A few months ago, I published a post on Delta’s transmissibility advantage, in which I argued that commonly accepted estimates of that advantage were likely overestimated and that in any case we didn’t have very good reasons to take them at face value. My argument was based on the distinction between a transmission advantage and a transmissibility advantage. A variant has a transmissibility advantage over another if, other things being equal, a person infected by that variant will on average infect more people. It has a transmission advantage if, in some particular context, people infected by it happen to infect on average more people. A variant can have a transmission advantage over another for a number of reasons. One of them is that it has a transmissibility advantage, but that’s not the only one. For instance, if a variant was introduced in a social network where most people don’t have immunity, it will spread more easily than variants that are circulating in social networks where most people have already been infected or vaccinated and are therefore less susceptible to infection. Thus, it’s dangerous to use a variant’s transmission advantage to estimate its transmissibility advantage, because if different variants are circulating in different contexts, and we have good reasons to think that’s often the case, one of them might have a transmission advantage over the other even if it has no transmissibility advantage, a transmissibility advantage but not as large as its transmission advantage or even a transmissibility disadvantage.
The problem is that, in practice, this is exactly what people do. They compare the growth rate of the new variant with that of previously established strains and use that to estimate its transmission advantage. This transmission advantage usually varies wildly across space and time, so they take the average and assume it corresponds to a transmissibility advantage, even if there is no good reason to think so. I also explained why, if people continue to use that method, they will eventually reach absurd conclusions:
If a variant is rapidly taking over, then even if it has no transmissibility advantage or only a modest one, it must have a large transmission advantage during its initial expansion, since otherwise it wouldn’t be taking over rapidly. Thus, if every time a new variant rapidly takes over in many places epidemiologists use its transmission advantage during its initial expansion to estimate its transmissibility advantage (even if the variant’s transmission advantage later collapses), they will eventually conclude that Omega or whatever has a basic reproduction number of 125, at which point it will perhaps finally dawn on them that such a methodology is not particularly reliable.
As it turned out, we didn’t even have to wait for Omega, we’ve reached that point already with Omicron.
For instance, here is what Tom Wenseleers, a Belgian professor of biostatistics, said about the expansion of Omicron in South Africa:
… [33-43%] 95% CLs. With a generation time of 4.7 days of the virus that would imply a 6 fold higher R value than Delta, if that would even be possible. To be confirmed, but not looking good… pic.twitter.com/VG839R2z04
— Tom Wenseleers (@TWenseleers) November 26, 2021
To be fair to him, he makes clear later that he is just talking about the effective reproduction number, not the basic reproduction number. In other words, he admits that the data don’t necessarily imply a transmissibility advantage, but merely a transmission advantage.
This is because, if we assumed that it reflected a transmissibility advantage, it would mean that Omicron has a basic reproduction number somewhere between 40 and 50 if you accept the estimates of Delta’s transmissibility advantage over the original strain that were derived using the same method. Of course, even epidemiologists don’t think it’s plausible that Omicron is that infectious, so they acknowledge that one can’t infer a transmissibility advantage from this transmission advantage. But as I pointed out several months ago, this was already true with Alpha and Delta, because the same method was used to estimate their transmissibility advantages over previously established strains. If this method produced conclusions that are not believable in the case of Omicron, it should cast doubt on the conclusions that were reached about previous variants using the same method. Therefore, the admission that we can’t use that method to infer Omicron’s transmissibility advantage over Delta has implications that go beyond the debate about how infectious Omicron is, though epidemiologists won’t point that out. However, they at least acknowledge that, in the case of Omicron, the inference from a transmission advantage to a transmissibility advantage is not reliable.
But if Omicron isn’t 6 times more transmissible than Delta, then how come it’s growing so much faster than Delta in South Africa at the moment? One explanation that epidemiologists often advance is that it’s better able to evade prior immunity. Indeed, it has several mutations on the spike that are believed to increase transmissibility and the prevalence of immunity has increased in South Africa since Delta took over, so this could certainly be part of the story. However, since as I noted previously the same variant’s transmission advantage often varies wildly across space and time even when it doesn’t have any advantage in terms of immune evasion or at best a very modest one, it should be obvious that it could be due to number of other factors we don’t understand beside the ability to escape prior immunity. In the case of Omicron, since it started to expand at a time when there were only a few hundred cases per day in South Africa and only a fraction of them are sequenced, measurement error could also be a big factor. Daily growth rates are measured by comparing the number of cases from one day to the next, so when you’re dealing with very small numbers, even a relatively small increase in absolute terms can result in a very large growth rate. But again there could be a number of factors. To be clear, as I already noted, there are good reasons to think that Omicron is highly infectious because it has several mutations that are associated with more transmissible strains, but there is no way to quantify how transmissible it is by analyzing the mutations it carries.
In any case, it doesn’t really matter. If this variant is really significantly more transmissible or better at evading prior immunity than Delta, then it will soon be everywhere and there is nothing we can do about it. Indeed, it has already been detected in several countries outside of Africa, so this wouldn’t be surprising. On the other hand, if it’s not more transmissible or better at evading prior immunity, there is no point in freaking out and closing borders or implementing other restrictions to prevent it from spreading. As many people have noted, closing borders to people coming from South Africa actually disincentivizes the kind of careful genomic surveillance that allowed South African scientists to detect Omicron early and warn the rest of the world about it. But perhaps it would be for the best, since as Richard Hanania noted, if we can’t detect new variants until they’re already everywhere, it will at least prevent governments in the developed world from taking stupid measures because they panic. Some people suggested that closing borders was a way to “buy time”, but it’s not clear what for exactly. As I argued a few months ago, SARS-CoV-2 is not going anywhere, it will continue to mutate because evolution doesn’t go on vacation and new variants will keep emerging, but immunity – whether induced by infection or vaccination – should still protect us against severe disease, so it makes no sense to freak out every time a new variant that might be more transmissible is detected. This is the world we live in now, so we have to accept it and move on. Buying time doesn’t actually buy you anything when there is no finish line.