The last may have not been heard about the dreaded Ebola Virus Disease, EVD, which claimed thousands of lives in West Africa including Nigeria as researchers have identified mutations in Ebola virus that increased ability of the virus to infect human cells during the 2013-2016 Ebola virus epidemics.
The findings have been reported by two independent teams of researchers as reported in Cell. Researchers from the World Health Organisation investigating how to stop Ebola The Ebola outbreak over the last two years had been adjudged the worst that ravaged the region the world has ever seen.
By the end of the epidemic in 2016, more than 28,652 people had been infected and more than 11,325 people were dead. In Nigeria, 20 cases and eight deaths were recorded before the country was declared Ebola free October 20, 2014.
Mutations: The new study which investigated whether the virus might have changed genetically in response to infection of such large numbers of people, found mutations of the gene that encodes the Ebola virus glycoprotein increased the virus’ ability to infect cells of humans and other primates.
By increasing infectivity in human cells, it is possible that these mutations increased Ebola virus spread during the outbreak.
Human disease outbreaks A co-author of one of the papers and Professor at the University of Massachusetts Medical School, Jeremy Luban, in the new research explained that: “Ebola virus is thought to circulate in an unknown animal reservoir and to only rarely cross over into people. When the virus does cross over, the effect has been devastating to those people who are infected. Until recently, the human disease outbreaks have been short lived, and the virus has had little opportunity to adapt genetically to the human host.”
Also reacting to the findings, a virologist at the University of Nottingham and co-author of the other paper, Jonathan Ball said: “If you introduce a virus into a new host, like humans, it may need to adapt to better infect and spread in that host.”
One particular mutation, studied by both groups, emerged early in the outbreak just as case numbers vastly increased and soon became the dominant virus type circulating in the outbreak.
Ball added that the Ebola virus mutations did not increase the ability of Ebola virus to infect cells from other mammalian species, including the presumed natural host of Ebola virus.
“We found that, as Ebola virus was spreading from human to human, it apparently didn’t have to worry about maintaining its infectivity in bats,” Ball stated.
The research teams are continuing their work to learn more about how these specific mutations made the Ebola virus more infectious for human cells. “It’s important to understand how these viruses evolve during outbreaks,” says Luban. “By doing so, we will be better prepared should these viruses spill over to humans in the future.”