There have been several suggestions that the relative nonvariance
of Ebola Zaire strains over the past 19-20 years reflects an unusually
stable Ebola-encoded RNA replicase. Without any evidence one way or t'other,
I think this is very unlikely. As noted RNA replicases have no proof-
reading attributes. And measurements of RNA replicase error-proneness
generally show comparatively similar results- i.e., 10-4 to 10-5 mistakes.
I would be curious in reading about hypotheses wherein certain replicases
could be 10-100 fold more accurate in their catalysis of polymerization of
new strands off complementary RNA templates.
It seems more likely that the stability of Ebola is a reflection of
selective pressures exerted on the infectiousness of progeny virions. For
example, capsid conformation requirements or relative constraints on surface
protein configuration (thus allowing adsorption to otherwise susceptible
cells) or other characteristics required for virus formation and infectious-
ness probably play an important role. Finally, the reservoir animal(s)
whatever their nature and immune system, exert a powerful selective pressure,
as noted by others.