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A recent model study painted a reassuring picture of a post-pandemic future in which SARS-CoV-2 transitions from dangerous pathogen to just another cold coronavirus in a few years to a few decades. This predicted loss of virulence, the authors emphasize, is based on a specific idiosyncrasy of the virus, namely that it rarely causes serious diseases in children.
Yet many experts agree that we should not be the least bit surprised at the authors’ conclusion, because all viruses become more transmissible and less pathogenic over time. After all, the seductive logic is: 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 evidence is still accumulating, early estimates by Nervtag, the UK advisory group for new and emerging respiratory virus threats, suggest that B117 may be about 30% more lethal.
But perhaps this is a single exception to a rule that is otherwise well observed, 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 to predict how evolution will shape the relationship between a pathogen and its host?
Law of diminishing virulence
It was the bacteriologist and comparative pathologist Theobald Smith (1859-1934) who began the story of the ‘law of diminishing virulence’ at the end of the 19th century.
By studying tick disease in cattle during the 1880s, Smith realized that the severity of the disease was determined by the extent of previous infection. Cattle that were repeatedly exposed to the pathogen suffered from a much more moderate disease than cattle that first encountered it. Smith reasoned that it was because host and pathogen conspired over time to form a mutually benevolent relationship.
The story then takes a clear antipodean turn. In 1859, the year Charles Darwin published his Big Idea, European rabbits were introduced to sport in Australia, with devastating consequences for the native flora and fauna. After rejecting Louis Pasteur’s offer of mass delineation by using chicken cholera as a biological control, the Department of Agriculture focused on the myxoma virus that causes the deadly but very species-specific disease, myxomatosis in rabbits.
By the 1950s, the myxoma virus had spread rapidly among the rabbit population. Recognizing the opportunities offered by this unique experiment, virologist Frank Fenner documented how the virulence of the disease decreased over a few years from 99.5% mortality to about 90%. This was seen as strong empirical evidence in support of Smith’s law of diminishing virulence – and sometimes it is.
Queensland State Archives / Wikimedia Commons
A challenge to the law of declining virulence
Around the same time, a talented young Australian mathematician named Robert May came across the work of his compatriot Charles Birch, a leading ecologist who was involved in regulating animal populations. Together with epidemiologist Roy Anderson, May pioneered the application of mathematical modeling to the ecology and evolution of infectious diseases. By the late 1970s, May and Anderson had developed the ‘exchange model’ for the development of virulence – the first conceptual framework in 100 years that challenged Smith’s general law of declining virulence.
The exchange model recognizes that virogenesis by pathogens does not necessarily limit the ease with which a pathogen can transmit from one host to another. It can even improve it. Without the supposed evolutionary costs for virulence, there is no reason to believe that the severity of diseases will decrease over time. Instead, May and Anderson suggested that the optimal level of virulence for any pathogen would be determined by a variety of factors, such as the availability of susceptible hosts and the length of time between infection and symptoms.
This last factor is an important aspect of the epidemiology of SARS-CoV-2. The long period between infection and death (if it occurs) means that SARS-CoV-2 has an important window to repeat and spread, long before it kills its current host.
The exchange model is now widely accepted. This emphasizes that each host-pathogen combination must be considered separately. There is no general evolutionary law to predict how these relationships will work out, and certainly no justification for arousing the inevitability of diminished virulence.
There is little or no direct evidence that virulence decreases over time. While custom pathogens, such as HIV and Mers, are often highly virulent, the reverse is not true. There are many ancient diseases, such as tuberculosis and gonorrhea, that are probably just as virulent today as ever.
A change in conditions can also drive the trend in the other direction. Dengue fever has plagued humans since at least the 18th century, but an increasingly large and mobile human population has presumably caused an increase in virulence over the past 50 years or so. Even the seminal case of the myxoma virus that kills the rabbit is uncertain. There was little decrease in virulence after Fenner’s earlier reports, and it even rose slightly.
Plausible but not inevitable
Obviously, these counterexamples do not in themselves prove that the virulence of SARS-CoV-2 will not decrease. Decreasing virulence is certainly plausible as one of the many potential outcomes under the exchange model.
Conversely, mutations can increase both virulence at the same time and transmissibility by increasing viral replication rate. Although we will have to wait until more evidence is certain – and the exact mechanisms may be difficult to determine, the emerging evidence surrounding the B117 variant is currently indicating an increased mortality rate.
Ed Feil, Professor of Microbial Evolution at the Milner Center for Evolution, University of Bath and Christian Yates, senior lecturer in mathematical biology, University of Bath
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