June Almeida was born in 1930 and raised in a Glasgow tenement. Her father was a bus driver. She left school aged 16 and became a hospital histopathology lab technician. She married a Venezuelan artist and emigrated to Canada, where she became an exceedingly talented electron microscopist. She was head-hunted by a virologist who had recently started at St Thomas’s Hospital in London, where in 1966 she discovered human coronaviruses in samples taken from volunteers infected with colds.
Until Sars in 2002-03, medical microbiologists paid little attention to coronaviruses; they were simply recurrent causes of the common cold and testing for them was not worth the effort. Since there was no treatment, and because testing took so long, the patient would recover long before the results came through. By contrast, molecular microbiologists studied coronaviruses in the late 1980s and early 1990s because techniques had become available to investigate virus nucleic acids. Coronaviruses were interesting to scientists – not because they caused important diseases but because they had particularly large RNA genomes. Long before they became medically important, we knew much about coronaviruses’ molecular biology.
Almeida had observed that the human virus she saw, B184, which had been isolated from cold sufferers at a boys’ boarding school had knobbed spikes jutting out of its surface, just like mouse hepatitis virus and avian infectious bronchitis virus. The name “coronavirus” was coined for them, derived from the Latin corona, or crown – which they are thought to resemble. Human ones cause around 20 per cent of common colds, and antibody studies show that we all eventually get infected. Different ones occur in pigs, dogs, cats, rabbits, mice, rats, cows, turkeys, chickens and bats.
It took much much longer to respond to Sars than to Covid-19, the official name for the new disease. The first case of Sars occurred in Guangdong Province on 16 November 2002. The World Health Organisation was not alerted until 11 February 2003, by which time there had been 300 cases in Guangdong with five deaths. The virus was not identified as a new coronavirus until 16 April. By 28 April there had been more than 2,000 cases worldwide.
Sars is an imperfect model for Covid-19. Although the disease has been isolated from patient’s stools (many other different coronaviruses also cause intestinal infections), the faecal oral route does not appear to be a significant route for infection. By contrast, the Sars outbreak in Hong Kong at the Amoy Gardens tower blocks (329 cases with 42 deaths) was caused by exhaust fans in the bathrooms sucking up faecal droplets from floor drains. For Covid-19, the most significant route of transmission is through respiratory droplets and surfaces contaminated with them.
The Covid-19 outbreak in China probably peaked at the end of January when Wuhan City was closed down. But the virus has been introduced by travellers to many other countries. At the time of writing there have been 80,430 cases in China (and 3,013 deaths), there have been 6,088 cases in South Korea, 3,513 in Iran and 3,089 in Italy. Virtually all of the UK’s 90 cases have been imported from these countries, and so Covid-19’s spread depends to a great degree on how successful other states are at containing it.
The UK plans, correctly, to now aim to slow the spread of the disease; the hope is that warmer weather will help. Influenza, after all, is seasonal and less pervasive in summer months. Flu is the model that pandemic planners use. Nevertheless, during the 2009 swine flu pandemic, the number of UK cases peaked in July. Lurid estimates of death numbers were officially publicised, but far fewer died.
So microbes present difficult dilemmas for politicians and experts. The classic example is swine flu in the US in 1976. A soldier died of the disease at Fort Dix, New Jersey. Experts thought that the time had come for a new pandemic; Asian flu had occurred in 1957 and Hong Kong flu in 1968, so the idea took root of a cycle of 11 years. Memories of 1918, when more US soldiers died of flu than through First World War battles, also abound.
A rushed mass vaccination programme was started. US President Gerald Ford was photographed receiving his jab. But the virus did not spread from Fort Dix and some people died soon after being vaccinated. The programme was stopped halfway through; the 11-year cycle proved to be nonsense. President Ford lost the 1976 presidential election to Jimmy Carter, and the head of the US Centres for Disease Control and Prevention was summarily sacked by the new administration.
My greatest concern over the new virus is that, as it spreads in the UK, the biggest impact will be on the elderly, who unlike the middle-aged and the young are far more likely to contract severe pneumonia and require intensive treatment. The biggest obstacle will almost certainly be staffing levels, so the plan to encourage retired expert doctors and nurses to return is wise. They will, of course, be at an increased risk of contracting the virus from their patients, so protective suits will be a premium requirement.
My favourite quote, as ever, is one attributed to the late film producer Sam Goldwyn: “Making predictions is difficult, particularly about the future.”
Hugh Pennington is an emeritus professor of bacteriology at the University of Aberdeen. He chaired inquiries into E coli outbreaks in Scotland and south Wales