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  • Alex Cloherty

SARS-CoV-2: An army, or a single violin?

I haven’t written about SARS-CoV-2 for a while on Microbial Mondays - I’ve been busy revising a scientific manuscript on it instead - but a recent Instagram post and associated article from The Tyee, an independent online newspaper from British Columbia, made me change my mind.

“We now face an army of COVID Viruses,” it proclaims, with the subtitle: “The pandemic has not ended. It is evolving, with big implications.”

The Instagram post actually came my way thanks to my dear friend Darby, who forwarded it in our group chat and asked, “Is this true?”

The short answer: yes, SARS-CoV-2, the virus that causes COVID, has evolved into many different variants and subvariants, to the point that it’s sometimes difficult for even virologists to keep track of the latest virus on centre stage. But, in my opinion, that isn’t necessarily a bad thing. It might even be the best-case scenario.

Now, this is a very well written article that I’m responding to, and I really recommend giving it a read. As a scientist actively studying SARS-CoV-2, I didn’t have any quarrel in terms of the scientific facts. I just didn’t necessarily agree with the (mostly implicit) implication that we should all be panicking about the new variants. That being said, I’ve been wrong before and I’ll be wrong again, and only time will tell who’s more correct - me or Andrew Nikiforuk, the author of the Tyee article.

With that caveat out of the way, let’s dive in.

Point one from the Tyee article: “One virus has become many.”

This is absolutely accurate. We started out with the so-called “wild-type” SARS-CoV-2, the original virus that somehow jumped from an animal to humans back in 2019. And now, we have a regular alphabet soup of variants and subvariants - the mix of which is constantly changing. My colleagues and I submitted a scientific manuscript detailing new findings from our lab about SARS-CoV-2 at the end of last year, and by the time we got the paper back from the journal following peer review, we already had to change some sentences in the discussion of the paper about which Omicron subvariants were dominating worldwide. The virus is moving so fast that it’s outpacing the traditional mode of academic research by miles.

So, I completely agree that “one virus has become many.” But the point that I was missing in the Tyee article was that we always knew that this would happen. Although “our actions, or inactions” may be helping to drive evolution in certain ways (and I’ll get back to this particular point in more detail in a future Microbial Mondays article), evolution is an unstoppable tide. Andrew Nikiforuk writes, “What was once a single violin has become a complex and expanding orchestra with no discernable conductor.” Indeed, the conductor is invisible, but the conductor has always been there, has remained constant, and is the same conductor to which the entire orchestra of life plays: evolution. It all comes back to Darwin, and although our actions surely impact the exact course of evolution, they do not impact its everlasting existence.

Indeed, every virus that humanity has ever come into contact with evolves, and more specifically, co-evolves with us. Just think of the flu. Influenza virus is a name that we use to refer to many different subspecies within one big virus family, and we have been living with that reality for centuries despite perhaps not always paying much attention to it. If I step back and take a less human-centric view of SARS-CoV-2, one main difference that I see between influenza evolution and SARS-CoV-2 evolution, is that there are a lot more humans paying attention to the latter versus the former. Put simply, from a purely biological standpoint, the fact that SARS-CoV-2 evolves doesn’t make it special. The fact that it evolves quickly also doesn’t make it unique - so does HIV, for example. Evolving is just what viruses do.

This isn’t to say that you should bury your head in the sand and stop reading about SARS-CoV-2 evolution. It’s interesting! I read about it, too! I have a very strongly held belief that learning about science should never be simply left to scientists, and that curiosity absolutely does not kill the cat. Curiosity educates the cat. I just think that being curious and interested doesn’t necessarily have to entail a doomsday-esque “constant vigilance”.

Which brings me to the next point.

Point two from the Tyee article: “The new COVID soup is a unique experiment in evolution.”

As I wrote above, the evolution of SARS-CoV-2 itself isn’t really very biologically unique, in my opinion. What is unique about this situation is that we are watching it so closely.

When SARS-CoV-2 hit the world in 2019, it hit a technologically advanced, globalised society. This means that we can follow its evolution with incredible accuracy and detail, like no previous generations could. It also means that if we want to, we can obsess about the latest mutations in the SARS-CoV-2 spike’s receptor binding domain! Again, I’ve done it too. In my opinion, it is this, the information overload, which is truly the situation that humanity has never really found itself in before, and which is the truly unique experiment. However, this is rather a sociological experiment on how we humans respond to having this abundance of information about a potentially deadly, constantly evolving, invisible foe, versus a unique biological experiment in that foe’s evolution.

As a matter of fact, humanity actually has already encountered a somewhat similar foe in the recent past - but this encounter was at a time when the human race was more busy with other things. Although the influenza pandemic of 1918 likely claimed even more lives than the Great War, World War I undeniably took precedence in our attention economy at the time. Maybe it was because we could more clearly see the enemies involved in the war, versus in the pandemic. I wonder sometimes if the opposite is happening today, when people are better versed in the latest Omicron subvariants circulating a given continent, than in the latest developments in Russia’s invasion of Ukraine. I think a lot of our perception of this particular pandemic comes down to our hyper-focused attention on it.

Anyways, back to the Tyee article. Under this sub-heading on the COVID soup experiment, Andrew Nikiforuk writes, “As leaders have shifted to the position that masks and tests are matter of personal choice rather than collective self-preservation, they have implicitly silenced a vital message to the citizenry about how pandemics actually come to an end. It is this: less transmission means fewer mutations; fewer mutations means less variation, the fuel of evolution. Reducing infections, then, puts the brakes on viral evolution.” Indeed, if a virus is not able to replicate - in this case, within us, by infecting us - it is a rule that then it can’t mutate. Evolution happens over generations, not within generations. But I take issue with another point in this paragraph: “how pandemics actually come to an end”.

Do they come to an end? I’m not so sure.

Think about the 1918 influenza pandemic. We still have influenza. And sometimes we even have nearly the exact same type of influenza that circulated in 1918. It’s an inescapable fact that it is really hard, and perhaps even impossible, to completely eliminate a virus - especially one that is airborne like SARS-CoV-2 or influenza. In fact, we have only ever managed to eliminate one virus, smallpox, in the entire history of humanity. And to do so, it took 22 years of a highly effective World Health Organization campaign. Or, 184 years if you count the time since the very first, rudimentary vaccine against smallpox (which also happened to be the first vaccine ever).

The point that I’m trying to make here, is that we may be well on our way to the best case scenario: that “one pandemic has morphed into regional epidemics” (and thus we also cover point four from the Tyee article), in a similar manner to what we see with influenza. At least, that was the future that I was hoping for at the beginning of the COVID-19 pandemic: that one day SARS-CoV-2 would become a seasonal virus with regular peaks and troughs of infection, and for which we would have vaccines and antiviral treatments. And to be honest, it happened a lot faster than I was expecting. Again, I’m not trying to negate the terrible impacts that SARS-CoV-2 has had on humanity - I’m just saying it could have been a lot worse (for instance, it could have well taken us longer to develop therapies and vaccines), and that I am somewhat sceptical of claims that we’ll ever be truly rid of this virus.

Now, on to point three from the Tyee article: “What were viral peaks are now a constant rising sea of infections with high and low tides.”

About that rising tide bit - that kind of depends on where you are.

In regards to the ‘rising tide’, Andrew Nikiforuk (who to be fair, is writing in Canada) is referring to this graph to the right, which was popularised by the Canadian evolutionary biologist T. Ryan Gregory (a great guy to follow on Twitter, by the way). It shows the cases of hospitalisation due to SARS-CoV-2 steadily increasing with each new variant. Looks bad, eh?

But that’s not the case everywhere. You can actually see rather the opposite trend in these graphs from the USA, the Netherlands, and the UK.

I really don’t know exactly why we see these different trends across the different countries. It could be the specific public health approaches of the different countries, or the general health of the populations, or specific actions taken by the population such as more or less travel and the tendency to mask or not. It could be due to differing current circulating strains across the countries, or it could be something entirely different that I haven’t thought of. It is clear that COVID-19 is still putting people in hospitals, and that this virus has exposed challenges in our health care systems. But I think it’s too early to say whether the tide will keep rising, or if it will simply ebb and flow with the seasons. In my opinion, Andrew Nikiforuk is most likely right that SARS-CoV-2 has “gone from an acute emergency… to an ongoing chronic reality,” - but again I think that that may be the best outcome that we could have hoped for with such a highly contagious, airborne virus.

Point five from the Tyee article: “Reinfections rarely happened. Now they are commonplace.”

Also true - and that is a direct consequence of there now being many different subtypes of SARS-CoV-2. You can imagine it like this: each time SARS-CoV-2 evolves, it is sort of changing one item of its clothing. The more it evolves, the more different the virus's outfit is. As we’ve covered before on Microbial Mondays, our immune system functions by remembering what a virus looks like, using a sort of immunological ‘wanted’ poster. If the virus started out wearing a clown suit, but a few months later saunters up your nose wearing an evening gown, your immune system is less likely to recognize it and tackle it right upon entry. And, voila, if the virus is able to sidestep your immune system thanks to its new duds, you can end up with a reinfection.

My only objection here is that I don’t know if we could have reasonably avoided increasing amounts of reinfections.

I imagine that fateful day in 2019 as an opening of Pandora’s box. Once SARS-CoV-2 was out, there was no putting it back in. It’s just too contagious, too floaty (by that I mean airborne - airborne viruses are notoriously difficult to contain), and too sneaky (in that it takes a while to develop symptoms, so you won’t automatically notice if you’re contagious). I’m not denying that humanity has made plenty of mistakes along the way in our attempts to contain SARS-CoV-2, but with a virus like this, I think once it was out of the box, eventual reinfections were inevitable.

And now lastly, point six from the Tyee article: “We can do more to blunt the evolutionary threat of COVID subvariants”

Here, Andrew Nikiforuk eloquently writes, “So the pandemic is not over. Viruses, one of the most abundant entities on this planet, don’t stand still. They mutate. They shift. They adapt.” He then goes on to list a series of actions that we could take to limit the transmission of the virus. I agree with all of them. And action points like “Set new standards to clean the air in our schools and workplaces to dramatically reduce viral spread in the public” would have a beneficial impact on not only reducing SARS-CoV-2 cases, but lots of other viral and bacterial infections as well.

I guess my only point here is that I think it’s time for a more holistic view of infectious disease. I’m simply not sure anymore if SARS-CoV-2 deserves to be the singular star of the show. Perhaps it is time, to borrow Andrew Nikiforuk’s analogy, to begin thinking of SARS-CoV-2 as only one violin in the orchestra of infectious diseases.

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