Bats are biological oddities: they harbour dangerous viruses without becoming ill, rarely develop cancer, and live far longer than their size predicts. Research decoding Myotis bat genomes reveals how those traits are genetically intertwined.
Scientists assembled and analysed the genomes of eight Myotis species, publishing in Nature.
Why bat longevity is genuinely strange
Across mammals, body size predicts lifespan reasonably well — larger animals generally live longer. Small mammals with fast metabolisms typically live a few years.
Bats violate this comprehensively. Some Myotis species live for decades at the weight of a small mouse, making them among the most extreme longevity outliers in mammals relative to size. They also fly, which imposes enormous metabolic demand and generates oxidative stress that should, by conventional ageing theory, shorten life rather than extend it.
The viral pressure argument
The genomic analysis found a genome-wide over-representation of positive selection in genes interacting with DNA viruses, and elevated copy-number changes in genes tied to RNA viruses.
Positive selection means these genes have been under sustained evolutionary pressure to change — the signature left by a long arms race. Copy-number expansion means the genome carries multiple versions of a gene, generally increasing the capacity of whatever it does.
One example is striking: the antiviral gene EIF2AK2 (PKR) appears in multiple copies in some Myotis bats, versus a single copy in most mammals. PKR detects viral genetic material and shuts down protein synthesis in response — a blunt, powerful defence. Having several copies suggests a lineage that has been fighting viruses hard for a very long time.
Why the three traits connect
“Pathogen adaptation, longevity, and cancer resistance — they are fundamentally linked,” said lead researcher Elise Lauterbur of the University of Vermont, whose team worked with Penn State.
The connection is not coincidental, and it is the paper’s central claim. Many virus-adapted genes also function in longevity and tumour suppression, because the underlying problems overlap. Detecting foreign or abnormal nucleic acid is relevant to both viral infection and to the genomic instability preceding cancer. Deciding whether a damaged cell should be repaired or destroyed is relevant to infection control, cancer prevention and tissue ageing simultaneously.
An immune system tuned by constant viral pressure toward exceptional vigilance may, as a side effect, be exceptionally good at eliminating cells on their way to becoming tumours — and at maintaining tissue quality over decades.
The chemotherapy observation
Little brown bats also showed unusual DNA-damage responses to high doses of chemotherapy drugs.
This is an informative experiment. Chemotherapy works by inflicting DNA damage severe enough that cells die, and how a cell responds — attempting repair, entering senescence, or self-destructing — reveals how its damage-response machinery is calibrated. Bat cells behaving unusually under that stress indicates their calibration genuinely differs from other mammals, rather than merely their gene sequences differing.
How the study was done
A methodological detail worth noting: tissue was sampled via gentle wing biopsies rather than by harvesting organs.
Wing membrane heals well in bats, so a small punch biopsy allows genomic material to be collected from a living animal that is then released. For a study spanning eight species, several of which face conservation pressures, that matters both ethically and practically — it makes sampling across wild populations feasible in a way lethal collection would not.
What this is and is not
This is comparative genomics: identifying which genes differ between species and inferring function from that pattern. It is a powerful way to generate hypotheses and a weak way to establish mechanism.
Signatures of positive selection indicate a gene mattered evolutionarily, not what it does now or whether it contributes to the trait of interest. Extra copies of an antiviral gene are suggestive rather than demonstrative, and the leap from “these genes are unusual in long-lived bats” to “these genes cause the longevity” requires functional work that has not been done.
Why it is worth doing anyway
The practical value is not in copying bats but in learning which pathways nature has already optimised. Evolution has run the experiment of building a small mammal that resists viruses and cancer while living for decades, and the genome is a record of which solutions worked.
Why bats matter for pandemic research too
The same biology that makes bats interesting for ageing research explains their recurring role in emerging infectious disease, and the connection is worth stating carefully.
Bats host a wide range of viruses without becoming visibly ill, which is what the genomic signatures in this study describe: an immune system tuned to tolerate viral presence rather than to eliminate it at any cost. Tolerance is a genuinely different strategy from resistance, and it has consequences.
An animal that survives infection without severe illness can carry a virus longer and shed it while behaving normally. Combined with bats living in dense colonies and, uniquely among mammals, flying long distances, that makes them effective reservoirs.
Understanding the molecular basis of that tolerance therefore serves two purposes at once — identifying pathways that might inform human ageing and immunity, and clarifying why certain viruses persist in these populations. The genes are the same; the questions asked of them differ.
That narrows an otherwise unbounded search space for human ageing and cancer research. It is basic science — the kind that seeds therapeutic ideas rather than producing them. Research news, not medical advice.