Item — HN Reader

Some counterpoint. A lot of the assertions, particularly the fact that delta is dramatically more transmissible than ancestral type, are reported as fact in the mainstream, but the evidence for this particular claim is thin. It certainly is true that delta is outcompeting the other strains. But inferring higher transmissibility from observational or ecological studies is not really sound. Most of the increases can be explained by human behavior - a third to a half of Americans are not fully vaccinated, and people are going out, not wearing masks, etc. Determining higher transmissibility in the virological sense is a difficult experiment and I don't think is really being done.

This is discussed in some detail in TWiV[777], a discussion with Ron Fouchier. If you use influenza as a model, the picture looks completely different - new strains are coming up all the time and outcompeting the older ones, but that's just because people have developed immunity to the older ones (antigenic drifts). The new ones are not fundamentally different or more transmissible. For people who don't want to listen to the whole thing, the main point is also made in a NYT opinion piece[2].

Pueyo claims that alpha is 60% more transmissible than ancestral type, but again the evidence doesn't strongly support this. Indeed, a preprint just came out[3] in which alpha looks pretty much identical to ancestral type when it comes to viral loads and clearance.

I've really enjoyed and appreciated Pueyo's writings. In particular, I think "The Hammer and the Dance" was groundbreaking and we could still learn the lessons from it. But I think this one is a miss: it could present real insight, but instead mostly propagates conventional thinking.

There's a really interesting science communication aspect to delta: it's basically a proxy for the (very true) statement, "the virus is still dangerous." In fact, one prominent evolutionary biologist accused the NYT op-ed of verging on "delta denialism". Accurately communicating reality in a way that is useful to people is fantastically hard, and we just don't have an ecosystem for it. I think this is the reason I've become addicted to TWiV and other similar highbrow sources - I hate being fed partial information and feel compelled to learn more.

[777]: https://www.microbe.tv/twiv/twiv-777/

[2]: https://www.nytimes.com/2021/06/27/opinion/covid-vaccine-var...

[3]: https://twitter.com/BallouxFrancois/status/14149092626571141...

2 comments

The article itself leads with the conventional media thinking about Delta, but to me it almost feels like it's a hook to lure in both those who follow or doubt the conventional thinking in order to lead them to develop a better understanding of the actual risks. I very much agree with you about the transmissibility. It's probably not much more transmissible but still enough to out-compete other variants, but there's a lot of other factors that greatly amplify the effective transmission rate. It's interesting the correlation between where the new variants spread and what type of vaccines were deployed there. Immunity against certain variants from past infection and vaccination is going to put pressure on variants to develop in a certain way. We'll probably soon see variants that are more transmissible against the Pfizer vaccine.

The evidence cited in the article is not just looking at prevalence graphs, it is a study that looks at within household transmission rates and thus public social distancing and mask wearing would have no effect.

And your [3] source explicitly warns against using their findings to compare infectiousness.

> I don't believe 'infectiousness" is necessarily the ideal term here. B.1.1.7 (Alpha) could be intrinsically more 'infectious' than previous 'non-variant' lineages in circulation (e.g. higher risk of initiating an infection with the same infectious dose of virions). 4/

Let me speak to the second criticism (I'm not sure I fully understand the first one). The quote in context from the paper is:

"there is no significant difference between B.1.1.7 and non-B.1.1.7 viruses in total infectiousness predicted by our model"

But "predicted by our model" is doing considerable work here, as the model doesn't take into account potential differences in what happens after someone is exposed to the virus, only what's measured in the study (viral shedding dynamics). So I think the critique of Prof Balloux is worth heeding: it would be a leap to conclude that alpha is definitely not more "infectious" than ancestral type when you take into account the broader meaning of "infectious." Even so, to my mind that places even more burden on demonstrating a biological mechanism.

It also refutes a major claim in TFA and calls into question the methodology used to support that claim: "In China, they estimated the viral load of Delta to be 1,000 times higher than that of the original variant." But when you look at viral load specifically, as is done in the Ke et al paper, you find no difference at all. A few things could be going wrong here, but my money would be on some problem in how that 1000 factor was "estimated."

Then don't extrapolate viral load to transmissibility like you did in your original comment. Stick to refuting the specific claims that you actually have evidence to address.

If you don't understand my summary of the first point, then read the source the article cited for the claim that delta is 60% more transmissible:

https://khub.net/documents/135939561/405676950/Increased+Hou...

Thanks for that citation. It is indeed among the strongest evidence for increased transmission. My point is that it is observational rather than biological evidence, which is not the same, and when you do observational studies, there can be many confounders.