruses and microorganisms. Within days, animals lacking CARDIB and related antiviral genes accumulated substantially more viruses than normal anemones. One immune gene that appeared only moderately important in the lab became clearly important in the natural environment. "This demonstrated that the pathway we discovered is not simply a laboratory phenomenon," Moran said. "It plays a crucial role in helping these animals cope with the viral challenges they face in nature."
The broader implication is striking: evolution didn't stick with a single antiviral blueprint. Different animal lineages, separated by hundreds of millions of years, appear to have developed distinct molecular solutions to the same ancient problem. For humans, MAVS acts as an on switch. For sea anemones, CARDIB acts as a brake that somehow makes the whole system work. It's a reminder that the human immune playbook, for all its sophistication, may be just one chapter in a much longer story.