The Ebola outbreak of the last few years was particularly tenacious and terrifying. Over 28,000 people were infected by the virus between 2013 and 2016, and over 11,300 died – greater numbers than all other Ebola outbreaks put together.
New research from the University of Nottingham and the University of Massachusetts has shown that the outbreak might have become so deadly because the virus managed to subtly adapt to become even better at infecting humans.
Two independent studies, both published on the same day in the journal Cell (here and here), have detailed that the Ebola virus developed a mutation that allowed it to enter human cells more easily.
“There was this belief that Ebola virus essentially never changes,” Dr Kristian Andersen, from The Scripps Research Institute in California and a co-senior author on one of the studies, 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.”
The researchers studied around 2,000 Ebola genome sequences that had been isolated from victims of the epidemic. They discovered a mutation, known as GP-A82V, changed the glycoprotein that the Ebola virus uses to enter cells. It’s thought the mutation arose early during the outbreak. This mutation made it easier for the virus to enter primate cells, including human cells, but not the cells of other mammals.
“This mutation is not just located in some random location of the viral genome,” study author Jeremy Luban of the University of Massachusetts said in the statement. “Amazingly, it’s located precisely at the tip of the molecule that the Ebola virus uses as a key to unlock and gain entry to human cells.”
Many factors were behind the cut-throat severity of the recent outbreak that ripped through Guinea, Liberia, and Sierra Leone from late 2013 until 2016. The World Health Organization points towards weakened health infrastructure, mobile populations with little to no border control, and cultural beliefs that include West African burial practices. However, this new research suggests that the GP-A82V mutation could have also contributed to the scale of the outbreak.
“I think our study reminds us that if you take a virus and allow it to infect a new host for a considerable amount of time, eventually it may acquire a set of mutations that will benefit it, for example increasing its ability to spread or changing the disease that it causes,” study author Professor Jonathan Ball of the University of Nottingham said in another statement. “In order to be prepared we need to know whether similar things are occurring in other outbreaks such as the ongoing Zika and MERS-coronavirus epidemics.”