Recent modeling study he painted a vivid 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 projected loss, the authors emphasize, is based on a specific strain of the virus, which rarely causes severe infection in children.
However, many experts agreed that we should not be surprised by the authors’ decision, as all viruses “become more susceptible and less pathogenic over time”. After all, the seductive logic goes, from an evolutionary point of view it makes no sense for a pathogen to harm the host it is responsible for surviving. According to this reasoning, violence is little more than a temporary evolutionary imbalance.
This comforting reasoning chain has been unjustifiably broken by stating “reasonable potential” that the highly portable new B117 variant is “associated with an increased risk of death”.
While the evidence is still emerging, early estimates from Nervtag, the New and Emerging Respiratory Virus Risk Advisory Group, suggest that B117 could be about 30% more lethal.
But this may be one exception to a well – observed rule, and we can still be confident that SARS-CoV-2 will go into obscurity. So what is the evidence for this idea? And how confident can we be in predicting how evolution will shape the connection between a pathogen and its host?
A declining law of decay
It was the bacteriologist and comparative pathologist Theobald Smith (1859-1934) who began the description of the “declining decay law” in the late 19th century.
Examining tick-borne cattle disease in the 1880s, Smith realized that the severity of the disease was determined by the prevalence of previous diseases. Cattle that had been exposed to the pathogen were again suffering from a much more moderate disease than cattle experiencing it for the first time. Smith reasoned that this was because a host and a pathogen cooperated over time toward an incompetent relationship.
The story then takes a very antipodean turn. In 1859, the year Charles Darwin published his great idea, European rabbits were introduced to Australia for sport, with a devastating effect on the native plants and animals. After rejecting Louis Pasteur’s mass offer délapinsation using avian cholera as a biological control agent, the Department of Agriculture turned to the myxoma virus that causes the deadly, but species – specific disease, myxomatosis in rabbits.
By the 1950s, the myxoma virus was spreading rapidly among rabbit populations. Recognizing the opportunities presented by this particular test, pathologist Frank Fenner reported on how the viability of the disease has decreased over a few years from mortality from 99.5% to about 90%. This has been taken as strong empirical evidence in support of Smith’s law of decline – and sometimes is.
Challenging the law regarding muscle contraction
Around the same time, a talented young mathematician from Australia named Robert May came across the work of his companion Charles Birch, a renowned ecologist working on animal population management. Together with epidemiologist Roy Anderson, May went on to apply mathematical modeling in the ecology and evolution of infectious disease. By the late 1970s, May and Anderson had developed the “trade” model for evolution – the first conceptual framework in 100 years to challenge Smith’s general law of decline.
The commercial model recognizes that pathogen density does not largely limit the ease with which a pathogen can move from one host to another. Maybe he will improve it. Without the generally accepted cost of violence, there is no reason to believe that disease severity will decrease over time.
Instead, May and Anderson suggested that the optimal level of virus for any pathogen is determined by a range of factors, such as access to susceptible hosts, and the time between infection and onset of disease.
This latter factor is a key aspect of the epidemiology of SARS-CoV-2. The long time between infection and death (if it occurs) means that SARS-CoV-2 has an important window for reproduction and transmission, long before it destroys its normal host.
The trade-in model is now widely accepted. It emphasizes that each host-pathogen combination must be considered individually. There is no common evolutionary law for predicting how these relationships will unfold, and there is certainly no reason to awaken the instability of a decline.
There is little direct evidence that life expectancy decreases over time. While newly emerged pathogens, such as HIV and Mers, are highly virulent, the opposite is not true. There are many old diseases, such as tuberculosis and gonorrhea, that seem to be as strong today as they have ever been.
A change in circumstances can also reverse the trend. Dengue fever has affected humans since at least the 18th century, but an increasingly large and mobile human population is thought to have seen a dramatic increase in the last 50 years or so. . Even the advanced case of the myxoma virus that kills rabbit is uncertain. There was little subsequent decline after Fenner ‘s early reports, and it could even go up a bit.
Credible but not inevitable
Indeed, these contraindications in themselves do not present evidence that SARS-CoV-2 violence will not decline. Depreciation is certainly plausible as one of many potential outcomes under the trade model.
At the same time, mutations can simultaneously contribute to both viruses and transmission by increasing the rate of viral reproduction. While we will have to wait until more evidence is conclusive – and the exact mechanisms may be difficult to verify – the evidence emerging around the current B117 version indicates more towards increased mortality.
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
This article is republished from The Conversation under a Creative Commons license. Read the original article.