I can’t remember​ the last time, before the current outbreak, when one of my patients died from flu. The strain involved in the last flu pandemic, the swine flu outbreak in 2009, was highly infectious, but milder than other pandemic strains have been. Of the 61.7 million people living in the UK in 2009, 457 died from it – comparable to the usual annual death toll for flu. The 1957 Asian flu and the 1968-69 Hong Kong flu pandemics were more serious; the death toll in each case was estimated at around a million worldwide.

I first found out about the current outbreak when I was called to a nursing home to see a patient in his nineties who had suffered two days of cough and fever. I knew Mr Wedderburn well; I used to visit him in his own home, before the slow creep of dementia made his life there untenable. He used to talk with me about his favourite books and music, but for the last couple of years he had been confused and distracted. Frail elderly people often have a less robust systemic response to infection than the young and fit, but even so, Mr Wedderburn was flushed with a temperature of 38°C, and was breathing much too quickly. As I listened to his lungs with my stethoscope his fingers picked at the bedcovers, and his feet knocked against his cot-bars. When I took a viral swab from his nose, he screwed up his eyes and muttered ‘Oh dear, oh dear.’

I phoned his niece: no, she didn’t think he’d want to be admitted to hospital if he were to deteriorate. ‘He’s an old man,’ she said to my relief, ‘I think he’d prefer to take his chances.’ That was Friday afternoon. Over the weekend I was on call for the GP night service, and visited three more nursing homes to assess cases of flu. A message came through from the health board: the swabs GPs were sending in were testing 74 per cent positive for influenza, but there was no evidence yet of a spike in deaths. When I returned to my own clinic after the weekend there were two papers on my desk: a lab report confirming Mr Wedderburn’s influenza, and a note reporting that he’d died.

‘It can’t just be flu,’ patients often say. ‘I feel absolutely dreadful.’ Sweats, fever, headache, muscle pain, breathlessness, cough: for many fit young people, a bad dose of the flu is their first intimation of mortality. Flu virus hijacks airway tissues, forcing the cells lining them to reproduce copies of themselves. That process irritates and inflames; sneezes and coughs spread new generations of the virus. Bacteria reproduce more easily in flu-debilitated, inflamed lungs, so if flu itself doesn’t give you pneumonia, other micro-organisms might – and this secondary infection can be more dangerous than the virus itself. You can do something about the dehydration and fever, but beyond that there’s little effective treatment once the illness is established.

Every autumn the fridge in my consulting room is stacked high with vaccines, and every October my colleagues and I jab hundreds of shoulders. Of the 3700 patients registered at my practice about a thousand are eligible for a flu vaccination, because of age, lung disease or some other infirmity. We don’t vaccinate just to protect the most vulnerable: the hope is that raising the background level of immunity among a selected population will slow the spread of seasonal flu among the rest. Usually just over a quarter don’t take up the invitation; this year we ordered 750 vials.

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. The pandemic had some influence on the lives of everyone alive today. Donald Trump’s grandfather Friedrich died from it in New York City. He was 49. His early death meant that his fortune passed to his son Fred, who used it to start a New York property empire. My wife’s great-grandmother died from it in Verona; her grandfather, aged eight, had to leave school and find work to support the family. Emilio died in 2011 aged 101. When I told a friend, the writer Andrew Greig, that I was writing this piece, he told me that his father, born in 1899, came down with Spanish flu while on leave from the war in France. ‘His convalescence delayed his return to the front, where his battalion was all but wiped out,’ Andrew said. ‘He always insisted Spanish flu saved his life, and without it, I suppose I wouldn’t be alive either.’

Laura Spinney’s book attempts to collate what is known about the pandemic, and takes a stab at examining its legacy: ‘The flu resculpted human populations more radically than anything since the Black Death,’ she writes. ‘It influenced the course of the First World War and, arguably, contributed to the second. It pushed India closer to independence, South Africa closer to apartheid, and Switzerland to the brink of civil war. It ushered in universal healthcare and alternative medicine, our love of fresh air and our passion for sport.’

The majority of deaths came in the three months between September and December 1918. The war probably didn’t spawn it, but certainly helped it spread: the US lost more soldiers to flu than to the war in part because so many of them spent weeks coughing together in barracks and transports on their way to Europe. Britain and Italy suffered between two and three times more deaths from the war than from the flu, while Germany’s war deaths outnumbered flu deaths six to one. Spinney quotes historians who claim that flu struck Germany harder than Britain or France; Erich Ludendorff was convinced it had robbed Germany of victory. 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. ‘As far as the “Flu” is concerned the whites have the whole big show to themselves,’ J. Franklin Johnson wrote to the Baltimore Afro-American. It was just as well, he added, or ‘health talks to coloured people would have been printed by the wholesale in 72-point type in the daily papers.’ Most flu epidemics have a U-shaped distribution curve, disproportionately afflicting the very young and very old. Spanish flu had a W-shaped distribution curve, with an extra peak of deaths in young, fit 20-40 year olds. Theories vary, but it’s possible that this population wasn’t exposed to the widespread Russian flu of the 1890s; it’s also possible that, being in peak fitness, they may have had a damagingly brisk immune response. Pregnant women were particularly vulnerable.

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 (Spinney writes about its devastating effect on the city of Mashed, where it probably arrived with a Russian soldier from the north).

As to the original source of the pandemic, there are three chief candidates: Kansas poultry farms, the army barracks of Etaples in northern France, and the Shansi province in China. In China, where flu was known as the ‘little plague’, there are reports of a flu-like epidemic in late 1917. A physician named Wu Liande thought he’d isolated the plague bacillus Yersinia pestis from the lungs of the victims (in 1910 Liande had helped rein in a Yersinia epidemic responsible for sixty thousand deaths). But sophisticated laboratory techniques hadn’t yet been devised, and it’s possible he diagnosed an incidental secondary infection. In late 1917 and early 1918 a Chinese Labour Corps of 135,000 men was transported from Tsingtao by ship to the US, across America by rail, then onwards to dig trenches in France. It’s possible that they carried the flu with them. A similar corps of 200,000 men was transported west through Russia.

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.’

In New York City the public health commissioner, Royal S. Copeland, eliminated rush hour by staggering shop, school and factory opening times. He was under pressure to close schools, but after infancy children were relatively unaffected by the virus, and Copeland argued that schools could help disseminate health advice to their communities. He opened 150 health centres to deal with the sick, and insisted that all flu patients who lived in shared accommodation be hospitalised. Public health information was distributed by an obliging press: the Italian-language Progresso Italo-Americano sold close to a hundred thousand copies a day in New York alone, and raised funds for an Italian hospital in Brooklyn. Copeland allowed children to go to school, but he banned them from theatres. 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. Across the world communities adapted traditional remedies: in China, public sweat baths, opium and herbal extracts; in India, hill tribes moulded figures out of flour and water, and waved them over the sick. In New Jersey William Carlos Williams, working as a family physician, wrote: ‘We doctors were making up to sixty calls a day. Several of us were knocked out, one of the younger of us died, others caught the thing, and we hadn’t a thing that was effective in checking that potent poison that was sweeping the world.’ ‘We were all in the same boat,’ wrote Maurice Jacobs, a doctor in Hull, ‘tossed about on pestilent seas, sick at heart and frustrated.’ In Odessa, in September, some Orthodox Jewish merchants organised a black wedding, shvartze khasene, to appease the flu. Spinney describes it as ‘an ancient Jewish ritual for warding off lethal epidemics that involved marrying two people in a cemetery … the bride and groom must be chosen from among the most unfortunate in society.’ According to the Odessan novelist Mendele Mocher Sforim, the bride and groom were ‘the most frightful cripples, degraded paupers and lamentable ne’er-do-wells as were in the district’.

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.

The seasonal flu vaccine I’ve been jabbing this year contains elements of three separate strains. There are two sorts of influenza A: H1N1 (a strain similar to the swine flu of 2009) and H3N2, the strain causing the current outbreak, recently arrived from the southern hemisphere (which is why the tabloids have been calling it ‘Aussie flu’). H3N2 mostly afflicts the elderly. The third strain is influenza type B, which affects children more severely than it does adults. Every year a team of vaccine advisers from the World Health Organisation analyses the prevalent strains around the globe and makes recommendations as to which should be included in vaccines.

Since viruses aren’t alive in the way that bacteria are, they can’t be grown on agar jelly. Virology was largely a mystery until 1931, when a Russian called A.A. Smorodintseff managed to breed viruses inside chickens’ eggs. In 1933 a ferret sneezed in the face of a researcher named Wilson Smith at the Medical Research Council unit in Mill Hill, London. Smith caught flu from the ferret. His subsequent paper in the Lancet showed that flu virus was the infectious agent, and that it could be transmitted between animals and people. In 1936 Smorodintseff invented flu vaccination: he took flu viruses and preferentially bred the ones that were poorest at reproducing. He injected these mild versions of the virus into two human subjects: they developed a low fever, but the jab seemed to confer protection against more virulent strains of flu. Some modern flu vaccines are weakened live versions of the virus, similar to the ones Smorodintseff grew, but the ones in my fridge are heat-treated to render them inert.

By exposing large sections of the public to a variety of H and N antigens, seasonal flu vaccination helps reduce the risk of another pandemic, but that risk can’t be eliminated. H and N variants are in ceaseless evolution, and flu viruses can hide for long periods in host animal populations, many of which don’t suffer any ill effects. This transmissibility between animals and humans is one key to its virulence; another is the ability of its antigens to mutate. 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.

Two thousand years ago horses were probably the main reservoir for flu, but the virus is now usually found in the digestive tracts of birds, or occasionally pigs (as in the case of swine flu). All three theories of the origins of Spanish flu point to birds as the source of the pandemic: the French virologist Claude Hannoun found a hundred different strains of flu in the birds of the Somme estuary; in China, flocks of ducks are traditionally herded through paddy fields to eat insects, and mingle there with wild birds; the evolutionary biologist Michael Worobey suggested that Spanish flu may have come from the poultry farms of the Midwest.

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.