Bats stand out among mammals for their ability to fly, their unusually long lifespans, and their rare incidence of cancer. A new study published in Nature, led by researchers at the University of Vermont and Penn State University, suggests the bat immune system may be central to that combination.

The international team found that the roots of bats’ long lifespans and cancer resistance trace back to how their DNA encodes genomic changes in response to pathogens. “Pathogen adaption, longevity, and cancer resistance—they are fundamentally linked,” said Elise Lauterbur, co-lead author of the study. “Many of the genes that have adapted to viruses in bats are genes that are also involved in longevity and cancer resistance.”

By analyzing bat genomes and running experiments on cultivated cells to simulate disease response, researchers traced how eight species of Myotis bats, one of the largest bat groups, evolved after past pathogen exposure. Screening for positive selection, or adaptation to viruses, revealed gene duplications and deletions, along with a key divergence from humans: people show strong selection for proteins that respond to RNA viruses like SARS-CoV-2 and influenza, while bats show outsized selection for proteins responding to DNA viruses like hepatitis B and herpes. That mismatch could leave both species vulnerable to disease spillover between them. The team also found bats carry a distinctive gene-copying mechanism for DNA repair, a process tied to longevity and resistance to age-related disease.

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To build the underlying genomes, the team collected wing tissue from Myotis bats in the American West using a biopsy method developed by co-lead author Juan Manuel Vazquez, avoiding the need to harvest organs. “Here is a way to do science for any animal on earth that doesn’t require killing the animal and is in fact compatible with better science,” Vazquez said. 

The researchers zeroed in on PKR, an antiviral gene present as a single copy in nearly every mammal but found in one, two, or three copies in various Myotis bats. Experiments splicing extra PKR copies into cells, then exposing them to a pox virus and a chemotherapy drug, showed that little brown bats, the longest-lived of the group, responded to high-dose damage by killing off affected cells. “The little brown bats start committing to kill off cells,” Vazquez said, describing it as a way of discarding cells that can’t be repaired. 

While the researchers caution it’s too early to apply these findings to human medicine, Vazquez said the results point to shared biological systems worth studying together. Lauterbur said she next wants to explore other underappreciated genetic adaptations, including gene copy number changes.