The more the epidemiological data seem to reassure our health authorities, the more nervous I get...

As seen in the graphs above, peaks in SC-2 wastewater concentration (used as a proxy for viral infectivity) are decreasing. This suggests reduced viral transmission despite the high infectiousness of circulating variants and the frequent occurrence of ‘silent’ transmission (i.e., via mildly or asymptomatically infected individuals). The lower the viral inter-host transmission, the more quickly a newly emerging SC-2 variant with a slight fitness advantage (e.g., LP.8.1.: see below)) can outcompete and dominate over other circulating variants. It is reasonable to assume that a low inter-host viral transmission rate enhances the role of selection pressure on viral (trans) infectiousness in determining which variant predominantly spreads. In this scenario, even a small fitness advantage (e.g., a slighter higher replication efficiency) could enable a new variant to displace others relatively rapidly over time. This is because each transmission event disproportionately favors the fitter variant. However, if the transmission rate of this newly emerging, more productive variant becomes too low (IMO, because of enhanced immobilization of infectious virus on URT-patrolling DCs), the virus may not spread enough for any new, more infectious variant to gain dominance quickly and drive a surge in viral infectivity and transmission. This is likely to drive the dominant spread of a new variant capable of overcoming the infection-inhibiting effects of strong viral adsorption onto URT-resident DCs. Instead of causing global replacement of circulating variants, such virulent variant (HIVICRON) will likely cause a very severe outbreak.