A genetic mutation may have helped the Ebola virus infect humans during the 2014 outbreak in West Africa, the New York Times reports.
Two studies appearing in Cell this week found that the virus became better adapted to human hosts, despite a 2015 Virology paper suggesting that the virus hadn't changed significantly.
In one of the new studies, researchers led by University of Massachusetts Medical School's Jeremy Luban focused on a mutation, GPA82V, that came about early in the outbreak and became highly frequent. The mutation affects a glycoprotein at its NPC1-binding site, and the researchers found that viruses with this mutation were better able to enter primate cells, including human cells. They noted that this increased infectivity was limited to cells with a primate-specific NPC1 sequence, suggesting that this was an adaption to a human host, Luban and his colleagues say.
They further report that patients infected with viruses with this mutation were more likely to die, the Times adds.
Meanwhile in the other study, the University of Nottingham's Jonathan Ball and his colleagues created synthetic glycoprotein constructs based on early isolates and on amino acid substitutions subsequently introduced into various viral lineages from the outbreak. They used these to create pseudoviruses that they then used to infect human and bat cell lines. They found that these substitutions, including the GPA82V mutation, increased human cell tropism while decreasing bat cell tropism to indicate that they are assisting adaptation to humans.
The Times says that that the virus has better adapted to humans worries Ball, who says another outbreak is likely. "You will see that virus trying to adapt to its new host," he says. "And the longer you let that spillover take place, the more chance it has to become better adapted."