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Could the key to COVID be found in the Russian pandemic?

From lethal pandemic to common cold: what we can learn from the events of 1889-90

June 4, 2020

3:20 PM

4 June 2020

3:20 PM

The killer came from the east in winter: fever, cough, sore throat, aching muscles, headache and sometimes death. It spread quickly to all parts of the globe, from city to city, using new transport networks. In many cities, the streets were empty and shops and schools deserted. A million died. The Russian influenza pandemic of 1889-90 may hold clues to what happens next — not least because the latest thinking is that it, too, may have been caused by a new coronavirus.

In addition to the new diseases of Sars, Mers and COVID-19, there are four other coronaviruses that infect people. They all cause common colds and are responsible for about one in five such sniffles, the rest being rhinoviruses and adenoviruses. As far as we can tell from their genes, two of these coronaviruses came from African bats (one of them bizarrely via alpacas or camels), and two from Asian rodents, one of them via cattle.

This last one, known as OC43, is the commonest of the cold coronaviruses. It comes around every winter and apparently sometimes reinfects people who have had it before. Unlike the other three, its origin is not lost in the mists of time but is known to be comparatively recent. Comparing its genetic sequence with that of its close bovine cousin, Dr Marc van Ranst at Leuven University in Belgium and his colleagues calculated in 2005 that they shared a common ancestor around the year 1890. (There is also a version of the same virus that infects pigs but it is slightly less close to the human and cattle versions than they are to each other.) That date was therefore probably when the virus jumped into the human species for the first time.

The date is intriguing because 1889-90, as previously stated, saw a terrible pandemic, the worst of the 19th century, caused by a respiratory infection. Moreover, it was preceded by a global outbreak of what was thought at the time to be pleuro-pneumonia in cattle. It has always been assumed that the 1889-90 Russian or Asiatic flu was indeed a form of influenza. But direct evidence of this is lacking, and some of the symptoms do not seem quite right for flu. Given how many people fell ill, implying little pre–existing immunity, it seems probable that it was a virus new to the human species, and the dating coincidence with OC43’s species jump is highly suggestive.

The first case is thought to have been in Bukhara, in central Asia in the spring of 1889, but by October, Constantinople and St Petersburg were affected. In December, military hospitals in the Russian capital were overcrowded, factories and workshops closed for lack of workers and ‘whole districts of the city were abandoned by the population’, according to one report. The symptoms were said to include headache, fever, aching bones, facial rash and swollen hands. The illness lasted for five or six days but sometimes left the patient exhausted for weeks.

The virus reached Paris in November. By the turn of the year, with hospitals full, patients were housed in military barracks and tents in the city’s parks. Many schools were closed. In Vienna the schools closed early for Christmas and stayed closed till late January. In Berlin, it was reported that many post-office staff were affected. In London so many lawyers fell ill that the courts were closed for a while. One day in January at St Bartholomew’s Hospital in the City of London, Dr Samuel West found more than 1,000 people crowded into the casualty ward, most of them men.


In every country, capitals and port cities were hit first and hardest because they had the busiest rail and ship connections. Celebrities were not immune. The Russian tsar, the young king of Spain, the president of France, the queen of Sweden and Lord Salisbury all fell ill. In Turin, the Duke of Aosta, who had briefly been king of Spain, died, as did Empress Augusta of Germany and Lord Napier. Mass-circulation newspapers engendered widespread alarm.

According to a modern analysis, the death rate peaked in the week ending December 1, 1889 in St Petersburg, December 22 in Germany, January 5, 1890 in Paris, and January 12 in the US. R0 has been estimated at 2.1 and the case fatality rate was somewhere between 0.1 percent and 0.28 percent: similar figures to today’s pandemic.

Contemporary newspaper reports say that like today’s epidemic, the Russian flu appeared to attack adults more than children, and in some schools the teachers were all affected but not the pupils. Like today’s virus, it was, intriguingly, reported to affect men much more badly than women. Newspapers were filled with statistics of mortality, anecdotes and reassuring editorials.

In 1890 the germ theory of disease was far from universally accepted, and viruses had yet to be distinguished from bacteria. The ‘miasma’ hypothesis that blamed such pandemics on the air remained popular, and the speed with which the illness had spread around the world seemed to indicate something other than person-to-person contact, though rail travel was in fact the cause. In an echo of today’s 5G fantasies, an editorial in the Lancet noted that there had been earthquakes recently: ‘Why should not this troublesome complaint have been produced by injurious emanations from the earth?’

By March 1890 the pandemic was fading in most places, just as common colds and flu do in spring today. The seasonal pattern displayed by colds and flus is so striking that it cannot be a coincidence that today’s pandemic was also in retreat by May all around the world, irrespective of the policies in place. By the northern summer of 1890 the virus was ensconced in the southern hemisphere, having reached Australia in March. It returned to Europe the following winter and for several years after.

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If OC43 was the cause of the 1889-90 pandemic — far from proven, of course — and given that it is the cause of perhaps one in 10 colds today, then it has evolved towards lower virulence. It is easy to see how this occurs with respiratory viruses, which are transmitted by people chatting and shaking hands. Mutations that affect the severity of the virus also tend to have an impact on whether people pass it on: if it sends you to bed feeling rotten, you will not give it to so many people. In the inevitable struggle for survival, the milder strains will gradually displace their nastier ones. This is why so many cold viruses affect us but so few kill us, except maybe when new to our species.

Perhaps, too, a degree of immune response in the population helps moderate the effects of the virus, even if not achieving full and permanent immunity. Some cross–immunity seems to exist today, whereby those who have had coronavirus colds do not catch, or do not suffer severely from, COVID-19.

Here is a disturbing thought: is lockdown preventing this evolutionary process, by confining the disease to settings where it can still thrive while being fatal, such as hospitals? Our fate is clear: without a vaccine or a cure, COVID-19 will fade, will be back, but will become less lethal till it is eventually indistinguishable from every other cold.

Matt Ridley’s new book How Innovation Works is out now. This article was originally published in The Spectator’s UK magazine. Subscribe to the US edition here.


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