A study published in Nature claims that Myotis bat longevity genes are intimately connected to immune function, offering researchers what they describe as a potential new window into the biology of ageing in mammals, including humans. The paper presents the first genomic analysis of eight Myotis bat species, and its authors argue the findings challenge the assumption that diseases of ageing and diseases of infection are entirely separate problems.
The research was led by Juan Manuel Vazquez, who began collecting bat tissue samples after joining UC Berkeley as a postdoctoral fellow in 2020. Working with Berkeley undergraduates, Vazquez set up mist nets over streams, ponds and rivers across the western United States at night, capturing bats, collecting small biopsy samples, and releasing the animals. He currently holds cell cultures from 259 individuals representing 32 species.
What the Myotis bat longevity genes actually show
The Myotis genus is an unusual research subject. Among the 1,511 known bat species, roughly 139 belong to this group, and closely related species within it can have dramatically different lifespans. One Brandt’s myotis, Myotis brandtii, was banded in Europe and recaptured 50 years later. The black myotis, Myotis nigricans, of South and Central America, lives only about seven years. Vazquez compared that contrast to a hypothetical scenario in which our close relative, Homo neanderthalensis, lived nine times longer than modern Homo sapiens.
The genomic analysis found that longer-lived bats carried higher levels of genes associated with fighting cancer. The results also showed substantial overlap between genes associated with ageing and those involved in disease defence. The company making the broader claim here is the research team itself, and they are careful to frame it as a connection rather than a mechanism: the data show correlation, not a worked-out causal pathway.
‘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.
Damaged cells and an unexpected response
One of the paper’s more concrete findings comes from laboratory work on cultured bat cells. Vazquez exposed cells from bat wing biopsies to toxic chemicals to observe how they responded to severe damage. In the longest-lived bat in his sample, the little brown bat (Myotis lucifugus), the response was not what his team anticipated.
Instead of activating genes that produce DNA repair proteins, the cells increased activity in genes that promote cell death. The cells, in effect, elected to destroy themselves rather than attempt repair. Vazquez noted that elephants, another long-lived, cancer-resistant species, appear to follow the same logic: if a cell cannot be saved, it is eliminated. Whether this represents a general principle or a convergent accident is one of the open questions the paper does not resolve.
Peter Sudmant, a Berkeley associate professor of integrative biology who studies the genetics of ageing and lifespan, framed the broader ambition plainly. ‘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,’ he said.
Myotis bat longevity genes and the virus connection
A second thread in the paper concerns the relationship between longevity genes and viral interactions. Vazquez’s collaborator M. Elise Lauterbur, now at the University of Vermont, had independently identified many of the same genes as ones involved in bat-virus interactions. ‘There is way more overlap than you would expect just by random chance,’ Vazquez said.
The analysis found that Myotis bats carry an unusually large number of genes producing proteins that interact with DNA viruses, such as herpes viruses. Humans and other primates show a different pattern, tending towards genes that interact with RNA viruses, including those responsible for COVID-19 and HIV. That evolutionary mismatch, the authors suggest, may help explain why viruses that bats carry without becoming ill can cause serious disease when they cross into humans.
‘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.’
Vazquez is continuing to investigate the genetic mechanisms behind longevity in a new faculty position at Pennsylvania State University. Sudmant, meanwhile, is examining how bat cells regulate immune responses and is using primate cell cultures to study the relationship between lifespan and DNA repair genes. The work was funded by the National Institutes of Health and the National Science Foundation.
