(1) (H/t: masgramondou). Matt Ridley tells the story of the 1890 Russian flu epidemic
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 S[ARS], M[ERS], and C[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 the[se] via cattle.
It sounds very familiar… (Note that at the time, not everybody even believed in bacteria — and the first virus was only discovered eight years later by Martinus Beijerinck.)
Genetic analysis by the Belgian virologist, Prof. Marc van Ranst at the University of Leuven, suggests OC43, one of the four common cold coronaviruses diverged away from a pneumonia virus in cattle around 1890. Matt Ridley describes the hypothesis that OC43 was the pathogen of the 1890 Russian Flu, then gradually evolved away to a much more contagious, but infinitely less harmful, form.
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. […] 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.[Sounds familiar?] […]
According to a modern analysis, the death rate peaked in the week ending 1 December 1889 in St Petersburg, 22 December in Germany, 5 January 1890 in Paris, and 12 January in the US. [The basic reproductive number] R0 has been estimated at 2.1 and the case fatality rate was somewhere between 0.1 per cent and 0.28 per cent: 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.
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.
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 ten 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.
(2) Die Welt reports that in the Italian city of Bergamo (classical music lovers may think of Debussy’s Suite Bergamasque) no fewer than 57% of 10,000 tested subjects had antibodies for COVID19. (This is most definitely in 1st-order ‘herd immunity’ territory.) Among a similar-sized (10,400) sample of healthcare workers, “only” 30% had antibodies (which is in the 2nd-order herd immunity range).
In a summary of the state of the epidemic so far, the German daily quotes virologist Prof. Christian Droste, who in an interview in Der Spiegel states that with our present state of knowledge, it is time to shorten the 2-week quarantine in case of exposure to just one week.
(3) A German-Norwegian collaboration, reports Die Welt, found confirmation of earlier indications that blood groups have an effect on disease progression. A+ are worst off (oh joy ;)), while O imparts a degree of protection.
Dass die Blutgruppe Krankheitsverläufe beeinflussen kann, ist grundsätzlich nichts Neues. So gibt es schon seit Längerem Hinweise darauf, dass Blutgruppe 0 auch vor schweren Malaria-Verläufen schützen kann, dafür aber anfälliger für Magen- und Darminfektionen macht, während Träger der Blutgruppen A, B oder AB besser gegen die Pest gewappnet sind.
[That blood groups can influence disease progression is fundamentally nothing new. There have for long been indications that blood group O can also protect for severe malaria [!!], but makes one more susceptible for gastro-intestinal infections, while carriers of blood groups A, B, or AB are more resistant to the plague.
Laut Blutspendedienst des Bayerischen Roten Kreuzes haben 37 Prozent der Bevölkerung die Blutgruppe A Rhesus Positiv und 35 Prozent die Blutgruppe 0 Rhesus Positiv.
[According to the blood donation service of the Bavarian Red Cross, 37% of the [German] population have blood group A+ and 35% O+.]
(4) A new Nature paper “Estimating the effects of non-pharmaceutical interventions on COVID-19 in Europe”
(This is a “postprint”, i.e., accepted version after peer review, but without copy-editing by the publishers and corrections in proof.) I will probably devote tomorrow’s edition to discussing this paper. (The hoary sketch comes to mind: “Why are you spraying pesticides on an organic garden?”
“Those aren’t pesticides, that’s a powder against elephants.”
“But there aren’t any bleeding elephants here!”
“Yeah, good stuff, huh?”)
(5) Apropos of nothing:
“Liberty is for science what air is for an animal: when deprived of liberty, [science] dies of suffocation as surely as a bird deprived of oxygen. […]
Thought must never submit —
neither to dogma,
nor to party,
nor to passion,
nor to special interest,
nor to a preconceived idea,
nor to anything but the facts themselves —
for when thought submits,
that means it ceases to be.”
—Henri Poincaré, Le libre examen en matière scientifique (1909)