Will coronavirus really evolve to become less deadly in decades to come?

 It was the bacteriologist and comparative pathologist Theobald Smith (1859-1934) who began the narrative of the "law of declining virulence" in the late 19th century

A recent modelling study painted a reassuring picture of a post-pandemic future in which SARS-CoV-2 transitions, over “a few years to a few decades”, from dangerous pathogen to just another common-cold coronavirus. This predicted loss of virulence, the authors stress, is based on a specific idiosyncrasy of the virus, namely that it rarely causes serious disease in children.

Still, many experts agreed that we should not be in the least surprised by the authors’ conclusion, as all viruses “become more transmissible and less pathogenic over time”. After all, the seductive logic goes, from an evolutionary perspective it makes no sense for a pathogen to harm the host on which it depends for its survival. According to this reasoning, virulence is little more than a temporary evolutionary imbalance.

This comfortable chain of reasoning was rudely broken by the announcement of “a realistic possibility” that the new highly transmissible B117 variant “is associated with an increased risk of death”.

Although the evidence is still accruing, early estimates from Nervtag, the UK’s New and Emerging Respiratory Virus Threats Advisory Group, suggest that B117 may be around 30% more deadly.

But perhaps this is a single exception to an otherwise well-observed rule, and we can still be confident that SARS-CoV-2 will slowly fade away to obscurity. So what is the evidence for this view? And how confident can we be in predicting how evolution will shape the relationship between a pathogen and its host?

Law of declining virulence

It was the bacteriologist and comparative pathologist Theobald Smith (1859-1934) who began the narrative of the “law of declining virulence” in the late 19th century.

Studying tick-borne disease of cattle during the 1880s, Smith realised that the severity of the disease was determined by the degree of prior infection. Cattle that had been repeatedly exposed to the pathogen suffered from much more moderate disease than cattle encountering it for the first time. Smith reasoned that this was because host and pathogen conspired over time towards a mutually benign relationship.

The story then takes a distinctly antipodean turn. In 1859, the year Charles Darwin published his Big Idea, European rabbits were introduced to Australia for sport, with devastating consequences for the indigenous flora and fauna. Having turned down Louis Pasteur’s offer of mass délapinsation using fowl cholera as a biological control agent, the Department of Agriculture turned to the myxoma virus that causes the lethal, but highly species-specific disease, myxomatosis in rabbits.