What doesn't kill you makes you stronger
Bats have been identified as natural reservoirs for viruses that have wreaked havoc in humans. These include rabies, Hendra, Nipah, Ebola, MERS and SARS, all of which have the potential to cause high morbidity and mortality in humans. How bats are able to live with these viruses with no obvious symptoms of infection has recently become the intrigue of scientists.
By scrutinizing the immune pathways of bats and observing how viruses respond to this at the cellular level, Cara Brook, lead author and a Principal Investigator with Bat OneHealth, together with her colleagues, have begun to unravel how the remarkable antiviral defenses in bats cells have pushed viruses that have evolved with bats to replicate faster. It is this rapid replication that causes severe damage in other species that have not evolved to cope with these viruses.
In most mammals, a viral infection would trigger an inflammatory response, which in turn sets off associated immune responses to limit the damage of an infection to host tissue. Inflammation can often have debilitating impact on the host, as anyone who has suffered the cold or flu would know. But bats are able to cope with inflammation. Scientists suspect that this could have resulted from the need to manage the metabolic stress associated with flight. Flying is so metabolically expensive, that bats are almost always in a near state of starvation. Most mammals would not be able to endure the daily demands of foraging, hunting, and staying warm while starving but bats seem to be able to manage this thanks to this impressive adaptation.
The authors explain that this mechanism could have enabled bats to live with a constant load of viruses in their bodies. Consequently, the constant challenge of replicating within a host with such a competent immune system has pushed viruses to replicate faster. These are the viruses that could pose the greatest challenge for cross-species pathogen emergence should they spillover into other species with less competent immune systems.
Relevant papers: