More than sixty years ago, puffing on an untipped Senior Service (we were allowed to smoke in those days) to cover up the reek in a dissecting room at St Thomas’s Hospital, I was struck down by a pandemic virus that had recently evolved in China. By the time I fell ill (its onset was very sudden) the virus had already killed more than 20,000 people in the UK, with 1150 dying every week at its peak, and 80,000 in the US. In the first UK wave, more than half the deaths occurred in the under-55s. It went for the elderly later, in its second wave. It killed quickly: nearly 20 per cent of its younger victims died before getting to hospital and two-thirds were dead within 48 hours of admission. But it has been airbrushed out of history, despite being by far the most lethal pandemic to affect Britain at any time in the hundred years after the ‘Spanish’ flu pandemic at the end of the First World War.

There was more vigorous debate about its name – why ‘Asian’ flu, why not ‘Asiatic’? – than about its impact on society, despite its lethality. Political memoirs, hospital histories and accounts of the NHS don’t mention it. It put no pressure on Intensive Care Units because none existed; ventilators were in their developmental infancy and were used mainly to treat patients with polio, as well as a few with tetanus, barbiturate poisoning or chest injuries; and there were no arguments about testing because tests were so slow that when the results were reported the patient was either better or dead. The impact of the virus was being measured by excess mortality, the number of deaths greater than expected. It is mentioned in medical and microbiological textbooks but not described in detail except to note that it was of low virulence because it killed many fewer than Spanish flu in 1918-19.

The Asian flu virus emerged in China in February 1957 and was spread to the rest of the world by people on ships, aircraft and the Trans-Siberian Railway. It arrived in England in July, taking off in September and October, going relatively quiet in November, and then rising in incidence again, peaking around Hogmanay. Vaccines were developed but not deployed on any scale because even their keenest proponents were unsure about their efficacy and not happy about the sore arm side effect. In the US the federal government disdained to support a vaccination campaign.

The spread of the virus was assisted by the dispersal of attendees from conferences, scout jamborees and youth festivals, and there were explosive outbreaks in military camps and boarding schools. But there was no social distancing. Public gatherings were not stopped. The virus was at its peak when Aneurin Bevan was heckled at the Labour Party Conference on 3 October 1957 for arguing that unilateral disarmament wasn’t possible, and it was still busy when CND held its first meeting at Westminster Central Hall on 17 February 1958. No noteworthy individuals fell ill with it, unlike the Spanish flu, which infected Woodrow Wilson during the peace negotiations in 1919.

In October and November 1957 the prime minister, Harold Macmillan, was kept busy not by the ongoing pandemic but by the events that followed the world’s first nuclear reactor accident, when Windscale Pile No. 1 caught fire. According to Lorna Arnold’s brilliant account, Windscale 1957: Anatomy of a Nuclear Accident, the pile physicist was ill in bed with flu when the fire took hold on 10 October. The deputy works manager, Tom Tuohy, who at immense personal risk played a key role in putting out the fire, was called in from leave at home where he was looking after his wife and children – who all had flu. President Eisenhower meanwhile was preoccupied by the Russians’ launching of Sputnik 1 on 4 October.

The Asian flu virus went on killing people every winter until 1968, when it was replaced by the Hong Kong pandemic virus.

After finishing my pandemic-interrupted dissection of an embalmed corpse’s brachial plexus, I stayed on at St Thomas’s. As a house physician I worked for Peter Sharpey-Schafer, an expert in the physiology of the circulation. Ron Bradley was a member of his team. He was an intensive care pioneer, specialising in measuring how well or badly a very sick patient was doing. He developed much of the technology as he went along. To start with, rather than the acutely ill patient being taken to the monitoring set-up, the equipment on a big trolley was brought to the patient. Ron and the anaesthetist who came with him were called the ‘deathwatch beetles’ because success was far from guaranteed.

A purpose-built intensive care unit opened at St Thomas’s in 1966. By that time I was working in the medical microbiology department, participating in virology as it moved from studying its subjects as entities that caused diseases in ferrets and mice to visible macromolecules. One of my colleagues was June Almeida, the brilliant electron microscopist who in that year discovered human coronaviruses using her microscope in the basement of the medical school. They had been isolated from young people with colds. Their medical importance was trivial, and it wasn’t until SARS and MERS that human coronaviruses showed their malignant potential.

The novelty of Covid-19 and its big differences from other coronaviruses (it is a lot less vicious than SARS or MERS but orders of magnitude nastier than common cold coronaviruses) mean that predictors of its future behaviour are obliged to use flu pandemics as a model. But Covid-19 is not flu. We don’t yet know if, as with pandemic flu, there will be a second wave of cases; or if, like flu, the virus will go on for years as a seasonal killer; or if better vaccines can be developed than for flu, which are least effective in the most vulnerable patients; or if antiviral drugs can be developed for Covid-19 that are as least as good as the anti-flu ones.