The Likely Future of COVID-19? More Than Polio, Less Than Flu

F. Perry Wilson, MD, MSCE


March 03, 2021

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This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study. I'm Dr F. Perry Wilson of the Yale School of Medicine.

After what we've all been through, it almost sounds crazy to talk about it, but we really should start thinking about what we would call "a victory" in the fight against coronavirus.

Lately there have been a slew of think-pieces about when life will get back to normal, but that's not really what I want to talk about. I'm thinking further into the future — 5 years, 10 years. What are the potential scenarios? And what can we honestly say means we won?

I'll start with the clearest victory: total SARS-CoV-2 eradication. The hashtag #zerocovid is certainly catchy, but even proponents would be quick to tell you that #zerocovid means elimination, not eradication. What's the difference? Eradication means that the virus has ceased to exist in the world, except perhaps in certain labs. Here is a comprehensive list of viruses that the human race has eradicated.


Rinderpest only infects cattle, by the way. Or it did. We eradicated it.

The reason we could eradicate smallpox was twofold: one, we had an effective vaccine; two, there were no animal reservoirs of the disease. (It probably jumped to humans from rodents 50,000 years ago, but in modern times we were the only vector.) That meant a global vaccination project could achieve eradication. And it did.

We have an effective vaccine — multiple, in fact — against SARS-CoV-2, but we also have the pesky problem that the virus can circulate in other mammals. It's hard to catch and vaccinate all the bats, so another species jump is always possible.

Can we move from eradication, then, to elimination? Here, the idea is that there is no acceptable limit of COVID cases. We get the rates as low as possible and then, when an outbreak inevitably occurs, we stop it from spreading. Think firemen putting out a housefire before it spreads to the whole neighborhood.

Possible? Maybe. But the problem — the secret weapon of COVID-19 — is asymptomatic spread. By the time we see those first cases, the horse might be out of the barn. Or, to avoid mixing metaphors, the invisible fire may have already spread.

This is the fundamental public health difference between SARS-CoV-2 and the more lethal SARS-CoV, which was responsible for the SARS outbreak in 2002. Also a virus with an animal reservoir, we haven't had a single case worldwide since 2005. If not eradicated, SARS was eliminated. This was possible, in no small part, because people were almost universally symptomatic while they were infectious. Remember the temperature screenings at airports? They work — if people who are infectious actually have fevers.

So while elimination is aspirational, I don't think we should set the bar for victory quite that high.

The next level I've seen tossed around isn't ambitious enough, though.

This is the idea that if we can get COVID cases to look more like the flu, we win.

Let's put some numbers to it. Flu deaths are variable but tend to kill about 25,000 individuals in the US each year. That works out to 68 a day. Currently, even with death rates falling, we're seeing around 2500 COVID deaths a day.


Some experts have said that if we can get COVID-19 deaths down to below 100 a day in the US, we've done as good as can be expected. We've transformed a raging scourge to another flu.

But here's the thing: I don't want another flu. If COVID never existed but flu suddenly got twice as deadly, wouldn't we all be freaking out? This bar is too low for me.

And I think we can do much better. In fact, for multiple reasons, I think we can get "endemic COVID" to rates much lower than those of endemic flu.

First, we have the vaccines. Flu vaccines vary year to year but tend to have about 50% efficacy — good, not great. The coronavirus vaccines have dramatically higher efficacy rates — up to 95% for the mRNA vaccines — and are even more protective when it comes to severe disease and death.


Second, flu is a fickle virus. Though the mutation rate of influenza A isn't as dramatic as some of the great mutators like HIV and HCV, it is dramatically higher than SARS-CoV-2, thanks in part to a proofreading enzyme that the coronavirus carries in its genetic makeup.


Why, then, are we seeing all of these variants? Simple. Every cell infected is a chance for a new mutation to occur: More people infected, more cells infected, more mutations — even with a virus that, on its own, is pretty stable. The implication is positive. If we can squelch the infection rate, the virus won't be able to evade our defenses as quickly, giving us a chance to keep it good and squelched, even more so than with flu.

The third edge we have against COVID-19 is its weird spreading pattern, though it's a double-edged sword. By now, we've all basically memorized that the R0 of SARS-CoV-2 is 2.5 or so, much higher than for flu, which is usually in the low 1s. But the idea that each infected person infects 2.5 additional people is just an average. COVID spread is considerably clumpier than that, with superspreading events driving a lot of transmission. This can be quantified by the k-number — the dispersion parameter. Flu A has a k of around 1, meaning that spread is pretty uniform. SARS-CoV-2 has a k of around 0.1, meaning that a small number of cases are responsible for a large number of secondary cases.


This could be good for us. It means that if we can get rates way down, we are more likely to see isolated outbreaks that we can quickly pounce on compared with the slow burn that we see in a typical influenza season. Of course, one big superspreading event in an indoor concert or something would set us way back.

My belief, if we do this right, is that 5 years from now, we'll still have coronavirus, but cases could be extremely rare, worthy of particular attention: local, regional, and national reporting — that sort of thing. We may not give it the smallpox treatment or the polio treatment, but it certainly doesn't have to be another flu.

F. Perry Wilson, MD, MSCE, is an associate professor of medicine and director of Yale's Clinical and Translational Research Accelerator. His science communication work can be found in the Huffington Post, on NPR, and here on Medscape. He tweets @fperrywilson and hosts a repository of his communication work at

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