Dynamic progression of RNApol functional properties, processivity () and fidelity () predicted by replicative homeostasis. Initial state (A, corresponding to panel A, Figure 7): in a newly infected cell, high-affinity wild-type:RNApol interactions will predominate resulting in high RNApol processivity but low fidelity causing high-level viraemia with broad virus phenotypic spectrum, maximizing cell tropism. Intracellular accumulation of variant viral proteins (B, c.f. panel B, Figure 7) reduces RNApol processivity but increases fidelity reducing viral RNA synthesis and consequently, viraemia before a dynamic, fluctuating equilibrium (C, c.f. panel C or D, Figure 7) develops in which inhibition of RNApol by variant viral proteins is balanced by increases in RNApol fidelity (with consequent synthesis of wild-type viral products tending to cause high RNApol processivity).