Covid-19 heterogeneity

From Southeast Asia coronavirus update by Tyler Cowen. He is discussing and speculating about why Vietnam, Thailand, Cambodia, and Laos have nearly zero Covid deaths or even cases.

Have you noticed that those four countries are right next to each other? (Within southeast Asia, most cases are in the relatively distant Indonesia and Philippines.)

I genuinely do not understand why this heterogeneity is not discussed much, much more.

Those countries also have very different institutions and systems of government and state capacity. Do you really think this is all because they are such policy geniuses?

Those countries have instituted some good policies, to be sure. But so has Australia, where there is a major coronavirus resurgence.

Inquiring minds wish to know. One hypothesis is that they have a less contagious strain, another is that they have accumulated T-cell immunities from previous coronaviruses. Or perhaps both? Or perhaps other factors are playing a role?

I do not understand why the world is not obsessed with this question.

Well, yes. There are mysteries galore. Why did Italy seem to be an early and massive victim? Why hasn't California been harder hit? Why is Israel suffering a second wave? And only Israel so far?

My refrain has been since the beginning - We don't know what is going on. And we still don't. There are a few things we think we understand but only a few and even some of those are kind of dicey.

Cowen has a follow-up post from a reader - A highly qualified reader emails me on heterogeneity by Tyler Cowen.

“Some thoughts on your heterogeneity post. I agree this is still bafflingly under-discussed in “the discourse” & people are grasping onto policy arguments but ignoring the medical/bio aspects since ignorance of those is higher.

Nobody knows the answer right now, obviously, but I did want to call out two hypotheses that remain underrated:

1) Genetic variation

This means variation in the genetics of people (not the virus). We already know that (a) mutation in single genes can lead to extreme susceptibility to other infections, e.g Epstein–Barr (usually harmless but sometimes severe), tuberculosis; (b) mutation in many genes can cause disease susceptibility to vary — diabetes (WHO link), heart disease are two examples, which is why when you go to the doctor you are asked if you have a family history of these.

It is unlikely that COVID was type (a), but it’s quite likely that COVID is type (b). In other words, I expect that there are a certain set of genes which (if you have the “wrong” variants) pre-dispose you to have a severe case of COVID, another set of genes which (if you have the “wrong” variants) predispose you to have a mild case, and if you’re lucky enough to have the right variants of these you are most likely going to get a mild or asymptomatic case.

[snip]

2) Strain

It’s now mostly accepted that there are two “strains” of COVID, that the second arose in late January and contains a spike protein variant that wasn’t present in the original ancestral strain, and that this new strain (“D614G”) now represents ~97% of new isolates. The Sabeti lab (Harvard) paper from a couple of days ago is a good summary of the evidence. https://www.biorxiv.org/content/10.1101/2020.07.04.187757v1 — note that in cell cultures it is 3-9x more infective than the ancestral strain. Unlikely to be that big of a difference in humans for various reasons, but still striking/interesting.

And as always with Cowen, much of the meat is actually in the comments to the posts.