From Wild-Type SARS-2 to Omicron: Towards a Theory of Corona Evolution

With additional thoughts on why mass containment probably made everything worse, by playing to the most central strategy of the virus

Scientific discourse on Corona remains focused on microbiological minutiae, while ignoring the broader behavioural patterns of SARS-2. This is especially frustrating, because our mass containment policies were at base attempts to change the behaviour of the virus, and their failure has prompted no introspection about the limits of our understanding.

Equally neglected is the evolutionary trajectory of Corona. Aside from simplistic, one-dimensional concerns about things like escape variants, almost nobody in mainstream scientific circles has tried to account for observed evolution or describe the various selection pressures SARS-2 faces.

Among the few people to have given serious thought to the evolution of viral pathogens is Paul Ewald, author of the book Evolution of Infectious Disease, as well as numerous articles explaining the evolutionary pressures on the virulence and transmissibility of viruses.

As he explains in this piece from 2011:

Much of the variation in the harmfulness of acute infections is associated with the dependence of transmission on host mobility. When transmission occurs by direct contact, infected hosts generally need to be mobile to facilitate contact with susceptibles. When transmission of pathogens does not depend on the mobility of infected hosts, evolutionary considerations predict that natural selection should favor high degrees of host exploitation and hence high degrees of virulence.

Basically, the virus wants to make as many copies of itself as possible. But, very roughly speaking, the more aggressively the virus copies itself, the sicker its hosts become. This places an upper limit on the virulence of viruses that depend on person-to-person contact, and it explains why widely transmitted respiratory viruses all fall within the same narrow range of pathogenicity and cause the same kinds of symptoms. The pandemicists raise money by wargaming pandemic viruses with 10% fatality rates, but in the real world, the truly deadly viruses never get very far. They’re all like SARS-1 – they put people in the hospital too soon.

But what about smallpox? And cholera, and yellow fever and dengue fever? Are these not deadly viruses?

They are, but they either don’t spread via direct contact, or they have other options. Smallpox falls into what Ewald calls a “sit-and-wait” category of transmission. These are viruses that have remarkable durability, remaining viable in the external environment for months or (in the case of Variola) even years. They can thus disable their hosts while still having hope of new victims. Yellow fever and dengue, meanwhile, are “vector-borne.” They depend on mosquitoes to hop from host to host, and they’re free to make their victims as sick as they want. “Waterborne” pathogens like cholera are similarly advantaged.

More importantly for our purposes, Ewald defines a fourth category of what we might call mediated transmission facilitating higher virulence. This is “attendant-borne” transmission, which occurs primarily in hospitals, where staff unwittingly circulate viruses among patients. Attendant-borne viruses, like their vector-borne and waterborne colleagues, are free to develop remarkably high virulence. Ewald believes that the 1918 influenza outbreak achieved its unusually high mortality via attend-borne transmission related to troop transports at the end of the First World War.

SARS-1, although never properly adapted to human hosts, also depended on attendant-borne transmission, and MERS is a more straightforward case of this phenomenon. But the clearest example of all is surely pre-Omicron SARS-2, which caused elevated mortality near the top of what we would expect for pandemic influenza; and which flourished nowhere as effectively as in healthcare institutions, including hospitals and especially nursing homes.

Remember that SARS-2 arrived in Europe no later than November 2019, and in America no later than December 2019. The West saw multiple months of community Corona transmission, in other words, without anybody noticing that anything was amiss. Hospitals remained as empty or as full as ever. As soon as we imposed lockdowns and started testing everybody, though, mortality spiked. These containment procedures involved nothing so much as identifying Corona patients and putting as many of them as possible in environments favouring attendant-borne transmission – from Corona testing centres to hospitals. And as the mass containment regime continued through 2021, SARS-2 began evolving towards greater virulence, as nosocomial and nursing home infections came to dominate the case statistics almost everywhere.

Omicron, whatever its origins, broke this dynamic. Unlike prior SARS-2 lineages, this is a classic direct-contact respiratory pathogen. With the advent of Omicron, Corona no longer spreads preferentially in healthcare institutions, and behaves much more like a mild flu or the common cold, with an emphasis on keeping its hosts healthy and mobile.

The worst thing we could do, from an evolutionary perspective, is continue the mass containment regime. We want to keep SARS-2 circulating via direct contact in the community. All such respiratory viruses, despite their stark differences, have been subject to the same convergent evolution, with remarkably similar effects on their human hosts. We must stop intervening in matters we don’t understand, or we’ll just continue our recent history, of always making everything worse.