Publication date: Oct 27, 2020
Now scientists have identified key ways in which bats can harbor these dangerous germs while apparently suffering no ill effects from them, which may reveal ways to deal with these contagions in humans.
In the past 20 years, researchers have discovered that bats host some of the most lethal emerging infectious diseases — including those behind maladies such as Nipah, Hendra, Marburg and MERS — yet the animals only rarely display clinical symptoms from such contagions.
One clue to this mystery was revealed in 2016 when virologist Lin-Fa Wang at Duke-National University of Singapore Medical School and his colleagues discovered that all known bat genomes completely lost the genes encoding molecules known as AIM2-like receptors.
In the new study, Wang and his colleagues introduced the genes for human AIM2-like receptors into bat kidney and immune cells grown in lab dishes.
However, installing AIM2-like receptors in bat cells did not restore other known inflammatory responses, such as activation of the enzyme caspase-1, which plays a central role in mobilizing immune defenses.
The researchers also discovered that in black fruit bats, the cave nectar bat (Eonycteris spelaea), and the vesper bat David’s myotis (Myotis davidii), a protein called interleukin 1 beta that is activated by caspase-1 in humans possessed modifications that made it less active in response to greater caspase-1 activity.
Although the absence of AIM2-like receptors might prove dangerous in some as-yet-unknown way to bats, presumably such a risk is more than offset by avoiding the harm from an overactive immune response to germs, Wang noted.
Instead, to minimize risk of zoonotic diseases from bats, “there are very simple low-tech solutions we could adopt, like reducing the wildlife trade, and reducing contact with bat colonies by not cutting down forests,” Daszak said.
|disease||MESH||emerging infectious diseases|