The secret to living longer may be hidden in bat DNA

Bats pack an unusual combination of traits into small mammalian bodies. Many live for decades, tolerate infections that can harm other mammals, and show signs of unusual cancer resistance. New genomic work suggests these traits may share part of the same evolutionary foundation.

An international team led by researchers at the University of Vermont and Penn State University built near-complete genomes and primary cell lines for eight closely related Myotis bat species. Their analysis linked viral adaptation, DNA-damage responses, cancer-related pathways and extreme lifespan changes across the group.

The study combined genome-wide searches for natural selection, structural-variation analysis and experiments in living cells.

“Pathogen adaption, longevity, and cancer resistance—they are fundamentally linked,” said Elise Lauterbur of the University of Vermont. “Many of the genes that have adapted to viruses in bats are genes that are also involved in longevity and cancer resistance.”

Using long-read sequencing and Hi-C scaffolding, the team assembled about 98.6% of nucleotides into 22 to 23 chromosome scaffolds per species. Each genome contained about 20,869 protein-coding genes with mammalian counterparts.

The chromosome arrangements were relatively stable, yet each genome contained roughly 6,813 to 8,013 structural variants compared with Myotis myotis. Most were shorter than 10,000 DNA bases and included inversions, duplications and translocations.

Copy-number changes were especially important because extra gene copies can later diversify in function.

“One of the things that copy number variation allows is for diversification of the function of the gene,” Lauterbur said. “So potentially, you now have two things you are good at instead of one.”

The researchers examined proteins that interact with viruses and found a striking split.

In Myotis and other bats, proteins interacting with DNA viruses showed strong enrichment for positive selection. Proteins interacting with RNA viruses did not show the same genome-wide pattern.

RNA-virus-interacting genes instead stood out for copy-number variation. These genes were significantly more likely to have expanded or contracted along the Myotis evolutionary tree.

The team checked the positive-selection pattern against 47 publicly available genomes from non-Myotis bats. Comparisons with several other mammalian groups suggested the bat pattern was unusual.

That points to two evolutionary routes: sequence changes in proteins associated with DNA viruses and gene-copy changes in proteins associated with RNA viruses.

One example centered on PKR, an immune and stress-response protein found across mammals. The team identified Myotis arrangements containing one, two or three copies of the gene.

The ancestral form, PKR2, appears to have been joined by a duplicated version, PKR1, near the root of the Myotis lineage. Both duplicated and non-duplicated forms persisted for tens of millions of years.

Functional tests did not show that having both copies simply produced a stronger antiviral response. When PKR1 and PKR2 were expressed together, they produced an intermediate shutdown of protein translation. Tests with two RNA viruses also failed to show stronger restriction from the combination.

High PKR activity could carry a cost because large doses affected cell viability. The pattern suggests an evolutionary balance between antiviral defense and damage to the bat’s own cells.

The team compared lifespan changes across an evolutionary tree containing more than 1,000 mammals. Bats showed some of the largest and fastest lifespan shifts despite relatively small changes in body size.

Myotis brandtii and Myotis lucifugus ranked in the 99th percentile for rapid lifespan increases relative to their ancestors. Myotis myotis ranked in the 93rd percentile, and Myotis grisescens in the 92nd.

Genome-wide selection tests found that many affected genes belonged to immunity, cancer and aging pathways. Cancer-related pathways were especially enriched in lineages associated with some of the largest lifespan increases.

The researchers examined M. lucifugus more closely. Of 65 genes in one high-fidelity DNA double-strand break repair pathway, 35 showed evidence of selection. Another related pathway contained 21 selected genes out of 37.

The team exposed primary skin cells from five bat species to neocarzinostatin, which causes double-stranded DNA breaks.

At low doses, M. lucifugus was the only species showing reduced cell viability after 24 hours and increased apoptosis, the programmed process cells use to eliminate themselves. At high doses, its cells showed the greatest viability loss and highest apoptosis.

Six hours after treatment, genes involved in stopping the cell cycle and promoting cell death became more active. Genes involved in division, growth and DNA synthesis declined.

Some of the strongest DNA-damage responses overlapped with genes associated with DNA-virus interactions. The connection remained significant when the analysis was limited to genes under positive selection in M. lucifugus.

The overlap supports the idea that antiviral defense and cellular damage control have not evolved independently.

The findings do not reduce bat longevity or cancer resistance to one gene. Instead, they point to overlapping changes involving immune defense, structural variation, DNA repair and cell-death pathways.

That makes bats useful for studying how evolution can reshape several age-related traits at once. The results also caution against assuming that an extra immune gene automatically provides stronger protection.

The nonlethal wing-biopsy method used to build the cell lines and genomes could also make long-term studies easier. Researchers can collect a small tissue sample without killing the animal and use it for genomic and cellular work.

“These are often studied as separate biological problems,” Lauterbur said. “But our results suggest that evolution may be shaping them together.”

For human medicine, the work remains exploratory. The findings identify pathways worth studying, not ready-made treatments. Their value lies in showing how one mammalian lineage linked antiviral defense with systems that also influence damaged cells, cancer risk and lifespan.

These five resources explore the wider evidence connecting bat antiviral defenses, genome evolution, aging and natural cancer resistance.

Bat genomes illuminate adaptations to viral tolerance and disease resistance: Reference-quality genomes from multiple bat species revealed unusually widespread selection in immune genes and identified adaptations affecting viral detection and inflammatory responses. (Nature, 2025)

Genomic and functional adaptations in the guanylate-binding protein GBP5 highlight specificities of bat antiviral innate immunity: Experiments across bat species showed rapid evolution and duplication of the antiviral protein GBP5, linking ancient viral pressures to species-specific immune functions. (PLOS Biology, 2026)

Limited cell-autonomous anticancer mechanisms in long-lived bats: Work with fibroblasts from long-lived bats found elevated p53-linked apoptosis and other unusual stress responses, while also showing that bat cancer resistance is more complicated than a single powerful cell-autonomous defense. (Nature Communications, 2025)

Experimental evidence for cancer resistance in a bat species: Tests across seven bat species found especially strong resistance to malignant transformation in Myotis pilosus and linked that phenotype to altered regulation of several cancer-related genes. (Nature Communications, 2024)

Bats as instructive animal models for studying longevity and aging: This review examines bats as models for healthy aging, covering DNA repair, immunity, inflammation, senescence and other traits that may help explain their exceptional lifespans. (Annals of the New York Academy of Sciences, 2024)

Research findings are available online in the journal Nature.

The original story "The secret to living longer may be hidden in bat DNA" is published in The Brighter Side of News.

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