I am asking this because as I look at the trajectory of this outbreak I am beginning to think that maybe this case count reflects large community-based transmission that has been ongoing for some time. I have thought that maybe the cluster at the seafood market was a “red herring” (pun intended) and came to light because of the epidemiologic linkage of patients and I am beginning to increasingly think that it may be the case. The Lancet paper on the 41 seafood market cluster tellingly reveals that patient number 1 had no contact with the market and became ill December 1 — weeks before this outbreak came to light. This suggests that this outbreak had been ongoing since at least November unbeknownst to clinicians. Remember, viral upper respiratory infections and even pneumonias largely go undiagnosed to a specific microbiologic level (to wit, I rounded this weekend and had multiple such cases that defied microbiologic diagnosis even in a nationally renowned quaternary care medical center).

In light of the above, the logical question is: if Patient 1 wasn’t linked to the market, where was the virus acquired? Who is Patient 0? We need serological anitbody-based surveys to see how prevalent exposure to this virus was pre-outbreak detection.

Phylogenetic analysis of the virus suggests a single introduction to humans but little variation in the limited human isolates available so far — they all share a common ancestor. However, does that suggest when the jump to humans occur? There are known rates of coronavirus mutations in humans and that can give some clue to how much divergence has occurred in humans and it appears that it has not diverged much at all. I wonder if this virus, like other coronaviruses, was circulating in the midst of a relatively forceful flu season and not diagnosed or noticed because many of the cases mimic influenza and other respiratory viruses. The data, based on assumed mutation rates, suggests this jumped no earlier than October 29, 2019 which would give the virus an almost 2 month head start to spread comingled in the flu season.The Makona variant of Ebola Zaire, which was the result of a single viral spillover from bats, circulated for 3 months before notice in Guinea.

If this is so, I expect case counts to rise as the virus circulates and deaths to rise as well (though at a much lower rate). Maybe this virus will become another established seasonal coronavirus with severity that is intermediate between the community acquired coronaviruses (OCV43, 220E, NL63, HKU1) and MERS and SARS? (Note that HKU1 can cause severe disease and may be an intermediate coronavirus as well)

I also believe if there is widespread community prevalence of this virus there is likely a significant severity bias in case reporting as well as in conceptualization of this viral syndrome. Imagine if you didn’t know anything about influenza and RSV and scoured adult ICUs and hospital floors. You would get a totally different picture of these diseases than if you were out in urgent care centers and PCP offices?

None of the above is meant to minimize this outbreak but my attempt to make sense of it.

If DA were here, I would ask him and know he would have an answer in a minute. It is at times like these that his giant, reasoned, prescient voice is what the world needs.