This year marks the centenary of Spanish flu, the most deadly pandemic in human history:
It is estimated that five hundred million people contracted it — a third of the global population in 1918 — and that between fifty and a hundred million of them died. Asians were thirty times more likely to die than Europeans.
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The spread of Spanish flu was quickened by the railway and steamer lines that girdled the planet, starkly illuminating global inequalities in security, nutrition and access to medical care. In India 6 per cent of the population died; in Fiji 5 per cent; in Tonga 10 per cent. In Western Samoa, for reasons that aren’t entirely clear, more than 20 per cent of the population died. Even harder hit were the Alaskan Inuit, with a death rate between 25 and 50 per cent: in some small Alaskan communities everybody died. Koreans and Japanese were infected at the same rate, but the Koreans, subject to chronic malnutrition, were twice as likely to die. In the US, Italian immigrants died at twice the background rate (the Italian neighbourhoods of New York had a density of five hundred per acre, ten to a room), while black populations were the least affected.
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The flu wasn’t Spanish at all. The name stuck when in May 1918 the Spanish king, the prime minister and his entire cabinet all came down with it. In Madrid, it was known as the Naples Soldier after a catchy tune then in circulation, while French military doctors called it Disease 11. In Senegal it was Brazilian flu; in Brazil it was German flu. Poles called it the Bolshevik Disease and the Persians thought the British were responsible.
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The first case of Spanish flu was recorded on 4 March 1918, when a military mess cook called Albert Gitchell in Camp Funston, Kansas, reported sick with a headache and fever. By the following day a hundred others had reported the same symptoms. A hangar was requisitioned to house the men, but flu has an incubation period of a couple of days, and had already moved on, aided by the war machine. By mid-April it had reached the Western Front, where three-quarters of French troops and half the British fell ill; 900,000 German soldiers were taken out of action. In April it also surfaced in South-East Asia, and in May, as the Spanish cabinet took to their beds, it was spreading through North Africa. On 1 June the New York Times reported it spreading through China (possibly for the second time), and later that summer it reached Australia. That was the first wave; through the summer of 1918 the pandemic seemed to be on the wane.
But in August a second and more deadly wave struck all at once in Sierra Leone, Boston and Brest. The virus seems to have mutated, making it more transmissible and provoking a more florid inflammatory reaction. Ten thousand died in Addis Ababa; Haile Selassie said that he fell ‘gravely ill’, but ‘was spared from death by God’s goodness’. In Prague Kafka became ill; in Dublin Yeats’s pregnant wife, Georgie, was stricken, as was Ezra Pound in London. In Zamora in north-west Spain the bishop ordered a novena — the community was to gather for nine consecutive evenings to pray to St Rocco, patron saint of pestilence, and to kiss his relics. Observant locals noted that afterwards ‘Zamoranos seemed to be dying in higher numbers than the residents of other provincial capitals.’
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When Charlie Chaplin’s Shoulder Arms came to New York in October, Harold Edel, the manager of the Strand Theatre, wrote: ‘We think it a most wonderful appreciation of Shoulder Arms that people should veritably take their lives in their hands to see it.’ Edel was dead within a week, of flu.
Although there was no effective treatment for the virus, aspirin was taken by the tonne (its German manufacturer, Bayer, was suspected of spreading flu through its pills); aspirin poisoning possibly killed some who would otherwise have survived.
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The structure of the flu virus was first seen in 1943, when effective electron microscopes became available. They are just 0.1 microns across, between a tenth and a twentieth of the size of the bacilli most often associated with pneumonia. It’s moot whether they are even alive: viruses are simply packets of protein and fat, together with some nucleic acids to encode proteins. The flu virus carries just eight strands of RNA, with which it creates copies of itself. Two kinds of protein jut out from its surface: Haemagglutinin is the skeleton key that allows the flu virus to slip into living cells; Neuraminidase is the battering-ram that bursts its progeny out. These antigens can be recognised by our immune system and used to destroy the virus; we name flu strains according to which H and N subtypes they carry.
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Animal ‘reservoirs’ allow flu strains to recombine until a new pandemic strain breaks out again — which it will. Every flu pandemic of the 20th century followed the emergence of a new Haemagglutinin antigen: H1 in 1918, H2 in 1957 and H3 in 1968.
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In 1951 a Swedish-Iowan pathologist, Johan Hultin, travelled to Alaska and sampled lung tissue from graves at Brevig Mission, one of the Inuit communities badly affected by Spanish flu. The graves were relatively well preserved in permafrost, but even so Hultin didn’t manage to get enough samples of the virus to reproduce it. In 1997 the virologists Ann Reid and Jeffery Taubenberger worked with a scrap of lung from a 1918 flu victim, preserved for seventy years in formaldehyde. They succeeded in extracting some damaged RNA, but again too little to reconstitute the virus. Hultin read of Reid and Taubenberger’s research and returned to Brevig Mission: he was again given permission to dig, and this time exhumed an obese woman whose lungs had been preserved in fat. Enough flu virus was recovered from the lungs to be sequenced, and the results, published in Nature in 2005, suggested that the 1918 virus was avian in origin, but that a mutation had rendered it fatally adept at infecting mammals. When the reconstituted virus was given to mice under barrier conditions the mice lost 13 per cent of their body weight and produced forty thousand times more infectious particles than mice with ordinary seasonal flu. Six days after infection, all the mice were dead. The virus is currently held in a high-security facility in Atlanta, Georgia. In 2016, around 1.7 million people died from tuberculosis, around a million from HIV/Aids, and around half a million from malaria. Computer modelling suggests that if the 1918 H1N1 virus were to break out of the facility in Atlanta it would cause around thirty million deaths.
Can I get a flu shot against that strain of H1N1, please?
+1 educational.