It is now three weeks since thousands of protesters first gathered in Trafalgar Square, and two weeks since London filled with even larger crowds, few of whom wore masks or kept two metres apart, and some of whom got involved in fights, resulting in arrests and injuries: a perfect recipe for spreading the coronavirus. Yet there has been a continuing decline in new cases of the disease and no uptick in calls to 111 or 999 about suspected Covid-19. By now, some effect should have shown up if it was going to. In June, London has seen fewer deaths from all causes than in a normal year. Why is this?
While respiratory viruses nearly always evolve towards lower virulence, essentially because the least sick people go to the most meetings and parties, this one was never very dangerous for most people in the first place. Its ability to kill 80-year-olds in care homes stands in sharp contrast with its inability to kill younger people. Fewer than 40 people under the age of 40 with no underlying conditions have died in Britain. On board the aircraft carrier Theodore Roosevelt, 1,100 sailors tested positive, many had no symptoms and only one died.
The summer weather is helping. Viruses are not easily caught outside, where ventilation, high temperatures and strong sunlight kill the virus. In addition, sunlight boosts vitamin D, which is protective against respiratory viruses; average vitamin D levels are especially low in Britons in winter because our public-health service does less than, for example, Germany’s to redress this deficiency.
The assumption expressed in the very term R0 was that everybody would initially be susceptible to catching this virus. But it soon became clear that this could not be the case. Frequent cases of family members not passing it on to each other baffled scientists. It turns out that there is lots of pre-existing immunity to the virus. Some seems to be generic protection conferred by so called innate immunity.
There is growing evidence that live attenuated vaccines such as polio and BCG have protective effects against other viruses by stimulating the production of interferons. More specific T-cell immunity resulting from previous infection with other common-cold coronaviruses is also widespread. Around 70 per cent of children under four show evidence of resistance to such coronaviruses.
This was a big part of the explanation for the vast over-estimates of death rates based on mathematical models. The virus was spreading like wildfire in hospitals and care homes where elderly people were far less resistant than the population at large. The modellers assumed these cases were coming into hospitals from the community when actually many were already in the care system. This wildly distorted their estimates. Outside such settings and large indoor gatherings, as the commentator Hugh Osmond has put it, the tinder was damp.
The influential Imperial College modellers have recently published a justification claiming that compulsory lockdowns are mainly responsible for the death rates being so much lower than they forecast, with other measures including school closure, public event bans, social distancing and self isolation only contributing 5 per cent of the infections averted.
However, they assumed, unrealistically, that all the reduction in coronavirus transmission was due to interventions. In reality people would have changed their behaviour anyway, and variability in people’s susceptibility to infection and number of contacts with others would have slowed its spread, as the pool of uninfected people most likely to become infected diminished.
Moreover, an expert scourge of dubious models, Nic Lewis, has shown that with arguably more realistic assumptions about the time between infection and death and how quickly interventions worked, their own model implies lockdowns did not make the largest contribution towards ending this wave of the pandemic. That is consistent with lockdown-free Sweden having also experienced a big reduction in transmission. Japan has one of the softest lockdowns and lowest death tolls.
Will there be another wave in the autumn? Most medics think so. But if we learn the lessons of the first wave – mainly that shielding the old and vulnerable is key – and we manage at least some effective contact tracing, then the winter wave should be more like a series of small, local outbreaks. A second national lockdown would be a huge mistake, given the harm the first one has done to everything from cancer diagnosis to mental health, let alone employment.
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