This COVID-19 article was republished here with permission from The Conversation. This content is shared here because the topic may interest Snopes readers; it does not, however, represent the work of fact-checkers or Snopes editors.
A recent modeling 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 a dangerous pathogen to just another common cold coronavirus. This predicted loss of virulence, the authors underline, is based on a virus-specific idiosyncrasy, namely, that it rarely causes serious illnesses in children.
Even so, many experts agree that we should not be at all surprised by the authors’ conclusion, since all viruses “become more transmissible and less pathogenic over time”. After all, it follows the seductive logic, from an evolutionary perspective it does not make 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 roughly broken by the announcement of “a realistic possibility” that the new highly transmissible B117 variant “is associated with an increased risk of death”.
While the evidence is still piling up, early estimates by Nervtag, the UK’s New and Emerging Respiratory Virus Threat Advisory Group, suggest that B117 could be about 30% more deadly.
But perhaps this is a single exception to a well-observed rule, and we can still be confident that SARS-CoV-2 will slowly disappear into 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?
Virulence decline law
It was the bacteriologist and comparative pathologist Theobald Smith (1859-1934) who started the narrative of the “law of declining virulence” in the late 19th century.
Studying tick-borne diseases in cattle during the 1880s, Smith realized that the severity of the disease was determined by the degree of previous infection. Cattle that have been repeatedly exposed to the pathogen have suffered from diseases much more moderate than the cattle that first encountered it. Smith concluded that this was because host and pathogen conspired over time for a mutually benign relationship.
The story then takes a distinctly antipode turn. In 1859, the year Charles Darwin published his Great Idea, European rabbits were introduced to Australia for sport, with devastating consequences for native flora and fauna. Having declined the offer of Mass of Louis Pasteur delapinsation Using avian cholera as a biological control agent, the Department of Agriculture turned to the myxoma virus, which causes the lethal but highly specific disease, myxomatosis in rabbits.
In the 1950s, the myxoma virus was spreading rapidly among the rabbit population. Recognizing the opportunities provided by this unique experiment, virologist Frank Fenner has documented how the virulence of the disease has decreased in some years of mortality from 99.5% to about 90%. This was taken as strong empirical evidence in support of Smith’s law of declining virulence – and occasionally it still is.
Queensland State Archives / Wikimedia Commons
A challenge to the virulence decline law
At about the same time, a young and talented Australian mathematician named Robert May met the work of his compatriot Charles Birch, an eminent ecologist who worked on the regulation of animal populations. Together with epidemiologist Roy Anderson, May pioneered the application of mathematical modeling to the ecology and evolution of infectious diseases. In the late 1970s, May and Anderson developed the “trade-off” model for the evolution of virulence – the first conceptual framework in 100 years to challenge Smith’s general law of declining virulence.
The exchange model recognizes that the pathogen’s virulence will not necessarily limit the ease with which a pathogen can transmit from one host to another. You can even improve it. Without the evolutionary cost assumed for virulence, there is no reason to believe that the severity of the disease will decrease over time. Instead, May and Anderson proposed that the optimal level of virulence for any pathogen will be determined by a number of factors, such as the availability of susceptible hosts and the length of time between infection and the onset of symptoms.
This last factor is a fundamental aspect of the epidemiology of SARS-CoV-2. The long period of time between infection and death (if it occurs) means that SARS-CoV-2 has a significant window to replicate and spread, long before killing its current host.
The compensation model is now widely accepted. He emphasizes that each pathogen-host combination must be considered individually. There is no general evolutionary law to predict how these relationships will develop, and certainly no justification for evoking the inevitability of diminished virulence.
There is little or no direct evidence that virulence decreases over time. Although newly emerging pathogens, such as HIV and Mers, are often highly virulent, the reverse is not true. There are many old diseases, like tuberculosis and gonorrhea, that are probably as virulent today as they ever were.
A change in conditions can also drive the trend in the other direction. Dengue fever has affected humans since at least the 18th century, but an increasingly large and mobile human population is believed to have caused a sharp increase in virulence in the past 50 years or more. Even the seminal case of the myxoma virus that kills rabbits is uncertain. There was little subsequent decline in virulence after Fenner’s first reports, and it may have even increased slightly.
Plausible, but not inevitable
Obviously, these counterexamples do not in themselves provide evidence that the virulence of SARS-CoV-2 will not diminish. The decline in virulence is certainly plausible as one of the many potential outcomes of the compensation model.
On the other hand, mutations can simultaneously increase virulence and transmissibility increasing the rate of viral replication. While we have to wait for more evidence to be sure – and the precise mechanisms can be difficult to define – the emerging evidence around variant B117 currently points more to increased mortality.
Ed Feil, Professor of Microbial Evolution at The Milner Center for Evolution, University of Bath and Christian Yates, senior professor of mathematical biology, University of Bath
This article was republished from The Conversation under a Creative Commons license. Read the original article.