Extinction and Speciation in Red Queen's Race of Influenza Virus.

The success of influenza as a virus is due to its ability to escape the human immune system memory by rapidly mutating its antigens. The continuous arms race between the virus and the adaptive immunity of its host population drives the need to update flu vaccines every few years. It also shapes a peculiar, spindly phylogenic-tree structure of influenza A (H3N2), with a single continuous backbone going forward accumulating antigenic innovations, while overall viral diversity at any given time remains limited. Thus, H3N2 flu evolves fast enough to reliably evade host immunity, yet it does not accumulate diversity, leading to divergence and eventual "speciation" in the sense of the loss of cross-immunity imparted by coexisting flu genotypes. What maintains this delicate balance? Under what conditions is the flu destined to extinction or speciation? From an epidemic-type model capturing this Red Queen's race between virus and host-immunity, we identify the time delayed (and nonlinear) feedback that stabilizes viral population (over a finite range of evolutionary parameters) so that the subspecies cloud moves as a traveling wave in the antigenic space, giving rise to a persistent but un-branching phylogenic backbone.