Ebola adapted to target human cells during the 2013-16 epidemic

Ebola Virus

A new study from The Scripps Research Institute (TSRI) suggests that Ebola virus gained a genetic mutation during the 2013-16 epidemic, which might have helped it better target human cells.

The research is published in the journal Cell. The new study accompanies a second paper in Cell led by an independent group of scientists at The University of Nottingham.

Scientists Spot Key Mutation

For the new study, researchers used a sequence catalog of viral genomes previously generated from 1,438 of the more than 28,000 known Ebola cases during the recent outbreak.

The new study in Cell is therefore an unprecedented approach to studying Ebola virus.

Every previous outbreak had been relatively small, so researchers had never before been able to examine the genomes from this many Ebola cases.

As they sorted through these sequences, a mutation on a site on Ebola’s outer protein, called its glycoprotein, caught the scientists’ attention.

Because the glycoprotein of Ebola virus binds to its receptor on host cells, mutations in that site can affect a virus’s ability to infect.

The researchers found that the version of Ebola virus carrying the mutation, called GP-A82V, emerged early in the epidemic before Ebola virus cases began increasing exponentially.

Overall, they estimate that the GP-A82V version of Ebola virus caused about 90 percent of infections in the recent outbreak.

Adapting to Human Hosts

Next, the scientists tested GP-A82V’s reaction to many types of animal cells and found that the mutation specifically helps the virus infect primate cells.

The researchers believe the size of the outbreak made detecting this kind of mutation more likely.

Scientists suspect that Ebola normally lives in bats–but with more human hosts, the virus had more opportunities to adapt to humans.

The researchers are not sure exactly how this mutation boosts the virus’s ability to enter human cells.

One hypothesis is that the mutation shifts nearby amino acids in the Ebola virus receptor binding domain, helping the glycoprotein better fit with the human host receptor–like a key in a lock.

Importance for Future Outbreaks

The researchers emphasized that the GP-A82V form of Ebola virus is most likely no longer a threat.

However, the findings are important because they answer the question of whether Ebola virus can gain mutations during outbreaks that can potentially change the function of viral proteins.

The researchers also see this study as an example of how genome sequencing can help researchers respond more quickly to epidemics and tailor therapies to the specific strain of a virus active in an outbreak.

The next steps will be to examine other mutations that showed up during the recent outbreak.

The researchers would also like to see if increased infectivity changes mortality rates and the likelihood of a person transmitting the disease.

Follow Knowridge Science Report on Facebook, Twitter and Flipboard.

News source: The Scripps Research Institute.
Figure legend: This Knowridge.com image is credited to NIAID.