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African straw-colored fruit bat may not be responsible for Ebola outbreak
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A recent analysis revealed that African straw-colored fruit bats may have evolved to resist Ebola virus infection, leading researchers to suggest these bats are an unlikely source of infection responsible for the 2014 Ebola outbreak in West Africa.
“We found that a very small sequence change in the NPC1 gene in African straw-colored fruit bats can make this type of bat seemingly resistant to Ebola,” Kartik Chandran, PhD, associate professor of microbiology and immunology and the Harold and Muriel Block Faculty Scholar in Virology at Albert Einstein College of Medicine, told Infectious Disease News. “This is the type of genetic signature that you might expect to see in a viral reservoir host. Looking for signatures like this and linking them to Ebola in other kinds of animals could give us some hint as to what the reservoirs might be.”
In a previous study, Chandran and colleagues discovered Ebola virus infects cells by attaching its surface glycoprotein (GP) to the host cell receptor NPC1.
Kartik Chandran
The researchers extracted cells from four bat species, including the African straw-colored fruit bat (Eidolon helvum), the hammer-headed fruit bat (Hypsignathus monstrosus), Büttikofer’s epauletted fruit bats (Epomops buettikoferi) and Egyptian rousettes (Rousettus aegyptiacus), and exposed them to seven filoviruses. African straw-colored fruit bats, which are commonly hunted for bushmeat in West Africa, were the only species that appeared to resist infection, according to the researchers.
To determine whether a defect occurred at the viral entry step, an expanded panel of kidney fibroblast cell lines from all four species were exposed to vesicular stomatitis viruses (VSV) bearing GPs spikes from the filoviruses. Infection was “substantially reduced” in the African straw-colored fruit bat cells for VSVs bearing the Ebola GP, the researchers wrote. They also found that the bats were somewhat resistant to Bundibugyo virus, another filovirus associated with human disease outbreaks.
“We mapped this resistance to a single amino acid change in the NPC1 gene of this bat,” Chandran said in a press release. “This tiny change prevents Ebola from binding to the NPC1 receptor.”
In contrast, infection was enhanced in bat cells that were genetically engineered to express human NPC1.
“Taken together, these findings indicate that [Ebola virus] infection is reduced in African straw-colored fruit bat cells because of a specific molecular incompatibility between the [Ebola virus GP] and the filovirus entry receptor,” Chandran and colleagues wrote.
Further investigation revealed the amino acid change in NPC1 occurred at residue 502 in the central region of the gene.
The researchers then screened a panel of mutants in the NPC1 region to determine whether a viral mutation could counteract the resistance. They found a single mutation at V141A in Ebola virus GP strengthened infectious activity in the straw-colored fruit bats. No known Ebola virus contains the V141A mutation; however, other viruses that cells from straw-colored fruit bats were susceptible to, including Sudan virus, contained this mutation.
“Those viruses already had the amino acid change that allowed the mutated Ebola virus to infect straw-colored fruit bat cells, so they didn’t have any problem binding to the different NPC1 receptors,” Chandran said in the release.
The researchers hypothesized the evolution of NPC1 in bats was driven by a co-evolutionary “arms race” between bats and filoviruses. A genomic analysis of NPC1 sequences in 13 bat species indicated the gene underwent positive selection to resist infection.
“We discovered that a gene segment derived from a filovirus found its way into some bat genomes at least 25 million years ago,” Chandran said in the release.
The evolutionary time span was almost twice as long as previously estimated, roughly 13 million years ago, according to the researchers. – by Stephanie Viguers
- References:
- Herbert AS, et al. mBIO. 2015; doi: 10.1128/mBio. 00565-15.
- Ng M, et al. elife. 2015; doi: 10.7554/eLife.11785.
Disclosure: The researchers report no relevant financial disclosures.