This preprint on SARS-CoV-2 transmission dynamics was a great read. The discussion about heterogeneity often focuses on numbers of contacts, but that always felt incomplete to me. As much as possible, we must link the models to the biology. (Thread 1/7)
The article posits different categories of super-spreading events.
- Individuals with many more contacts
- Individuals with high viral load
- High risk facilities (meat-packing plants, prisons, etc)
- Opportunistic scenarios (cruises, night clubs, choirs, etc) (2/7)
The last category of opportunistic scenarios reflects temporary clustering of people. For a short period of time, people have many more contacts (e.g. Biogen conference). These are further exacerbated by the presence of loud speaking/singing. (3/7)
The article describes many different observed super-spreading events. It is through these examples that we can start to identify patterns (indoors, crowded, conversation). Importantly, preventing these can have a dramatic impact on the outbreak, making control easier. (4/7)
Finally, they do a nice job explaining the theoretical reasons why overdispersion can make outbreaks appear so explosive. It is because many seeded cases don't cause secondary infections, so we only observe what has taken off, more likely to be a super-spreading cluster. (5/7)
The same point is made here. Given how frequently people travel, there were surely many introductions into the US from China and then later Europe. Not all of these took off. But that offers insight into those rare early deaths, like in Santa Clara. (6/7)
Finally, models that consider only heterogeneity in contacts (and no variation over time) are likely missing an important part of the puzzle. My feeling is that the dynamics are much more complex than we're accounting for.
Tagging authors @joel_c_miller @svscarpino (7/7)
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