Our panic over COVID-19 is being driven by media fictions: not the latest scientific data

At this time, the world’s health literacy — our ability to make judgments about information concerned with our health — is facing a severe test. We need to be attending to the facts, not the fiction, about COVID-19.

A copy of 'The Stand'
Useful reading material at the present time?

On the other hand, with plenty of time to kill, I felt that picking up one of the fattest novels on my bookshelf would be a good move. And as I hope I don’t lack a sense of irony, I’ve begun re-reading Stephen King’s The Stand. For those of you who don’t know, this epic horror novel, first published in 1979, describes how a genetically-engineered ‘superflu’ virus that comes to be called ‘Captain Trips’ wipes out 99.4% of the world’s population within a few weeks.

Fortunately, King is a novelist, and COVID-19 is nowhere near as infectious nor deadly as Captain Trips. But there are still things to learn from this work of popular fiction — coupled with a proper analysis of the emerging epidemiological data — when it comes to understanding how the media narrative on COVID-19 is being defined and what the consequences have been. I argue that we must alter certain basic informational assumptions about this virus and how the current crisis began, if we are to learn our way out of — that is, develop an exit strategy for — the regime of restrictions, isolations and lockdowns that many of us now face.

King was asked to make substantial cuts to his original manuscript for publication, but many of these passages were restored in the extended edition of The Stand published in 1990. In the opening pages of this longer version, Captain Trips is given a very specific point, and time, of origin — June 13th 1990, at a US Air Force base in California, where the virus was being developed as an agent of biological warfare. An accident wipes out most of the base personnel: security guard Charles Campion escapes with his family, but not until after he has been infected. From him can be traced all the subsequent deaths.

It is intuitively and logically correct to assume that when a new virus begins to infect human hosts, there must be someone who, like Campion, was Patient Zero: the person to whom, for whatever reason, the virus first jumped and — crucially — who then stayed alive long enough to pass it on to other humans. In the case of the Human Immunodeficiency Virus, or HIV — the virus that causes AIDS — analysis of its genetic structure and evolution, retrospectively applied to stored tissus samples, have suggested that it first emerged, and was transmitted between humans, in the city of Kinshasa (then called Leopoldville) in what is now the Democratic Republic of the Congo. (See Sharp and Hahn 2011.)  These first infections with HIV occured some 50 to 70 years before the disease it causes, AIDS, was first specifically identified in the US in 1981, through analysis of an otherwise inexplicable outbreak of rare conditions such as TB and Kaposi’s sarcoma in New York City [See, for example, Hymes et al (1981) ]. The virus HIV was then identified as the virus that causes the syndrome in 1983 in two separate studies [Gallo et al 1983 , Barre-Sinoussi et al 1983 ].

Jakarta airport
In Jakarta airport, where I might, or might not, have picked up my bug

Keep these facts in mind and let me tell you about my recent experience of a mystery infection. In late November 2019 I went on a work trip to Java, Indonesia. A few days after I returned I was hit by a bout of illness, of a sort and severity to which I am not typically prone. Although far from being at death’s door, I had a fever, headache and a deep, deep fatigue. I said to family, friends and work colleagues at the time that for five days I felt as if I were about 80 years old. (I am 50, in case you were wondering.)

Well aware of the fact that on my recent journey, I might have contracted something nasty, like malaria or dengue, I brought my health literacy to bear and, as a first step, reviewed available online information and, at least in an initial way, self-diagnosed. I read — yes, on Wikipedia — that as I was not vomiting, I probably didn’t have dengue, at least. In the end, I decided that I might have contracted Chikungunya virus: I had never heard of this before, but the description of symptoms broadly matched, and this was a disease present in Java and I had certainly been bitten by mosquitoes there (the disease vector in this case). Accurate or not, this self-diagnosis was at least  reassuring as the information I could then find on Chikungunya suggested that I would be sick for a few days, but it was not a serious illness and would clear up by itself. And this is, indeed, what happened. Had I not started feeling better I would have gone to the doctor, but there turned out to be no need.

Some level of hindsight is now unavoidable. My self-diagnosis was informed enough, but as there was never a reason to back it up with tests — and certainly not tests for COVID-19 — I have absolutely no idea what actually did wipe me out between 4th – 8th December. Nor now will I ever know, nor will the five other people that I know of in my (relatively small) town who were taken out for up to two or three weeks in late December and January by ‘the flu’, four of whom drink or work in the  pub I typically frequent, incidentally. With no retrospective testing available, who is to say whether we all might, in fact, have had COVID-19. Or just the ‘usual’ flu. Or I did indeed have Chikungunya and was nothing whatsoever to do with my friends’ later cases of flu. All are possible explanations. Faced by this kind of uncertainty in any medical diagnosis, one can look for other data that indicate the presence of an infection, and as there is no particular cluster of COVID-19 infections currently showing up centred on Hebden Bridge, aren’t I just being a little egotistical — behaving, perhaps, like one of those attention-seekers who ring up the police and confesses to multiple crimes they didn’t commit?

Yet it is quite plausible that I could have contracted COVID-19 in Jakarta airport, say, or on one of the crowded planes on which I flew. Let’s face it — if I started feeling like that tomorrow, I’d be straight into self-isolation mode, as would anyone else right now. The thing is that the “point of origin” myth extends not just to the assumption that the virus originated in Wuhan — but that its discovery marks the date of the first cases, and that no one in the UK (or Italy, Germany, etc.) could possibly have been infected before Christmas. COVID-19 almost certainly existed in various parts of the world prior to its identification in Wuhan. It would be extremely illogical to think otherwise. Even if Wuhan itself were the place where the first virus of this species popped out of an animal host and went “Ah, humans!” this will have taken place well before December 2019, with any early deaths attributed to other causes — as will have been AIDS deaths in Leopoldville and elsewhere prior to 1981. But it is actually very unlikely that the mythical meat market around which cases first seemed to cluster was the origin of COVID-19 any more than the Mineshaft sex club in New York was where HIV made the jump.

ESA image showing Italian smog
An image from the European Space Agency, showing a spike in poor air quality over Northern Italy in February 2020

Instead, Wuhan is the place where COVID-19 first became an informational concept. It is this concept — and the related concepts that it has produced in a domino effect, such as testing, cause of death, social distancing, lockdowns — that are spreading from Wuhan: the place where the number of cases, and their severity, first became high enough to catch the attention of medical science. Much the same is then true of the second major cluster of infections, in Northern Italy. So what other factors might explain this?

One strong possibility is that both are places with notoriously poor air quality. Wuhan’s citizens protested about this in July 2019. Recent data released by the European Space Agency indicate clearly that not only is Northern Italy’s air quality the worst in Europe, it is the worst by a significant margin. See this image for instance, showing smog in February 2020. In addition, how Italy has tested its citizens is also markedly different from the regime followed in South Korea — still the nation to have conducted the most tests. There has been a concentration in Italy on testing those who are already sick, whereas the Koreans have tested more broadly. See this report from Switzerland which includes a link to the report of the Italian National Institute of Health.

Thus, there are many reasons and factors, beyond just the basic mortality rate, which explain why COVID-19 has become such a crisis in Italy — but to extrapolate these factors out into an assessment of the global impact, and base such restrictive policies on this extrapolation, is foolish. And fresh data are emerging all the time that suggest some well-publicised calculations of mortality rates are far too high. Up to date analysis of the Wuhan data by Mizumoto et al (preprint) suggest that though nearly 20% of Wuhan’s population may have been infected, they estimate the infection/fatality ratio as 0.12%: which is actually lower than for other existing coronaviruses (like the flu). And it is also clear that there a very significant proportion of those infected with COVID-19 show no symptoms of it. Some half to three-quarters of all cases may be asymptomatic, according to this report from Italian newspaper La Repubblica (in Italian).

Due to all of these things, it is extremely likely that — as might have happened to me and my acquaintances, and will have been happening, across the world, for some time — many of us may have already been infected by COVID-19 and either not known this at all due to lack of symptoms, or (prior to about February, anyway) mistaken it for the seasonal flu or some other virus. Illnesses and even deaths will have been attributed to other causes. And the informational concept that is ’cause of death’ still remains largely unclear and is very unreliable data. If someone has cancer or some other serious condition, contracts COVID-19, and dies — what did they die of? The UK government’s chief health adviser, Sir Patrick Vallance, admitted that his figure of “half a million” deaths due to COVID-19 should not be seen as meaning these would be in excess to normal mortality rates. In the UK, some 600,000 people die annually, and as stated on Thursday 19th March:

The coronavirus deaths will not be on top of this. Many would be within this “normal” number of expected deaths. In short, they would have died anyway. It was a point conceded by Sir Patrick at a press conference on Thursday (19th March) when he said there would be “some overlap” between coronavirus deaths and expected deaths – he just did not know how much of an overlap.

Prof. Ioannidis of Stanford University

Let us also heed the words of John P.A. Ioannidis, professor of medicine, of epidemiology and population health, of biomedical data science, and of statistics at Stanford University and co-director of Stanford’s Meta-Research Innovation Center. [I think he has authority, don’t you?]

Reported case fatality rates, like the official 3.4% rate from the World Health Organization, cause horror — and are meaningless. Patients who have been tested… are disproportionately those with severe symptoms and bad outcomes. As most health systems have limited testing capacity, selection bias may even worsen in the near future.

The one situation where an entire, closed population was tested was the Diamond Princess cruise ship and its quarantine passengers. The case fatality rate there was 1.0%, but this was a largely elderly population, in which the death rate from Covid-19 is much higher.

Projecting the Diamond Princess mortality rate onto the age structure of the U.S. population, the death rate among people infected with Covid-19 would be 0.125%. But since this estimate is based on extremely thin data — there were just seven deaths among the 700 infected passengers and crew [emphasis added]— the real death rate could stretch from five times lower (0.025%) to five times higher (0.625%).

Professor Ioannidis goes on to say:

One of the bottom lines is that we don’t know how long social distancing measures and lockdowns can be maintained without major consequences to the economy, society, and mental health. Unpredictable evolutions may ensue, including financial crisis, unrest, civil strife, war, and a meltdown of the social fabric. At a minimum, we need unbiased prevalence and incidence data for the evolving infectious load to guide decision-making.

Bloom Street
A mostly deserted Bloom St. Manchester, on 21st March

I do not dispute that right now it is wise to limit the spread of the virus. Social distancing seems sensible. But not lockdowns and the panic, distress and economic damage that they cause? And how long can this last? What happens in two weeks’ time? Have we created a pointless and dangerous new dichotomy in society, between the ‘infected’ and the ‘not infected yet’ — which will now define everyone as a potential risk, and a dangerous miscreant if they do not obey orders — a sudden extension of incarceration to entire populations, locked in their houses, their towns, their countries?

I want to keep this post apolitical, but regardless of one’s ideology, we need an exit strategy from all this and we need it soon. And if it is to be democratic, sensible, and not lead to fear — it needs to be based in part on people saying, ‘In my opinion, I have already been infected — I am not in a high risk group — and any danger will soon pass’. It cannot but be otherwise.

This is not irresponsibility — it is a necessary step to retrieving our trust in one another. If we don’t get this back, or we wait for our now-paranoid governments to tell us when we can start living together in our communities again — then we really are in big trouble.

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