Conceptual progression of intracellular viral replication events, including variable RNApol fidelity and processivity, restriction of antigenic diversity and immune recognition under influence of Replicative homeostasis. Panels (A->E) changing frequency distribution of viral RNA and protein quasispecies, panels (a->e) cellular events. Initial state (panels A,a) viral replication occurring in cells devoid of molecular inhibitors of RNApol high affinity wild-type envelope (Enve, green): RNApol interactions predominate, causing rapid low-fidelity viral RNA synthesis and, consequently, a broad spectrum of viral proteins expressed on cell surface at concentrations below TOD. As variant viral proteins accumulate within cells (panel b) and variant viral envelope: RNApol interactions increase, RNApol fidelity increases while processivity decreases, restricting the distribution of viral RNA and proteins, reducing antigenic display on cells. As variant viral envelope: RNApol predominate (panel c), the frequency distribution of expressed viral proteins is restricted so the individual concentration of some proteins increases beyond TOD, allowing immune recognition and polyclonal, low affinity antibodies to develop, blocking cellular egress of viral proteins, further increasing variant viral envelope: RNApol interactions, thus immune responses force viruses to reveal wild-type epitopes by restricting antigenic diversity. High affinity responses once developed (panel d) preferentially reduce intracellular concentration of wild-type viral proteins further increasing variant viral envelope: RNApol interactions still further restricting RNApol processivity to the point of viral latency (panel e).