During the West African outbreak which killed more than 11,300 people between the years of 2013 and 2016, the Ebola virus mutated to more effectively infect human cells, reports now state.
This is the finding of two teams who published studies on Thursday in Cell, a scientific journal. The virologists were able to identify a mutation that changed a part of the virus which fits into "receptors on the exterior of the host cell," as the Washington Post notes.
Ebola evolved into deadlier enemy during the African epidemic https://t.co/c3sutizh83Jeremy Luban, a virologist at the University of Massachusetts Medical School and a lead author on one of the studies, shared that mutant versions of the molecular key were "better at fitting into the lock and got into the cell better." He states that once inside the cell, the virus could act by hijacking its "reproductive machinery and begin making copies of itself." Following the first appearance of the mutated strain, it was clear that it dominated the epidemic. It's reported that at least 90 percent of those who were infected had contracted the mutant strain of the virus.
— NYT Science (@NYTScience) November 4, 2016
"It's very difficult to prove that a mutation like this is responsible for the severity of the epidemic.... But it would have to be a pretty amazing coincidence," Luban said.
The most recent outbreak of Ebola began in Guinea in late 2013 and was the largest in history. There were 100 times more people that were infected than in the previous outbreak which meant that the virus had a never- before- seen level of opportunity to evolve and mutate. During the outbreak which infected 28,000, it was suspected that the virus would pick up such a mutation that would assist it in infecting more people, just as was discovered. This is how it reproduced and the natural selection assisted in its spread.
The Washington Post shares why it was difficult to detect the mutations while the outbreak was occurring.
"... early analyses of new mutations in the Ebola genome didn't identify any that appeared to be adaptive. And there were plenty of nonbiological factors to explain the intensity of the outbreak, particularly the poor public health infrastructure in the hardest-hit areas and the delayed international response."Jonathan Ball, a lead author of an additional paper and a professor at the University of Nottingham in the U.K., stated "as virologists we weren't really convinced. We thought... some of these changes might be affecting the biology of how the virus behaves."
Ball had colleagues reconstruct the tree of evolution of the Ebola virus and pinpoint the places that the pathogen adopted a genetic change. They noticed one specific mutation- including a single nucleotide change on a gene that was responsible for building the glycoprotein "key"- which appeared persistent.
How Ebola got so deadly https://t.co/BsRRs4aRKIThe Ebola virus is so dangerous that it's rarely experimented on in labs, yet Ball's team attached the discovered mutant glucoprotein to a different virus and tested its ability to take over and infiltrate the host cells. They discovered that the mutant was more efficient at infiltrating the cells of humans as well as other primates when compared to the standard version of the virus. However, the mutant virus was less able to infect the cells of bats, which is presumed to be the animal that harbors the Ebola virus between outbreaks in humans.
— TIME (@TIME) November 3, 2016
"Once it's in humans, that's the new host," Ball said, "It's really got to acquire adaptations and get the most fit for in human-to-human transmission." And that's what it appears the Ebola virus did.
Luban shares his conclusions on the findings he and his team made during this attempt to determine as to whether the virus had in fact mutated.
"We think that the mutation is actually an adaptation to humans. It's kind of a signal to us that this mutation was selected for by replication of the virus in people, which I would argue is further evidence that this mutation is significant and is not just a coincidence."[Feature Image by John Moore/Getty Images]