There’s a new variant of cov-19, the UK strain, that is something like 70% more infectious than previous strains. At this point its lethality seems about the same as earlier strains.
Virologists, most of them, did not expect this. I did.
Let’s consider some simple examples. Imagine that you have someone – a single individual – with what we will call a normal strain, A. On average, in the current situation, it has an R0 well above 1.
What is the most likely outcome? Most likely, he doesn’t spread it to anyone, and it dies out. Overdispersion: most people don’t do much spreading, and a few do a lot. Let’s say that 20% of those infected do all of the spreading. Right off the bat, 80% of new strains die out, just because of this pattern.
Now, imagine that we simultaneously introduce two new strains, A and B with a 50% greater R0%. for each, a single individual.
There are four possible outcomes: A spreads widely, B spreads widely, both and A & B spread widely , both A and B disappear.
Most likely both will disappear (~64% chance) .
There’s a fair chance that A will spread while B is lost, and a moderately larger chance that B will spread while A is lost.
There is essentially zero chance that both will spread widely: even if both manage to avoid being lost by chance in the beginning, B will grow faster than A and replace it.
So, suppose you introduce one person with A, and one person with strain B: can you judge the relatively infectivity by which one succeeds? No – there’s a significant chance that the less-infective one will win out.
Now consider a situation in which A is already common, and a single case of B is introduced. what are the possible outcomes?
- B is lost by chance. ( > 80% probability)
2. B replaces A – happens if B is lucky enough to get past the risk of extinction when rare. But once it gets up to a few hundred copies, it will surely replace A.
What can we conclude if B is rapidly replacing A ( as has been the case with the new UK strain)?
That it surely has significantly higher transmission, significantly higher R0.
Many virologists thought this very unlikely, and some said that you could never know that a new variety had higher transmission from mere incidence data: you must understand the biological mechanism. Are they correct? Obviously not.
Why did they think that a new, more transmissible variant of COVid-19 was unlikely? I would say there are several reasons. One, they typically deal with viruses that have been around for a long time, like measles ( > 1000 years) . An old virus is going to be pretty well-adapted to to humans. Probably it’s at a local optimum, where small changes would reduce infectivity. But you don’t expect that high degree of optimization in a virus that’s brand new in humans: while spreading to very many people, more than 100 million, greatly increases the chance of transmission-increasing mutations. Fisherian acceleration.
Like most biologists and MDs, most virologists don’t know any theory, and in fact don’t _believe_ in theory. For this they occasionally pay a price.