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WASHINGTON, Nov. 3 (Xinhua) -- The Ebola virus gained a genetic mutation that appears to make it better able to infect humans during the West African outbreak that killed more than 11,000 people between 2013 and 2016, two independent teams of researchers said Thursday.
Previously, Ebola is thought to circulate in an unknown animal reservoir and to only rarely cross over into people to cause the devastating outbreak. Scientists believed the virus has had little opportunity to adapt genetically to the human host, according to the studies published in the U.S. journal Cell.
"There was this belief that Ebola virus essentially never changes," Kristian Andersen, a co-author of one of the papers and director of infectious disease genomics at the Scripps Translational Science Institute, said in a statement.
"But this study tells us that a natural mutation in Ebola virus - which occurred during an outbreak - changed infectivity of human cells."
To investigate whether the virus might have changed genetically during the outbreak, the research teams examined the publicly available Ebola virus genomic sequences that had been isolated from victims of the epidemic.
One particular mutation, studied by both groups, were found to emerge early in the outbreak just as case numbers began increasing exponentially.
This mutation, GP-A82V, changes the glycoprotein that Ebola uses to enter cells. Animal cell research showed it increases the virus' ability to enter cells of humans and other primates, but not cells of other mammals.
Jonathan Ball, a virologist at the University of Nottingham and co-author of the other paper, said GP-A82V even decreases the ability of Ebola virus to enter cells from fruit bats, the presumptive animal reservoir for Ebola virus.
Overall, the researchers estimated that the GP-A82V version of Ebola virus caused about 90 percent of infections in the recent outbreak.
"The reports published today provide further insight into possible reasons the outbreak of Ebola virus in West Africa may have been so much larger than previous outbreaks," said Ed Wright, senior lecturer and virologist at the University of Westminster, who was not involved in the studies.
"The studies identify specific changes to the virus' genes that emerged as the outbreak unfolded. It appears the virus was adapting so it could infect human cells more efficiently."
