Headaches. Loss of smell and taste. Extended fatigue after initial infection. Frequent relapses. Cases of depression, insomnia, and even psychosis. People self-medicating with quinine. A disease which primarily strikes the old and those with underlying conditions.
No, I’m not describing COVID-19, I’m talking about the 1889–1890 Russian “flu.” And yes, quinine, the ancestor of hydroxychloroquine, enters the picture too. Because history, I guess.
The Fight Over Russian Flu
Seroarchaeologists, who attempted to identify the strain causing Russian flu by studying the immune systems of elderly people who would have been exposed, think that the Russian influenza, which infected a good chunkof St. Petersburg before expanding along rail routes to kill a million people worldwide, was an H3 strain of the flu.
But there’s an alternative theory, circulating since 2005. This theory centers on two things:
- The symptoms listed, which, as we all now know, are not so strongly associated with flu.
- An epidemic of bovine pneumonia that preceded the pandemic.
Enter OC43. OC43 is an endemic human coronavirus. We’ve all probably had it at some point. Of the four coronaviruses that cause the common cold, it’s the most common.
And it’s very closely related to a bovine coronavirus…and genome mapping indicates the split took place in the nineteenth century. That’s as close as we can get, but the timing is right.
This is, of course, speculative. OC43 is so common that seroarchaeology could never prove this.
Until this year, of course, the argument was academic and only of interest to virologists.
As SARS-CoV-2 sweeps the globe, though, it might be of rather more than academic interest.
The Pattern of The 1889–1890 Pandemic
The outbreak appeared to start in Bukhara, a central Asian city in the Russian Empire, where it killed a lot of people and then spread to Saint Petersburg. From there, it was basically in Europe. Through the Baltic shipping trade, it went to Scandinavia. And it made it across the Atlantic quickly too.
It was a very, very contagious disease. Its spread was, of course, helped by lack of knowledge.
Unlike COVID-19, it affected young people as well as the elderly.
There was a small first wave, then a huge second wave. That wave died out (there was no social distancing then), but sporadic outbreaks continued until 1895.
The ultimate end to the pandemic: The virus became endemic and weakened, whether through mutation or herd immunity. Nobody now worries about catching OC43 (although, like all common colds, it occasionally kills immunocompromised or extremely frail individuals).
What does this Teach Us About COVID-19?
First of all, it depends on who is right about the virus causing the 1889 pandemic. If it really was flu, nothing.
If it was OC43? Then we have a pattern which might be more accurate than comparison with the 1918 flu.
That pattern is a large initial outbreak, a repeating pattern of smaller outbreaks, and then the virus “disappearing” as it becomes mild and endemic. In other words, we are actually dealing with, literally, a pandemic cold. (Obviously that doesn’t mean it shouldn’t be taken seriously). The death rate and R0 also seem to be similar to COVID-19. COVID-19 has spread in a different way because of higher population and different movement patterns, but it’s still hit cities before rural areas.
If SARS-CoV-2 behaves like OC43 then, without a vaccine, we are looking at several years of interrupted normality; we’ll be able to go back to normal, but we’ll have to keep an eye on things and be prepared for another outbreak. Wastewater monitoring may prove to be the best way to spot them before they become serious. However, while the virus will always be with us, the pandemic won’t.
A vaccine, even one with only 50% effectiveness, would accelerate this process. It’s possible a COVID-19 vaccine will not prevent infection, only serious illness, and that would start to push it into the endemic stage faster.
But again, this is speculation. I personally am kind of buying the coronavirus theory based on the available data, but my degree is in archaeology, not epidemiology.
So, put this down as opinion…and also a fascinating sidetrack into the history of epidemics.