The danger of scientific dogmatism
Science that challenges the Covid orthodoxy is being too easily dismissed.
The Covid-19 pandemic has been treated as a Year Zero phenomenon. We were told this was a novel (indeed, an unprecedented) deadly disease that threatened millions of lives. This was the Big One, which demanded an extraordinary response, from lockdowns to the now mandatory wearing of masks.
Given how little we first knew about this new virus, and the ways it attacked the human body, this initial fearful reaction was perhaps understandable. But is it still? After all, we know so much more about Covid-19 now. Yes, it certainly is novel and deadly, particularly for the elderly and those with comorbidities. But unprecedented? Unlikely, if the historical record of other epidemics is taken into account. Indeed, almost every influenza epidemic in the past was, like Covid, initially understood to have been novel, but was later proved, through serological studies, to have had previous eras of prevalence long before its emergence.
Yet this novel coronavirus has been treated as something completely different, as an almost singular pestilence of Biblical proportions. It has been met with the kind of doom-laden fatalism with which Medieval man would have been all too familiar.
But we are not in Medieval times. Mankind is not at the beginning of the scientific revolution. There is a vast amount of accumulated scientific knowledge about past epidemics that we can draw on. And, while it may not provide easy answers, it might at least raise important questions about the wisdom of our response to Covid-19.
Take, for example, the key concept of direct spread through human interaction, which underpins many of the social restrictions in place to combat Covid. This idea has also been used to explain the emergence and transmission of influenza for hundreds of years. But in the late 1970s, the concept of direct spread as the sole mode of influenza transmission was challenged by Robert Edgar Hope-Simpson, a British general practitioner most famous for showing that shingles was a reactivation of the chicken-pox virus.
His highly accessible, pioneering study, The Transmission of Epidemic Influenza, was published in 1992 after a lifetime of study that began with the great epidemic of 1932-33, the years in which he entered general practice.
Hope-Simpson raised several key questions about influenza transmission. How, for example, could direct spread account for the simultaneous appearance of influenza in places far apart – especially before global travel was ubiquitous? The universally observed abruptness of the onset of some influenza epidemics and their equally abrupt endings – without any lockdowns or social distancing – underlined the most puzzling aspect of influenza: how could its seasonal character be explained?
Hope-Simpson’s challenge to the idea of direct spread was first published in 1979 in the Journal of Hygiene, and he published further evidence in support of his case over the next seven years. His key argument was that influenza epidemics are caused by a previous ‘seeding’ of the virus in the community. Symptomless carriers spread the virus around, until seasonal variations in solar radiation reactivate the virus in its human carriers, which allows the virus to emerge among the non-immune. He suggested that the influenza virus is seldom transmitted by the human host because the influenza illness rapidly adopts a persistent non-infectious mode – the ex-patient carries this persistent influenza infection for a year or two before it may be reactivated by seasonal changes.
Hope-Simpson further suggested that the speed of movement of epidemics is therefore unaffected by the speed and complexity of human communications (an idea that, if applied to a coronavirus, would also challenge the conventional tale of Covid-19’s spread from Wuhan in China through human travel).
Influenza epidemics, he contended, must have travelled at the same speed in previous centuries because they are determined by the seasonal stimulus underpinning all natural phenomena, rather than by direct human-to-human spread. The impressive empirical data he gathered from across the globe showed that novel influenza strains appear in different parts of the globe, and that they always spread annually south and then north through the world population. His data showed that tropical regions have very different triggering mechanisms to northern temperate regions, which generate two different prevalence curves.
Hope-Simpson’s challenge to the idea of direct spread was based on the antigenic shift of the influenza A virus and the recycling of its major serotypes. Antigenic shift is the process by which two or more different strains of a virus, or strains of two or more different viruses, combine to form a new subtype. This is what is triggered by the seasonally mediated reactivation of influenza genomes. He hypothesised that an individual person would only harbour the particular influenza A virus genome from their first ever infection. This would explain why only some, rather than all, people become infected when an epidemic is reactivated.
Hope-Simpson was not dogmatic. He was a scientist who made no claim that this was ‘the science’. He was the first to warn that ‘the hypotheses advanced in the new concept are likely to be superseded in part or altogether as more information is gathered. This is the destiny of all hypotheses.’ But he cautioned that ‘it seems certain that the current concept of direct spread is impeding our understanding of influenza’.
What really needs explaining is why the theory of direct spread has remained an orthodoxy, despite both the empirical data that challenges it and its inability to explain many features of influenza epidemics. Hope-Simpson provides a possible answer. In a passing reference, he mentions the research of a Dr John Haygarth, a general practitioner who undertook a detailed study of the spread of the 1775 influenza epidemic in Chester, in north-west England. Haygarth’s subsequent experience during the 1782 epidemic convinced him of its contagious nature. His findings were eventually published more than 20 years later, as Of the manner in which the Influenza of 1775 and 1782 spread by Contagion in Chester and its Neighbourhood. Haygarth writes:
‘But a contrary and, as I think, a very pernicious opinion has lately been supported by physicians of great respectability, and authors of the highest reputation, not, indeed, in this, but in other enlightened nations, have ascribed not only this but many other epidemics, even the plague itself, to a morbid constitution of the atmosphere, independent of contagion. To determine whether this doctrine be true or false, is of the highest importance to mankind. Knowledge, in this instance, is power. So far as it can be proved, that a disease is produced by contagion, human wisdom can prevent the mischief. But the morbid constitution of the atmosphere cannot possibly be corrected or controlled by man.’
This shows that the concept of direct spread was important because it reinforced a sense of human agency. Knowledge was indeed power – the power of mankind to ‘prevent the mischief’. The idea that ‘the constitution of the atmosphere’, rather than human interaction, underpins the seasonal reactivations of influenza was unthinkable. It challenged humanity’s capacity and aspiration to control nature. The concept of direct spread sustained a sense of control even in the face of ignorance about what was causing these epidemics. (It was only in 1933 that the ultramicroscopic parasite that causes flu was discovered.)
Knowledge still is power. But, as with all science, it can ossify and become an orthodoxy that bars the way to further study. And in the battle against Covid-19, there are similar examples of just this process of orthodoxy and dogmatism, which could be holding back our attempts to understand the virus.
For example, on 17 September 2020, the British Medical Journal published an article that received little attention, titled ‘Covid-19: Do many people have pre-existing immunity?’. This questioned whether Covid was a novel pandemic virus and whether there was no pre-existing immunity to it. It highlighted at least six studies that reported T-cell reactivity against Covid in 20 per cent to 50 per cent of people with no known exposure to the virus. These reactivity results were shown to exist in the US, the Netherlands, Germany, Singapore, Sweden and the UK. Evidence of Covid in human sewage was found to have existed in Brazil and in Spain in November 2019.
This is a remarkable finding that would throw much of the current approach to Covid-19 into a tailspin. Alessandro Sette, an immunologist from La Jolla Institute for Immunology in California, told the BMJ: ‘At this point there are a number of studies that are seeing this reactivity in different continents, different labs. As a scientist you know that is a hallmark of something that has a very strong footing.’
And he should know. In late 2009, months after the World Health Organisation declared the H1N1 ‘swine flu’ virus to be a global pandemic, he was part of a team working to explain why the so-called ‘novel’ virus did not seem to be causing more severe infections than seasonal flu. His answer was that pre-existing immunological responses in the adult population prevented its spread: B cells and, in particular, T cells were blunting the severity of the disease. This data forced the WHO and the US Centers for Disease Control and Prevention (CDC) to change position. Having assumed that most people ‘will have no immunity to the pandemic virus’, they now argued that ‘the vulnerability of a population to a pandemic virus is related in part to the level of pre-existing immunity to the virus’.
In 2020 this lesson seems to have been entirely forgotten. The recent past, let alone the past brought to life by Hope-Simpson, is truly another country.
While it is impossible to draw definitive conclusions from a small set of studies, they are still hard to dismiss. They raise the question and perhaps the exciting possibility that pre-existing immunity could be more protective than future vaccines. This suggests there are many different ways to deal with and react to the emergence of a novel virus. But because of the unquestioning focus on suppressing viral transmission there is very little research now being conducted into pre-existing immunity.
The reason Hope-Simpson’s book is so disquieting is that it raises serious doubts about a still current scientific orthodoxy. He didn’t claim to have all the answers – he was posing questions. But that is how knowledge advances. If there is a wider truth in Hope-Simpson’s influenza thesis that might also apply to a coronavirus, and we have seen in the T-cell immunity studies that there could be, then it raises serious questions about the current social-distancing approach to the pandemic.
But here’s the real concern. For the first time in history, draconian measures to restrict the spread of a virus have been in place throughout the summer, the period when, historically, a virus can circulate with very little mortality impact. This is precisely the period when more immunity and protection could have been built up. This could mean that the impact of Covid this winter could be worse than it needs to be. The rise in cases and hospitalisations globally suggests this is precisely what is happening.
The tragedy here is that mankind’s intervention might not have prevented ‘the mischief’. It could well have become part of the ‘mischief’, amplifying the ‘morbid constitution of the atmosphere’.
This is testament to a deeper problem – namely, that those in control of society no longer see humanity as problem-solvers but as part of the pestilence. Without a belief in human agency, society is left with no option but to hold on to existing knowledge – knowledge that may well now stand in the way of scientific progress.
Dr Norman Lewis is a writer and managing director of Futures Diagnosis.
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