A salient question to ask at this time is whether or not it is possible for rates of viral mutation to be self-modified. The rationale: if the information-replication and associated encoding mechanism that this viral family of entities represent is autonomously oriented towards maximal self-reproduction, and if accelerated mutation becomes a sustainable form of maximising probability of self-replication, then we might expect the continuing proliferation of variants.
The other side of this particular coin is that, while antigenic drift (and, perhaps, shift) as a function of the sustainable continuity of any viral system in a host population is perhaps inevitable – the measures of epidemiological interdiction applied against it have a tendency to inadvertently and inversely select for “successful” candidates. Human populations represent an extended phenotype of the viral information-encoding system but what is it about this particular virus (or the time, place and integrated complexity of the extended phenotype) that makes it so catastrophic and consequential? What, in effect, is the blind-spot here?
Are viruses as autonomously self-propagating information patterns bound to eventually and accidentally discover mechanisms of accelerated metamorphosis in and as novel self-encoding patterns? Beyond questions of attribution, this raises a question of whether or not such drift and associated rates of change is itself usefully manipulable as a viral Achilles’ heel.|
There may also be a general observation regarding complex information system self-propagation to be made here. The underlying pattern is not specific to an instance but represents a general, broad class of recursive information-system entities. If we might look anywhere for assistance, it might be to the foundational properties and logical self-inflection of complex systems.