Saturday, December 5

The coronavirus is evolving. Whether it becomes more lethal or not can depend on us | Coronavirus


LMaking the virus that causes Covid-19 to circulate more or less freely is dangerous not only because it risks overwhelming hospitals and endangering lives unnecessarily, but also because it could delay the evolution of the virus to a more benign and potentially even doing is more lethal.

Although the data are still incomplete and the measures crude, it is possible that this effect is already influencing the difference in death rates between Sweden, which took a relaxed approach to containment until recently, and Norway, whose measures have been much more stringent. Sweden has more than three times as many deaths per 100 cases as your neighbor.

The explanation for this surprising gap may lie in part in natural selection and the biological arms race between a pathogen and its host. Within any population, there is genetic variation. Viruses are no different. Some versions of the virus will be a little more dangerous to human health, more virulent, others less. If the conditions are right, the somewhat more virulent ones will begin to predominate and cause more damage.

Under this interpretation of the Sweden-Norway discrepancy, it is not that Sweden has one version of the virus and Norway has another. It’s just that conditions in Sweden have allowed those slightly more virulent variants that already exist in the virus population to flourish. For a truly spectacular, albeit extreme, example of the same mechanism at work, take a 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 sketchy at the time, it is considered that at least 25 times more lethal than any other flu pandemic in history. The fact that it was so exceptional demands an explanation, and evolutionary biologists have provided it in the exceptional conditions that prevailed on the Western Front that summer.

However, before we get to that, let me take a step back. A pathogen, or disease-causing organism, does not “want” to kill its host. His only evolutionary goal is to survive and reproduce, and if he has to kill to achieve that goal, so be it. It causes damage because it needs the cellular machinery of its host to replicate and transmit to a new host. We feel sick because it is diverting our bodily resources and because of our own immune response.

When a new pathogen emerges in humans, having jumped out of an animal reservoir, it is not adapted to us. If it is too virulent, it runs the risk of immobilizing its host through illness or death before it can spread to a new one; it is not virulent enough and is a weak transmitter, another evolutionary dead end. Scientists have recently shown that a successful pathogen is one that evolves at an intermediate level of virulence, so that it can spread without causing too much damage.

Humans shape that process, because we also adapt to the pathogen. We put obstacles in their way, in the form of containment measures, vaccinations, and eventually herd immunity. Although host and pathogen endlessly adjust to each other, a novel, highly virulent virus that encounters these obstacles will evolve to become less virulent faster, so that it does not go extinct before finding new susceptible hosts.

Going back to 1918. The first wave of the pandemic, in the northern hemisphere spring of that year, resembled a common 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 fluid. What happened to make the flu virus much more virulent?

Evolutionary biologist Paul Ewald of the University of Louisville in Kentucky has pointed to the proximity of men in the trenches, and to the fact that, far from being immobilized, the sick were transported to successive pools of susceptible hosts, from trench to store, by train, and thereafter through a series of hospitals .

Masked women hold stretchers during the Spanish flu pandemic in St. Louis, Missouri, USA, in October 1918.
Women in masks hold stretchers during the Spanish flu pandemic in St. Louis, Missouri, USA, in October 1918. Photography: Brochure ./Reuters

The tragedy of that situation, in other words, is that humans did the work of the virus. It had no need to reduce its virulence to continue spreading; in fact, it was in their evolutionary interests to flag it and broadcast even faster, as there was no cost to doing so. From the trenches of Flanders, largely through troop movements, the lethal insect was transported across the world, where it did so much damage before finally finding its footing with humanity, much later than it would have done from another way. This pandemic strain circulated in the world, in modified and milder forms, until 1957 – when it was overthrown by the one that caused the next flu pandemic, the so-called Asian flu.

Viruses have another metaphorical trick up their sleeve. Some of them may temporarily survive outside of a living host, for example on doorknobs and keyboards. This alters the rules of participation in the arms race, making them less dependent on their hosts to spread, and helps determine the level of virulence to which the virus eventually gravitates. The virus that causes Covid-19, Sars-CoV-2, is as durable as the flu virus on surfaces and in the air, leading Ewald to suspect that it is targeting a level of virulence comparable to that of seasonal flu. Seasonal flu causes one death for every 1,000 infected people, on average. Sars-CoV-2 is killing approximately 10 times that rate At the time.

It’s too early to interpret the data on Covid-19, in part 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 improvements in care, but we may already be seeing a viral evolution in falling mortality rates. As epidemiologist Andrew Noymer of the University of California, Irvine, has he pointed, this would happen anyway, over time. But here’s the thing: we can speed it up, if we want to. We probably already are, in some parts of the world.

“If we invest in measures like quarantine, we are favoring viral strains that are so mild that people do not know they are sick,” says Ewald. His colleague at the University of Louisville, biologist Holly Swain Ewald, has argued that such measures are key drivers of the reduction in virulence. If so, they probably contributed to the different death rates in Norway and Sweden. Protecting people through public health measures also gives us time, postponing the time when many people contract the disease until it is much milder. That could make a big difference for all those people in the world who do not have access to adequate medical care.

The ball is in our court, to a great extent. We have a say in how long this pandemic lasts and how many people die. That has been said before, but here is the evolutionary argument for it. The key to understanding is that we are not passive bystanders; we form the virus as it forms us. Eventually, Covid-19 will be no worse than the flu, or perhaps even the common cold caused by one of your relatives. Let’s get there as fast as we can.

• 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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