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.
See the study for more info:
More updates on Ebola:
Elisa Hofmeister ‘18
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