Bats’ remarkable ability to withstand decades of strenuous flight while keeping infections, inflammation, and cancer in check may offer new clues to healthier human aging
Bats are unusually long-lived for animals of their size. Small mammals generally burn energy quickly and die relatively young, yet some bats survive for several decades. Brandt’s myotis, Myotis brandtii, holds the bat longevity record after one individual banded in Europe was found alive 50 years later.
That biological puzzle fascinated Juan Manuel Vazquez when he was a graduate student at the University of Chicago. At the time, too few high-quality bat genomes were available to explain why some species age so slowly. After joining UC Berkeley as a postdoctoral fellow in 2020, he began building the biological collection needed to investigate the question himself.
With help from Berkeley undergraduates, Vazquez traveled across the Western U.S., stretching mist nets above streams, ponds, and rivers after dark. The researchers collected tiny wing biopsies from captured bats before releasing them, concentrating on species in the genus Myotis.
Bat Genomes Reveal a Longevity Link
In a study published in Nature, Vazquez and his colleagues analyzed the genomes of eight Myotis species. Their comparison linked longer lifespans with stronger representation of genes involved in immune defense and cancer suppression.
The connection suggests that healthy aging and resistance to disease may be different outcomes of the same biological machinery. An immune system that remains effective without producing uncontrolled inflammation could help an animal eliminate infections, remove dangerous cells, and limit the gradual tissue damage associated with aging.
“Bats evolved to live for a long time without getting diseases, which suggests that we don’t necessarily need to look at diseases of aging and diseases of infection as completely separate fields,” Vazquez said. “We can look at these bats and try to understand how, in the same way you can improve your immune system to fight off viruses, maybe you can improve your immune system so it doesn’t decline in old age. Or maybe bats can help us find ways to fight off tumors so our immune system doesn’t get tired, and that can also help us deal with other stresses of life and not exhaust our immunity.”
This approach addresses a larger evolutionary mystery sometimes called Peto’s paradox. Animals with more cells and longer lives should, in theory, accumulate more cancer-causing mutations. Yet species such as bats, whales, and elephants have evolved defenses that prevent their size or longevity from producing the expected surge in cancer.
Damaged Cells Face a Swift End
To examine those defenses directly, Vazquez grew cells collected from bat wings. (He currently has cell cultures from 259 individuals representing 32 species.) He then exposed the cells to toxic chemicals that cause severe damage.
Cells from the little brown bat, Myotis lucifugus, responded in a strange way. Instead of increasing the activity of genes responsible for DNA repair, they activated genes that promote cell death. Rather than risk repairing and preserving a dangerously damaged cell, the bat’s biology appeared to favor eliminating it.
“We found the literal opposite of what we expected if you treat the bats with a lethal dose of this chemical,” he said. “The longest-lived bat in North America decides, ‘I can’t save this ship,’ and immediately switches gears to prioritize killing off the cells that are damaged. The elephant, another cancer-resistant species that is long-lived, has the exact same strategy—if you can’t save the cell, kill the cell.”
This cellular self-destruction, known as apoptosis, is one of the body’s main safeguards against cancer. A damaged cell that continues dividing can pass mutations to its descendants, while a cell that destroys itself removes that threat before a tumor can develop.
Nature’s Solutions to Healthy Aging
The finding shows why the diversity of animal life can serve as a library of potential solutions to human disease, according to Peter Sudmant, a UC Berkeley associate professor of integrative biology who studies the genetics of aging and longevity.
“By looking across the diversity of life and the remarkable longevities of different species, we hope we can better understand the interplay between DNA damage and the immune system to enable us to have full and healthy life spans,” Sudmant said.
“If you start looking at long-lived species like elephants, whales, and bats, you start finding ways that nature has actually already resolved a lot of these problems in human health,” Vazquez added.
Bats have had roughly 60 million years to refine those solutions. Today, they account for about 20% of all mammal species, inhabit every continent except Antarctica, and occupy ecological roles ranging from insect hunters and pollinators to fruit and nectar feeders.
A Remarkable Range of Lifespans
Scientists have identified 1,511 bat species, including about 139 in the genus Myotis. That single genus contains an extraordinary natural experiment in aging because closely related species can have dramatically different lifespans.
Brandt’s myotis can live for half a century, while the black myotis, Myotis nigricans, of South and Central America survives for only about seven years. Vazquez compared the gap to an imaginary situation in which our close relative, Homo neanderthalensis, lived nine times longer than modern Homo sapiens.
Comparing close relatives is especially useful because many aspects of their biology are similar. Differences in lifespan are therefore easier to connect with specific genes, immune pathways, or cellular responses than they would be in comparisons between distantly related animals.
The demands of flight may have helped shape these unusual defenses. Flying requires an enormous and sustained release of energy, which can expose cells to metabolic stress. Vazquez likens a bat’s nightly search for insects to running several ultramarathons every day.
Powerful Immunity Without Runaway Inflammation
Bats also live with immune systems that appear unusually active. They can host a remarkable assortment of viruses while avoiding the damaging inflammation that would make many other mammals seriously ill.
A weak immune response can allow an infection or tumor to spread, but an excessive response can injure healthy tissue. Bats appear to have evolved ways to maintain potent antiviral defenses while keeping inflammation under tight control.
“Bats have evolved this incredible fitness capacity, this incredible ability to deal with disease, and this incredible ability to be able to prevent cancer,” Vazquez said. “That means that, by understanding how bats have evolved to do all these things that other mammals haven’t, we can find completely new and unexpected ways of dealing with the normal things that cause human diseases.”
Whenever Vazquez identified a bat gene associated with lifespan, collaborator Elise Lauterbur, then at the University of Arizona, had independently connected the same gene with interactions between bats and viruses.
Longevity Genes Double as Viral Defenses
“There is way more overlap than you would expect just by random chance between the genes that are associated with longevity and genes that are associated with viral interactions,” Vazquez said.
Another unexpected pattern involved the type of viruses that appear to have shaped bat evolution. Myotis bats possess an enhanced abundance of genes encoding proteins that interact with DNA viruses, including herpesviruses. Some of these proteins can help viruses infect cells, while others strengthen defenses by increasing the expression of interferon, a hormone central to antiviral immunity.
“DNA viral interacting proteins were strongly enriched for selection in bats in contrast to most other mammals, where there is a very strong enrichment for selection for both DNA and RNA viral interacting proteins,” Sudmant said.
Why Bat Viruses Can Be So Dangerous
Unlike bats, humans and other primates have more genes that interact with RNA viruses, including HIV and the virus that causes COVID-19, than with DNA viruses.
The mismatch between human and bat immune evolution could help explain why some viruses cause severe disease after crossing between the two groups. A virus adapted to one host’s defenses may behave very differently when it enters another species with unfamiliar immune vulnerabilities.
“Humans and bats are badly suited to each other,” Vazquez said. “That is one of the reasons why we have to be careful working with bats—it’s a two-way street for zoonoses. We don’t want to give the bat something, and we don’t want to get something from the bat. That mismatch is definitely something we should look into more.”
Protecting Viral Targets Without Harming DNA
People can acquire infections from wildlife, but humans can also introduce pathogens into bat populations. Careful handling protects researchers as well as animals already threatened by habitat loss and infectious diseases.
Vazquez, now a faculty member at Pennsylvania State University, continues to investigate the genetic regulation of longevity using cultured bat cells. Sudmant is focusing more closely on how cells balance antiviral activity with protection of their own DNA.
“One thing that I’m really excited about is the trade-off between how a bat protects itself by producing proteins that attack the genomes of viruses but also protects its own genome from being attacked by those proteins,” Sudmant said.
A defense powerful enough to destroy viral genetic material can also threaten the host’s own genome if it is not precisely controlled. Understanding how bats manage that risk may reveal strategies for preserving immune strength without accelerating cellular damage.
Sudmant is also studying cell cultures from numerous primate species to explore the genetic basis of longevity and its relationship with DNA repair.
Reference: “Insights into longevity and virus-driven adaptation from Myotis bat genomes” by Juan M. Vazquez, M. Elise Lauterbur, Saba Mottaghinia, Léa Gaucherand, Sarah Maesen, Michael Singer, Sarah Villa, Melanie Bucci, Devaughn Fraser, Genavieve Gray-Sandoval, Zeinab R. Haidar, Melissa Han, William Kohler, Tanya M. Lama, Amandine Le Corf, Clara Loyer, Dakota McMillan, Stacy Li, Johnathan Lo, Carine Rey, Samantha L. R. Capel, Kathleen Slocum, Melissa Sui, William Thomas, Janet Debelak Tyburec, Rachel Brem, Richard Miller, Michael Buchalski, Jose Pablo Vazquez-Medina, Sébastien Pfeffer, Lucie Etienne, David Enard and Peter H. Sudmant, 26 August 2026, Nature.
DOI: 10.1038/s41586-026-10932-7
This study was funded by the NIH/National Institutes of Health and the U.S. National Science Foundation.
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