Blamed for the Corvid-19 coronavirus outbreak, bats have been receiving some bad press. With an unusually low inflammation response that lets them incubate viruses, new research shows that it might not be the bat, but their unique immune system that is probably the culprit.
Emerging infectious diseases or EIDs pose a significant threat to public health and in more recent years have emerged with increasing frequency.
The vast majority of the latest EIDs are zoonotic in nature, meaning they have been transmitted from an animal that happily hosted them to another species, such as a human, where they proved deadly.
Not all zoonotic diseases are created equal and they vary in the severity of the disease when transferred to a human as well as their capacity, once transferred from an animal, for sustained human to human transmission.
Bats cause challenges as they are able to carry many viruses that have the potential to cause serious diseases in people. These include rabies, Ebola, Nipah and SARS. What's interesting is that the bats rarely get sick from these viruses that can prove deadly to humans and other animals.
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New research published this week in the journal eLIFE is helping scientists to understand what's so special about bats that means they can safely host these diseases and how bats might actually be helping viruses to become more deadly to other animals.
The study took two bat viruses, Ebola and Marburg, and used them to infect three types of cells in a lab. Two of the cell types were from different species of bats and the other was from an African green monkey.
After infection, the researchers monitored the spread of the virus across the cells to see how quickly they could pass the infection on as well as what happened to the cells that were infected.
Using these experimental results the researchers were then able to apply mathematical simulations to calculate how quickly the two viruses would infect other cells within both bats and monkeys.
They found while the spread occurred much more quickly in the bat cells, most of the cells survived whereas although the spread was slower across the monkey cells, all of the cells were completely destroyed.
The reason for this seems to be the unique molecular mechanism that bats possess in their immune system. In the event of a virus attack, bats and humans produce a signalling molecule called interferon-alpha, however, in bats its production is super-fast. This rapid signalling means that the other cells in a bat can quickly go into a defensive antiviral state, which allows the bat cells to resist the viral onslaught. Monkey cells, like human cells, don't possess this high-speed ability and are quickly overwhelmed and die.
Although their high immune response hinders the viruses ability to kill bat cells, it also seems to benefit the virus by allowing it to remain in the host's system for long enough that it can adapt to its over-defensive state. This gives the virus time to ramp up its replication rate without causing damage to the bat, allowing it to adapt and change through mutations. These amped-up mutated forms of the virus can be much more deadly if they jump to a different host, such as a human, whose slower interferon-alpha response hasn't been exposed to them before.
These new results show the importance of the signalling protein interferon-alpha as well as how unique features of the bat's immune system help to protect it. Who knows, maybe the bat that caused this could also be the key to finding antiviral medications for humans in the future.