In hopes of viral pressure on Nigerian authorities to try to recover the girls, campaigns have started on the White House website, on Change.org and on Facebook to demand: "Bring Back Our Girls". All this may or may not help, but it's worth trying.
Recurrent viral pressure has acted on host-encoded antiviral genes during primate and mammalian evolution.
When these interactions modify the host in a way that has lasting effects on viral selection pressure, niche construction will be in operation.
Due to faster mutation rates, short generation times, and more intense selective pressures, viral genomes may be genetically distant from the known reference genomes.
The evidence for the above comes from comparing the low CpG selection pressure in the innate immune genes observed here to the viral CpG selection pressure observed here and in Ref. [4].
Together, our data strongly suggest that the combined effect of these HLA-driven selective pressures on viral evolution is predictable and that viral founder effects are overlaid by rapid adaptation to local HLA population frequencies.
These roles and the resulting interactions present specific constraints and selection pressures on viral genes that contribute to the accumulation of genetic change with a rate characteristic to each viral protein.
Critical next questions include the extent to which crop-associated selection pressures drive viral pathogenesis.
The most plausible interpretation for this is that the stronger the selective pressures on viral population (imposed by antiviral treatment and host immune response), the higher the initial reduction in genetic variability.
In addition, this extensive diversity means that, at both the individual as well as the population level, the human immune response exerts a complex array of evolutionary selective pressures driving viral evolution [13], [14] in equally intricate, sometimes even conflicting [15], [16] ways.
