How dangerous by percentage of total human mortality are the variable functional outcomes of speciated viral populations with their parallel functional trajectories, relative, comparatively, to the original correlated function of human mortality from an original strain; amidst a total resultant population of viruses of multiple species. And, what variables define rate of speciation amidst the existing definitions of human viral host and host population statuses (the infected)?
I ponder whether the initially minor statistical anomaly of a newly fecund British viral speciation: the now emergent Anglican viral species that has propagated itself into a viable pathogenesis with its own increasing population; has drastically altered projected human mortality rates. And, with this new population being within the greater global virus/host virulence variabilities of the original viral species; is this phenomenon of mutagenesis and emergent species viability itself statistically indicative of a total global change in the rate of population growth for COVID19; inclusive of any and all added lethality from speciated populations which also might then predate upon dispersed isolated colonies of Hominids and other host reservoirs within Mammalia and Aves in particular. Then, via an additional zoonoses induced mortality; might this breadth of virulence therefore outpace the inoculation rate set in place against the original species of COVID19 and/or lead to the alteration of hominid mortality projections and their descriptive functions due to the increased biotic bandwidth of the mortifying sequences.
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