Human beings are in an evolutionary race with SARS-CoV-2, and we need all the help we can get

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On Thursday, the BBC reported that a patient who had tested positive for COVID-19 a record 505 straight days had died. Also on Thursday, NBC News reported that a woman in Spain had contracted the omicron variant of COVID-19 just 20 days after contracting an infection from the delta variant. 

These situations are at the extremes. The patient with the extremely long case of COVID-19 had serious medical conditions that suppressed their immune system. The woman with the two cases in less than three weeks was a health care worker whose job placed her at high risk of exposure. But there is something to draw from both these cases—something that was true a year ago, and is still true today. 

Every person infected brings around 10,000,000,000 new examples of the SARS-CoV-2 virus into existence. Every single one of those is subject to mutations. Those mutations then get winnowed by the one evolutionary pressure that faces viruses: getting that R0 number ever higher. …

COVID-19 is a brand new disease when it comes to people. No one, but no one, has a natural immunity. There is no handy closely related but mild infection (ala cow pox) that might provide some with protection. The newness of COVID-19 makes it almost infinitely more threatening that diseases we’ve been dealing with for ages.

COVID-19 is still engaged in a process in which unguided mutation is searching out the best way to infect human cells. The newness of that process can be seen in the huge gains being made in each generation of variant. Alpha was twice as infectious as the original variant that ravaged Europe and the U.S. Delta is over twice as infectious as Alpha. You do not see that kind of change in well-established, long-term disease.

That was written before the omicron variant appeared. By best estimates, omicron BA.1 is 3.19 times more infectious than delta. Omicron’s BA.2 subvariant is about 30% more infectious than the BA.1 subvariant. That puts estimates of the basic reproductive number (R0) for COVID-19 at around 16 to 18, putting it on par with pertussis and measles, which were the most infectious viruses in circulation. The version of COVID-19 that first appeared in China before moving on to other countries had an R0 value of between 2.0 and 2.5. The rapid increase in that number shows that this is a virus that still has a lot of potential for explosive growth. It’s still learning to get around the immune system, and that includes learning how to get past the effects generated by both vaccines and previous infection.

This is still a very new virus with an association with Homo sapiens that is just getting started. And it’s never been more important to limit the number of infections, reduce the SARS-CoV-2 virus’ opportunities to produce trillions of new attempts to break barriers, and not let everything that’s happened so far become only a prelude.

Before going further, it’s worth pointing out that SARS-CoV-2 is neither malicious nor aware. It’s not capable of making plans. It doesn’t “want” anything. It is a quasi-living particle capable of reproduction with changes that are driven by a combination of random chance and selective pressure. To a large extent, that’s true for every living thing, but nowhere is it more true than with viruses. 

In a 2013 paper, researchers from the University of Valencia said this: “RNA viruses are among the fastest mutating and evolving entities in nature.” SARS-CoV-2 is an RNA virus. Compared to a DNA virus like the variola virus behind smallpox, it changes more rapidly. And, in large part because the time of contact between human beings and SARS-CoV-2 is so brief, those changes can have significant effects.

Here is a quick look at just one measure of how rapidly SARS-CoV-2 is changing.

In two years, SARS-CoV-2 has moved from being a virus with rate of infection that was roughly 50% greater than the flu, to one that matches up with the most infectious viruses known. There is no guarantee that this represents its upper bound. In fact, the drastic improvements seen from alpha to delta and delta to omicron suggests that there may be still quite a lot of “headroom” for SARS-CoV-2 on this single vector.

Of course, infectiousness isn’t everything. Smallpox is sitting back there at the bottom of the chart, barely twice as infectious as the flu, but no virus in history may be responsible for more human deaths than smallpox. In just the last 100 years before it was driven to extinction by a worldwide campaign of isolation and vaccination, smallpox accounted for an estimated 500 million deaths. That’s enough to cover everyone in the United States. And Canada. And Mexico. With another 10 million or so left over.

That’s because around 30% of people who caught smallpox died. For COVID-19, that number is around 1.2%. One person in 100 dying out of sight in a hospital is simply easier to overlook than a third of your family expiring after being consumed by pus-spewing sores.

Notice that there is no guarantee it will remain that way. The influenza virus—another of those pesky, rapidly changing RNA viruses—had been infecting humans for thousands of years before a version appeared in 1918 that greatly kicked up both the R0 and the mortality.

There’s nothing in any of these viruses driving them toward being significantly more lethal or significantly less lethal. Smallpox killed a high number of those infected, year in and year out, for thousands of years. If killing off a third of those infected had generated a significant selective pressure on the virus to be less lethal, you can bet the number would have dropped. It didn’t. 

(Side note: For Ebola virus, increased lethality may actually be the result of selective pressure, as this virus is often transmitted by the handling of dead bodies.)

Right now, we’re still at the beginning of our relationship with SARS-CoV-2. We’ve already passed through a kind of Dunning–Kruger stage were we thought, or at least pretended, that we understood this virus and the disease it generates. We’re just starting to squeak past that to a point where we can admit our ignorance. We don’t know what kind of sequela are waiting for us years down the road. We’re only starting to become aware of horror stories like the one novapsyche covered in this diary. 

A study from Tulane has come out that strongly suggests that, even in mild forms or onsets of the disease, even with asymptomatic presentation, the brain may experience diffuse yet profound insult in the form of  “innumerable” microbleeds.

All of this just means that the idea that we should “just live with” COVID-19 and pretend that it doesn’t exist is an invitation to disaster of inestimable scale. That patient who tested positive over 505 days didn’t just have a persistent infection from SARS-CoV-2, they had a “unique” infection. Every single person infected generates unique infections, with genetic structures that are subtly different from the virus they had going in. If one of those unique versions happens to be more infectious, it stands a chance of being the next variant of concern, and what it does to us, from brain bleeds to death, barely matters.

It’s a race. And we can’t afford to stop running.