Immune arms-race in bats may make their viruses deadly to people

Strong immune system may save bats but make their germs harder for humans and others to survive

Egyptian fruit bat hanging upside down

Here’s an Egyptian fruit bat, a species known to sometimes shed Marburg virus, a germ that can be deadly to humans.

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When it comes to viruses, ones from bats can be super-deadly. You might think that would mean bats frequently get ill. In fact, many bats can safely host germs that would sicken or kill other species — including humans. Now a study using cells grown in a lab hints at why viruses from these flying mammals can be so dangerous.

Bats can host a wide variety of viruses with the potential to cause deadly human outbreaks. Among them are the germs that cause Ebola, Nipah and severe acute respiratory syndrome, or SARS. Previous work had suggested a bat’s immune system is uniquely adapted to tolerate viruses. For instance, their infected bodies can limit the ability of that germ to trigger dangerous inflammation. But such defenses may also push viruses to evolve in ways that allow them to rapidly spread from cell to cell. And if that altered virus now spreads to some species lacking a bat-like and strong immune system, the new victim might get super-sick — and maybe super-fast. 

That’s what a team of researchers reported February 3 in eLife.

The study is “an important piece of the puzzle in understanding why viruses [from bats] may be emerging and impacting people and other animals” says Kevin Olival. He’s a disease ecologist for EcoHealth Alliance in New York City. This group’s mission is protecting wildlife and public health from emerging new diseases. One example of such a disease: the killer pneumonia caused by the new coronavirus known as 2019-nCoV. 

“There’s a lot we can learn from bats about their immune system,” Olival says. It would be wise, he says, to “take some of that information to think about our own health.” It might even lead researchers to design better drugs to fight viruses that have been carried by bats, he says.  

Scientists have pinpointed bats as the source of several outbreaks of viral disease in people. Bats are now the leading U.S. cause of rabies. Insect-eating bats may have been the source of the 2014-to-2016 Ebola outbreak in West Africa. Egyptian fruit bats appear to safely carry Marburg virus, which in other species creates a hemorrhage-causing disease similar to Ebola. Other bat species are the reservoirs of SARS-like coronaviruses. There is suspicion that new bats may have at one time hosted at least an ancestor to the 2019-nCoV, which as of February 12 had sickened more than 45,000 people and killed at least 1,100.

For a long while, scientists have puzzled over why bat viruses tend to be so deadly when they infect other animals.

Cara Brook is an ecologist at the University of California, Berkeley. She and her colleagues investigated in the lab how two bat viruses — Ebola and Marburg — might spread after infecting one of three types of cells. One cell type comes from African green monkeys. It lacks a virus-fighting immune response. Cells from the Egyptian fruit bat have an immune response, but only if infected with a pathogen. The last are cells from the black flying fox, a type of bat. These cells appear to be “perpetually trying to fight viruses,” Brook says. 

The team infected these three types of cells with a virus that they tweaked. The tweaks coated the virus with the proteins that either Ebola or Marburg use to enter and infect cells. The researchers then monitored the spread of the test virus among cells. While all of the monkey cells died, more of the bat cells survived. The researchers also used mathematical calculations to estimate the conditions that best described what they were seeing. 

Viruses use their hosts’ cells to copy themselves. In a bat — and exposed to its immune system — the test virus appeared to have a much higher rate of cell-to-cell spread, the researchers found. How quickly the germ spread depended on how fast the lab cells were able to mount an immune response. Another factor that affected spread: the share of cells that were already in a virus-fighting mode when the experiment began.

It’s not good for a virus to kill its host. When the host dies, the virus risks dying off with it. From the germ’s point of view, it would be best if the host survives — at least long enough for the germ to copy itself many, many times and then infect many new hosts. If the host has an immune system that can defend it against rapidly replicating viruses, a virus need to might evolve to spread faster. Then, if and when it gets loose in other species, the virus might be especially virulent (able to sicken quick and widely). 

It’s like an arms race. “If you have an immune response [against the virus], it has to be matched by the virus replicating faster,” Brook says. And if a quick-spreading virus from bats were to infect another species that lacked bat-like defenses? “It would probably cause extreme virulence,” she says. 

More than 1,400 bat species exist, Olival notes. The new study focused on just two of them. In fact, he points out, “other bat species might have totally different responses.” 

And, Olival adds, “Bats are not the only mammal that are reservoirs for [viruses spread to humans by animals].” He wonders how the new findings might apply to other animals that carry deadly viruses, such as rodents. “The question is not only how do bats cope with viruses, but how do other mammal species that are reservoirs cope with the viruses they carry.”

Equally important, Brook emphasizes, “I don’t want people to walk away wanting to kill all the bats.” After all, closely related animals are more likely to spread viruses to one another. Bats and humans are not close relatives. So, she says, “Bat viruses are not likely to spillover to human populations.” But when they do, she notes, it can be very, very bad news.

Erin I. Garcia de Jesús is a staff writer at Science News. She holds a Ph.D. in microbiology from the University of Washington and a master’s in science communication from the University of California, Santa Cruz.

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