As rumours of a government plan to begin easing lockdown on 11 May (already several weeks after many European countries) were quashed by Michael Gove, sceptics of lockdown madness and dissenting scientists have continued to voice their concerns.
At the weekend it was the turn of Professor Johan Giesecke, one of the world’s most senior epidemiologists and an adviser to the Swedish government (he hired Anders Tegnell who is directing Swedish strategy), and the first Chief Scientist of the European Centre for Disease Prevention and Control. In an interview with UnHerd, he explains why the lockdown policies of the UK and other European countries are not evidence-based, why the correct policy is to protect the old and the frail only, and why the initial UK response, before the ‘180 degree U-turn’, was better and would eventually lead to ‘herd immunity’ as a ‘by-product’. He is scathing about Professor Neil Ferguson’s doomsday Imperial College paper, saying it was ‘not very good’, that it was much too pessimistic, and that he has never seen an unpublished paper have so much policy impact. Covid-19 is a ‘mild disease’, he says, similar to influenza with a fatality rate of around 0.1 per cent. In his opinion it is the novelty of the disease that scares people, and it is likely already to be very widespread.
German-American epidemiologist Knut Wittkowksi agrees with much of this. He has published a paper arguing that the epidemic is already well into decline in most countries around the world, and that in many cases this happened before or without lockdown. In Sweden, for example, ‘where no lockdown was implemented’ there is ‘no difference in the shape of the epidemic or the height of its peak [compared] with the other Scandinavian countries.’
He argues that the window in which lockdown intervention is helpful in slowing the virus, without causing more problems, is very narrow and, to all intents and purposes, impossible to pinpoint ahead of time. He observes: ‘In China and South Korea (and the first wave in Iran), incidence peaked after about two weeks and then declined. In Europe and in the US this is taking twice as long. The shorter duration of the epidemic in China and South Korea, however, does not demonstrate the effectiveness of social distancing, because the social distancing started too late to be effective. Instead, the longer duration in Europe is consistent with premature interventions in Europe prolonging the epidemic (“broadening the curve”).’
Data from the German government confirms that the reproduction rate of Covid-19 had already fallen below 1 (indicating the decline of the epidemic) before lockdown on 22 March, and there is similar evidence in Switzerland.
How can it be that epidemics have peaked and gone into decline before or without lockdown? General hygiene measures and public caution are likely to have helped. Another possibility is that collective immunity has already been achieved or is on the way, either because the 60 per cent threshold of people developing antibodies through catching the virus has been reached, or because an innate immunity (or cross immunity) to the virus within part of the population has reduced the antibody threshold required for collective immunity.
Oddly, this concept of innate immunity hasn’t featured much in public discussion about Covid-19 to date, or even in the scientists’ models, it seems. But could it explain why the epidemic has been dying down sooner than expected (before or without lockdown), and with fewer hospitalisations and deaths than expected?
One healthcare professional on the Lockdown Sceptics website explains the concept: ‘The first response of the immune system to an invading pathogen is mediated by what’s called innate immunity. Innate immunity is not pathogen-specific. It is a range of bodily defences that include local inflammation, fever and the engagement of cells called Natural Killer Cells to literally consume the pathogen – as well as others I won’t go into. It’s complex! Healthy young people and adults under around 40 seem to be able to see off the virus with just their innate immunity. This is good, it means the virus didn’t present much of a threat to them. They don’t have antibodies only because they didn’t need to produce them. They are not ‘immune’ in the antibody sense, but they aren’t particularly vulnerable either. If the innate immune system doesn’t defeat the pathogen, that’s when the adaptive immune system kicks in and the chain of events that leads to antibody production is kicked off.’
If this is what’s going on, it means it would not be necessary (or realistic) for 60 per cent of the population to develop antibodies for the horrible-sounding ‘herd’ immunity to be achieved. It would also explain why the proportion of those with the virus or with antibodies keeps coming back in surveys much lower than expected – 15 per cent with antibodies in Gangelt, Germany; 15 per cent infected out of those who shared a household with people who had caught the disease in Shenzhen, China; 22 per cent with antibodies in Robbio in Lombardy, Italy; 17 per cent infected on the Diamond Princess cruise ship; 13.7 per cent on the Dutch submarine MS Dolfijn; 14.3 per cent on the USS Theodore Roosevelt. However some more recent surveys have found more: 32 per cent with antibodies of people on the street in Boston, Massachusetts; 37 per cent infected (though none with symptoms) in a Boston homeless shelter; 59 per cent infected on the French aircraft carrier Charles de Gaulle.
These results confirm that the virus is, as many epidemiologists have suggested, much more widespread than the test data suggests, so it is much less deadly than initially thought and we are much closer to collective immunity. But will cases surge when the restrictions are lifted? Ironically, Knut Wittkowski suggests they might in places where the lockdown was imposed early enough to prevent the spread. But elsewhere, as in most of Europe, the lockdown (where there was a lockdown) was, he says, far too late to achieve that (it is more likely to prolong the epidemic) anyway, so a second wave is unlikely.
This is presumably because in those places some form of collective immunity has already developed or is well on the way, possibly aided by the innate immunity described above. If innate immunity is involved, the different infection and antibody rates found in the surveys could be explained by the fact that innate immunity is not as strong as antibody immunity and its resistance may be overcome by, for example, greater exposure such as might come from higher population density.
In the meantime what the public needs to hear from the government is reassurance, a better sense of perspective and fewer messages that promote unwarranted panic – that we’re getting the equipment needed and that the NHS now has sufficient capacity, that they are speeding up screening, testing and protecting front-line health workers. It’s the Government’s responsibility to get us out of the economic catastrophe it has led us into; to listen to a wider range of scientific voices and to look hard at the data emerging from around the world; to share evidence that the epidemic is on the decline and that infection rates and death rates are not as high as originally feared (not so different to some recent flu epidemics), and finally that we have to learn to live with this disease – mitigating it as best we can – as we do with so many others for which there is no definitive solution.
This is the basis from which they can begin to lift the lockdown, as many countries already are doing.