We’re all different, and that (probably) matters for infection with COVID-19

Felipe IV de castaño y plata, by Diego Velázquez

Above is Diego Velazquez’s portrait of Philip IV of Spain. He is not the best looking royal, and has what is sometimes called the Habsburg jaw, i.e., a very large jaw, attributed in this case to a lot of cousin marrying by his royal dynasty, the Habsburgs. They were rather inbred. Lab experiments on how diseases are transmitted are often done on mice. Now you might think that lab mice have little in common with the Habsburgs, but in fact they do haveone thing in common: the mice are also inbred. I think biologists want to avoid the variability that would occur if the, say, 50 lab mice they are doing experiments on, have a lot of genetic variability. So they are deliberately inbred.

But at least most commoners are not inbred, and this may matter for understanding transmission of COVID-19. Data on infecting lab mice with a corona virus that is in the same family as SARS-CoV-2*, finds that over a the dose range of about a factor of 100, you go from very little infection to almost 100% infection. Maybe this result would also apply to infecting a room full of Hapsburgs, but it may not to a room full of unrelated commoners.

As I pointed out in an earlier post, increasing the probability of infection for norovirus from small to high, requires more like a factor 10,000 increase in dose, than a factor 100. And even at very high levels, not all are not infected. This study was on (non-Hapsburg) humans. For the norovirus it is, I think, well understood that some of us have won the genetic lottery when it comes to resisting norovirus, while others of us have not, and so are much more susceptible.

It seems likely that the same applies to COVID-19, i.e., that some of us are better equipped genetically to resist COVID-19, while others are more susceptible. As far as I know, we don’t have good data on what these genes are. So we can’t test your DNA and see if you are more or less susceptible to COVID-19. It is not useful like that. However, it may help us understand why in superspreader events**, some people get infected and some do not, even though they may all be exposed to relatively similar doses of SARS-CoV-2.

* For example, that collected by Watanabe and coworkers in 2010 (see the appendix).

** For example, the event at the Skagit choral practice in USA, where perhaps 53 of the 61 in attendance were infected. See the analysis of Miller and coworkers.

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