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LMaking the virus that causes Covid-19 circulate more or less freely is dangerous not only because it risks overwhelming hospitals and therefore endangering lives unnecessarily, but also because it could delay the evolution of the virus into a more benign and potentially even making it more lethal.
Although the data are still inaccurate and the measures crude, this effect could already influence the difference in death rates between Sweden – which until recently took a relaxed approach to containment – and Norway, whose measures have been very more stringent. Sweden has more than three times the number of deaths per 100 cases than its neighbor.
Part of the explanation for this startling gap may lie in natural selection and the biological arms race between a pathogen and its host. Within any population there is a genetic variation. Viruses are no different. Some versions of the virus will be slightly more dangerous to human health – more virulent – others less so. If the conditions are right, the slightly more virulent ones will begin to predominate and cause more damage.
According to this interpretation of the Sweden-Norway discrepancy, it is not that Sweden has one version of the virus and Norway another. It’s just that conditions in Sweden have allowed those slightly more virulent variants that already exist in the viral population to thrive. If you want a truly spectacular, albeit extreme, example of the same mechanism at work, look at the 1918 flu pandemic.
That pandemic killed at least 50 million people, the vast majority of whom died in the second wave – in just 13 weeks between September and December 1918 – and although the data was even more fragmented then, it is believed to have been at least 25 times more lethal. than any other flu pandemic in history. The fact that it was so exceptional requires an explanation, and evolutionary biologists have provided one under the exceptional conditions that prevailed on the Western Front that summer.
Before I get to that though, let me take a step back. A pathogen, or disease-causing organism, does not “want” to kill its host. Its only evolutionary goal is to survive and reproduce, and if it has to kill to achieve that, then so be it. It causes damage because it needs its host’s cellular machinery to replicate itself and transmit to a new host. We feel bad because it is absorbing our bodily resources and because of our own immune response.
When a new pathogen emerges in humans, after jumping out of an animal tank, it is not suitable for us. If it is too virulent, it risks immobilizing its host by illness or death before it can spread to a new one; not virulent enough, and is a weak transmitter – another evolutionary dead end. Scientists have recently shown that a successful pathogen is one that evolves to an intermediate level of virulence, so that it can spread without causing too much damage.
Humans shape this process, because we also adapt to the pathogen. We put obstacles in its way, in the form of containment measures, vaccines and ultimately herd immunity. Although the host and the pathogen infinitely adapt to each other, a new, highly virulent virus that encounters these roadblocks will evolve to become less virulent faster, so that it doesn’t die before finding new susceptible hosts. .
Back to 1918. The first wave of the pandemic, in the Northern Hemisphere spring of that year, resembled a normal seasonal flu, but when the second wave broke out in August the disease was barely recognizable. Now his victims were turning blue and suffocating as their lungs filled with liquid. What happened to make that flu virus so much more virulent?
Evolutionary biologist Paul Ewald, of the University of Louisville in Kentucky, stressed the close proximity of humans in the trenches, and the fact that – far from being immobilized – the sick were being transported into successive pools of sensitive hosts, from trench to tent. to train, and then through a series of hospitals.
The tragedy of that situation, in other words, is that humans have done the virus work for it. He didn’t need to reduce his virulence to continue spreading – in fact it was in his evolutionary interest to compose and transmit it even faster, as there was no cost to do so. From the trenches of Flanders, largely through troop movements, the lethal insect was transported around the world, where it caused the shocking damage it did before finally finding its balance with humanity, much later. than he would have done otherwise. That pandemic strain circulated around the world, in modified and milder forms, until 1957, when it was ousted from the one that caused the next flu pandemic, the so-called Asian flu.
Viruses have another trick up their sleeve. Some of them can temporarily survive outside of a living host, for example on surfaces and in the air. This alters the rules of involvement in the arms race, making them less dependent on their hosts for spread and helps determine the level of virulence at which the virus gravitates. The virus that causes Covid-19, Sars-CoV-2, is as durable as the flu virus outside of a living host, which leads Ewald to suspect that it is heading towards a level of virulence comparable to that of seasonal flu. Seasonal flu causes an average of one death for every 1,000 infected people. Sars-CoV-2 is killing at about 10 times that speed right now.
It’s too early to interpret the Covid-19 data, partly because no one knows how many people have been infected – and there are many other factors in the mix, such as the changing age profile of the patient population and improved care – but we could already see viral evolution in declining mortality rates. As did epidemiologist Andrew Noymer of the University of California, Irvine underlined, this would have happened anyway, over time. But here’s the thing: we can speed it up if we choose it. We probably already are, in some parts of the world.
“If we invest in measures like quarantine, we’re favoring viral strains that are so mild that people don’t know they’re sick,” says Ewald. His colleague at the University of Louisville, biologist Holly Swain Ewald, said such measures are key factors in reducing virulence. If so, they likely contributed to the different death rates in Norway and Sweden. Protecting people through public health measures saves us time, postponing the time when many people get the disease until it gets much milder. This could make a huge difference for all those people around the world who don’t have access to adequate health care.
The ball is in our court, to a large extent. We have a say in how long this pandemic lasts and how many people die. It has been said before, but here’s the evolutionary argument for it. The key thing to understand is that we are not passive spectators; we form the virus as it forms us. In the end, Covid-19 will be no worse than the flu, or perhaps even the common cold caused by one of its relatives. Let’s get out of here as fast as possible.
• Laura Spinney is a science journalist and author of Pale Rider: The Spanish Flu of 1918 and How it Changed the World
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