Before the 2014 outbreak in West Africa, Ebola was long thought to be a virus that primarily impacted bats. But during the recent epidemic, that all changed—killing more than 11,300 people in six countries— because the virus adapted to more effectively target human cells, a new study suggests.

The research, published Thursday in the journal Cell, identified a genetic mutation called GP-A82V that was likely responsible for 90 percent of Ebola cases in the 2013-2016 epidemic. That outbreak led to 28,000 human infections.

“There was this belief that Ebola virus essentially never changes,” Kristian G. Andersen, The Scripps Research Institute (TSRI) infectious disease researcher, said in a news release. “But this study tells us that a natural mutation in Ebola virus—which occurred during an outbreak—changed infectivity of human cells.”

Andersen and his colleagues reviewed a sequenced catalog of viral genomes from 1,438 Ebola cases from the recent outbreak. They noticed a mutation on Ebola’s outer protein, called the glycoprotein, which is significant because mutations in this area can influence a virus’ infectiousness.

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“This receptor-binding domain of the virus has been the same since the first Ebola outbreak in 1976,” Andersen said in the news release. “This is the only time we’ve ever seen a mutation in this domain.”

Researchers observed that GP-A82V surfaced early during the outbreak before the number of illnesses began increasing. The sheer number of Ebola cases during the epidemic made possible spotting such a mutation in humans, they said.

To check their results, researchers observed that when infecting primate cells with the mutation, the virus was better able to infect the animals.

“We think this shows that when you have large outbreaks, of Ebola or other viruses, you could have these events where they may evolve to become more successful in a new host,” first co-author Nathan Grubaugh, a TSRI research associate, said in the release.

Although study authors aren’t sure how GP-A82V may improve Ebola’s ability to target human cells, one hypothesis is the mutation may change amino acids in this receptor-binding area, thereby helping the glycoprotein better fit with the human host receptor.

While researchers plan to study other possible mutations during the recent outbreak, they noted GP-A82V will be eradicated once all Ebola cases with the mutation disappear.

They also plan to study how boosted infectivity may influence mortality rates and a person’s transmission risk.

“We don’t know how these findings translate to Ebola virus infection of complicated organisms, including humans,” Grubaugh said in the release. “For future studies, that will be critically important to find out.”