‘Slow-living’ animals that reproduce less quickly could be reservoirs of disease



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‘Slow-living’ animal species that reproduce less quickly and live longer could be reservoirs of diseases that jump to humans, a new study finds.

Some species “live fast and die young” with an effort to reproduce, such as rabbits and hares, while other “slow-living species retain more energy to survive, such as badgers, bats. and primates.

Slow-living species also harbor a greater diversity of parasites and pathogens, such as some hantavirus-carrying rodents in parts of North America.

British researchers say animal host survival traits – whether energy conservation or reproduction – can help predict reservoirs of zoonotic diseases and the vulnerability of populations to disease-induced extinctions.

The European badger (pictured) is defined as a slow-living species, which is generally more likely to act as reservoirs of infection that can spread to other species

The European badger (pictured) is defined as a slow-living species, which is generally more likely to act as reservoirs of infection that can spread to other species

Experts have focused on endemic diseases that coexist with host species for long periods of time, as opposed to the current coronavirus pandemic, which is spreading rapidly around the world.

Experts measured what they called demographic competence – the ability of a host species to survive in large numbers while maintaining high levels of infection.

Their study found that slow-living species often have a higher demographic competence for persistent infections.

They are therefore more likely to act as reservoirs of infection that can spread to other species, the study suggests.

Rabbits and hares have a significantly faster life cycle, while bats (pictured) and primates have a significantly slower life cycle than expected for their body size.

Rabbits and hares have a significantly faster life cycle, while bats (pictured) and primates have a significantly slower life cycle than expected for their body size.

“ Wildlife diseases pose a threat to the survival of endangered species around the world, and we know there is a risk of disease spreading between closely related species of wildlife, livestock and humans ” ‘said study author Professor Dave Hodgson at the University of Exeter. .

“These contagion events are known to be influenced by similarities in immune systems and by increasing levels of contact between humans and wildlife caused by the exploitation of natural ecosystems such as tropical forests.

“Our results highlight the potential to use other, more ecological characteristics, such as lifespan, reproductive capacity and population size to identify and predict wildlife reservoirs from which new diseases could emerge.

For their study, the researchers used mathematical models to explore the types of animal species and diseases that are likely to coexist for long periods of time.

The coronavirus (pictured) has drawn attention to rapidly spreading infectious diseases, but the new study - from the University of Exeter - focuses on endemic diseases that coexist with host species for long periods of time.

The coronavirus (pictured) has drawn attention to rapidly spreading infectious diseases, but the new study – from the University of Exeter – focuses on endemic diseases that coexist with host species for long periods of time.

They found that demographic competence is generally higher in hosts whose populations are regulated by survival versus reproduction.

“ In addition to seeing that slow-living species can be reservoirs of infectious diseases, we show a setback that species with low population competence may not be able to coexist with new diseases and therefore might suffer from local or complete extinction ”. said study author Dr Matthew Silk of the University of Exeter.

Dr Silk said there are some differences between species when it comes to calling them fast or slow living – like rodents.

“For their size, rodents are fairly neutral on the fast-slow continuum, maybe more on the fast side,” he said.

“Obviously, many rodents are also important reservoirs of zoonotic diseases, which shows how many factors play a role.”

It is also important to note that the pace of life of the host species is not the only important factor affecting demographic competence.

“The characteristics of the pathogen itself – such as its ease of transmission and its likelihood of killing a host – will also play a key role, as will the social behavior of the host species,” he said.

“We also need to consider the role of immunity – the differences in the immune system that we know exist between fast and slow hosts can influence how long individuals are sick and whether they can be re-infected.

Other relevant factors include population densities and a species’ proximity to humans.

The study was published in the journal Nature Ecology and Evolution.

HOW BATS CAN ACT AS A ‘TANK’ FOR VIRUSES WITHOUT GETTING SICK

A study suggests that molecular mechanisms allow bats to tolerate zoonotic viruses, such as coronaviruses.

Bats act as “ reservoirs ” for many zoonotic viruses, including SARS-CoV, MERS-CoV, Ebola virus, and possibly SARS-CoV-2, the pathogen to the origin of the current coronavirus pandemic.

Aaron Irving, Wang Linfa and their colleagues at Duke-National University in Singapore claim that bats adopt unique strategies to prevent overactive immune responses, which protects them against diseases caused by zoonotic viruses.

The team looked at three species of bats – Pteropus alecto (black fruit bat), Eonycteris spelaea (cave nectar bat) and Myotis davidii (David’s myotis bat).

They have identified mechanisms that balance the activity of key proteins that play a major role in mediating immunity and inflammatory responses.

These mechanisms allow bats to harbor and transmit zoonotic pathogens without triggering the harmful consequences of immune activation, such as symptoms in humans infected with the coronavirus.

One of the mechanisms used by bats is to reduce levels of caspase-1, a protein that triggers a key inflammatory cytokine protein, interleukin-1 beta (IL-1β).

Another mechanism they use hinders the maturation of IL-1β, thanks to a finely tuned balance between caspase-1 and IL-1β.

“Suppressing hyperactive inflammatory responses improves longevity and prevents age-related decline in humans,” said Professor Wang Linfa.

“Our results may offer potential perspectives for the development of new therapeutic strategies capable of controlling and treating human infectious diseases.

The study was published in Proceedings of the National Academy of Sciences.

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