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Summer in question

May 18, 2020

My previous post painted a bleak few months ahead. One thing that might change that completely is if Covid-19 proves seasonal, and goes way for the summer, as the flu does. The interesting thing is that not only does no one know the degree to which this disease is seasonal, given that it is new, there also isn’t a good understanding of what makes some diseases so seasonal:

Researchers have speculated that changes in ambient temperature and humidity may make these viruses less viable by affecting their outer proteins and membrane, or by altering how quickly the virus-carrying droplets from mouth and throat evaporate. On the other hand, the change in infection rate might be due to the ways that people change their behavior with the seasons, going from being enclosed in offices and schools to opening windows and spending more time outdoors. (Getting more sunlight, which drives Vitamin D production and might enhance the immune system’s defenses, might play a role, too.) More subtly, it’s also possible that changes in temperature and humidity affect our bodies in ways that make them more or less vulnerable to viral infection.

While the summer free from this disease would be a welcome respite, it doesn’t seem to be doing that. Here in the coastal bend, where it already is high summer, we have had a recent surge in cases. And spread seems to be accelerating in Texas in the last week.

One of the silver bullets that might be developed quicker than a vaccine is a monoclonal antibody treatment. The interesting there is that it would prove a generic approach to infectious disease, much like vaccine development. A process that identifies new pathogens, or new strains of old ones, when they first appear, and then quickly develops monoclonal antibody remedies, essentially replicates at the social level part of what our individual bodies do biologically. That would be a major advance against infectious diseases generally.

One respondent recently said to me that the only importance to an epidemiological model is its ultimate projection of deaths. Which is wrong. No one can predict that at this point, no more than they can what the final score is in a professional football game, when at five minutes of play one team first scores a field goal. For the disease, it depends on what people do, it depends on what governments do, it depends on what treatments are developed and how fast, and it depends on what the disease does. No one knows any of that. The models cannot predict any of that. The models are not meant to prophesy, but to provide mathematical tools for thinking about those possibilities. I hope for a summer respite, and for a monoclonal antibody treatment in the fall, and for a vaccine not long after that. Each of those is dicey. If we get all of those, the US death toll will be quite effectively capped. Perhaps at less than twice what it is now, just ten weeks in. If we get none those nor any other good turns, the death toll could become horrendous.

I worry that many Americans, tired of the various measures taken so far to slow the spread, ready for summer, are thinking this almost is over. My own suspicion is that we still are in the first quarter.

A fishmonger in France had this disease in December, before anyone was looking for it outside China, and before it could have been diagnosed as such. Again, the early history of this disease is not yet known.

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