Mutated Gene Increased Infectivity of Ebola in 2013-2016 West African Epidemic
Brian P. Dunleavy has been covering health and medical research for more than 25 years, for United Press International and EverydayHealth.com, among other outlets. He is also the former editor of Infectious Disease Special Edition. In addition, he has written on other subjects for Biography.com, History.com, the Village Voice and amNewYork, among others. He holds a master’s degree from the University of Missouri School of Journalism.
Studies find that a mutated gene that encodes the Ebola virus glycoprotein increased its ability to infect human and primate cells in the 2013-2106 West African epidemic.
All viruses mutate, and such mutations are the bane of the infectious disease specialist’s existance, as these mutations can make the illnesses they cause less susceptible to drug treatment, and, in some cases, more severe or even infectious.
Now, research published November 3 in the journal Cell, suggests that viral mutations in Ebola increased its ability to infect human cells, contributing to the tragic scope of the 2013-2016 West African epidemic, in which there were nearly 30,000 cases and more than 11,000 fatalities.
“Ebola virus is thought to circulate in an unknown animal reservoir and to only rarely cross over into people,” said Jeremy Luban, MD, a co-author of one of the two papers on the subject and a professor of molecular medicine at the University of Massachusetts Medical School in a press statement released by the journal. “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. It’s important to understand how these viruses evolve during outbreaks. By doing so, we will be better prepared should these viruses spill over to humans in the future.”
To investigate the genetic changes in the virus that occurred during the epidemic, the two research teams, which were operating independently of each other, collected Ebola genomic sequences from different time periods and compared them. In essence, they found that mutations of the gene that encode the Ebola virus glycoprotein increased its ability to infect human and primate cells—but not fruit bats, which are believed to be its natural hosts—perhaps contributing to its wide spread. One of these mutations, according to both groups, emerged early in the outbreak and became the dominant form of the virus that circulated throughout the region.
“If you introduce a virus into a new host, like humans, it may need to adapt to better infect and spread in that host,” Jonathan Ball, co-author of the other study and a virologist at the University of Nottingham in the UK. “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.”
Brian P. Dunleavy is a medical writer and editor based in New York. His work has appeared in numerous healthcare-related publications. He is the former editor of Infectious Disease Special Edition.