The Ebola outbreak in West Africa was the largest in recorded history, prompting researchers funded by the Medical Research Council to question whether or not the virus had mutated to become more transmissible between human hosts. In a newly published paper, it was that there were small changes to glycoprotein (GP) amino acids. These mutations were likely responsible for the increase in efficient human cell infections.
The researchers studied two lineages of the virus: A and B. Lineage A was present in Guinea at the beginning of the outbreak, and lineage B was present for a much larger geographical area and later in the outbreak. It was deduced that Lineage B had a point mutation in the receptor-binding domain of GP at residue 82. The glycoproteins of the virus are commonly responsible for viral entry into a cell, so researchers focused their efforts studying how this mutation affected viral entry.
It was determined that lineage B of EBOV was nearly twice as infective as A in human cells. This result was traced back to the point mutation at GP 82, and is likely responsible for the size of the outbreak in the human population. Interestingly, lineage B is LESS efficient at entering bat cells, indicating that an evolutionary change has occurred in some Ebola strains, and that humans are becoming a more important host to the virus.
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Elisa Hofmeister ‘18