How Little We Know about the Cov-SARS-2 Virus

Things that we do not understand concern us.  Things we cannot control frighten us.  When we can neither understand nor control something it terrifies us.  So far, the novel coronavirus has both confounded our attempts to understand it and in mid-April, when the number of new cases was rapidly climbing almost every day, we seemed to have little control over it.

Since then the numbers have been steadily improving.  Last week in the U.S. there were fewer than half the fatalities attributed to COVID as mid-April, notwithstanding the relaxation of lockdowns around the country.

Of course, elected officials have been quick to claim credit for the improvement.  The problem is that there is no explanation, or at least not one that I can discern, that accounts for the wide variation in outcomes.

First, there are stunningly different outcomes between southeast Asia and the rest of the world.  In eight countries in southeast Asia, none have suffered more than 1 fatality per 100,000 people.  Europe’s average is 24 fatalities per 100,000, with countries like Spain and Italy over 50 per 100,000.  Even Norway, which instituted one of the earliest and most severe lockdowns, had 4 per 100,000.  The U.S. is at 30.  New York City is a staggering 200+, depending on what fatality count you use.

There is nothing that we know now that explains a 100-fold difference in the outcomes between some European countries and some southeast Asian countries.  Many have attempted to attribute the difference to various non-pharmacological interventions (NPIs), frequently mistakenly attributing causation to coincidence.

For example, there have been a number of media and social media accounts attributing the better outcome in Asia to a more extensive mask-wearing culture.  But the studies that have looked for a correlation between wearing masks and community transmission of a respiratory infection have found relatively nominal reductions or were inconclusive.  Certainly, no study has found anything that even vaguely approached a 100-fold reduction.

Others have suggested better contact testing and tracing, earlier interventions, greater social distancing, a different strain of the virus, genetic difference in the immune systems of the respective populations, greater social cohesion, more autocratic governments . . . and the list goes on.  There is probably some validity to many of these explanations.  After all, it only makes sense that the farther you are from someone who is infected, the less likely you are to be infected.  But there is certainly no data available now that demonstrates that any particular NPI was a decisive factor in the divergent outcomes.

Frustratingly, we may never fully understand why the virus has behaved like it has.  Over a century after the Spanish Flu pandemic, there is still widespread debate over what happened, including even how many died in it.  We have far better technology and public health infrastructure today, so we will likely eventually put together a clearer picture of what happened in this pandemic, but we may never have answers to some of our questions..

Of course, in today’s supercharged partisan environment, both sides have rushed to provide explanations convenient to their political narratives.  I find this partisan posturing tedious and, for the most part, not at all factually or scientifically based.  For now, it is utter intellectual hubris for anyone to suggest that they have an explanation for the course of the disease to date, much less the ability to predict what is likely to happen in the future.