Versions of COVID-19

The disciplines of virology and clinical medicine collaborate closely. For instance, the diagnostic tests that allow clinicians to ascertain if a patient is indeed infected with SARS-CoV-2 were crafted by virologists, while virologists learn from clinicians how the virus impacts its human hosts.5 At the same time, the object of these two disciplines is different. Virologists study all kinds of viruses, and their objects of inquiry include viruses’ genes, history, hosts, levels of virulence and transmission routes. This means that, for virologists, ‘COVID-19 is a contagious disease due to an infection by a specific type of coronavirus: SARS-CoV-2’.6 In the world of virologists, the surge of COVID-19, while new in its particulars, was an accident waiting to happen. They had been warning us for decades that serious pandemics were going to arise from virus jumping from animal to human populations. The starting point for clinicians is not the SARS-CoV-2 virus, but the ways it affects its human hosts. For clinicians, COVID-19 is a disease that causes havoc in the bodies of unfortunate patients. This turned out to be full of surprises.7 The particular assaults on lung capacities and blood clotting mechanisms that clinicians observed in their patients with COVID-19 were new. Existing interventions were adapted, pathophysiological pathways unravelled. Hence, while there are marked crossovers between pursuing a virus and treating a patient’s body, the precise objects that these two disciplines operationalise are not the same.

While clinicians were trying to save their patients’ lives, outside hospitals, preventive measures were implemented. These were oriented around blocking the most probable routes the virus might take from one host to another. People were warned to wash their hands, cough into their elbows and avoid handshakes. They were asked to maintain a significant distance between their bodies. In this context, physicists of fluids started to wonder what distance might be significant enough, given the behaviour of fluids. They operationalised COVID-19 as a disease caused by a virus hitchhiking from one body to the next, dissolved in bodily fluids, and set up laboratory experiments to discover how far bodily fluids travel. Volunteers were asked to breath, cough or sneeze and the researchers rendered the resulting droplets visual.8 These experiments showed that the emitted droplets, both large and small, cluster together and are propelled forward in clouds. This means that their reach is a lot farther than the 1–2 m distance recommended in public health advisories.

Most biomedical researchers were not impressed. For even in the absence of preventive measures, most people with COVID-19 were less contagious than, say, people who have measles, known to be transmitted by small droplets. The physicists might have shown that, under experimental conditions, aerosols may possibly travel from one body to another, but the biomedical experts wanted to know the probability of this transmission route resulting in people becoming infected with SARS-CoV-2. They did not envision individuals, but populations. Hence, they turned to infectious disease epidemiology, the discipline for which COVID-19 is a contagious viral disease spreading in its own specific ways through human populations. In epidemiology, the transmission of the virus is not experimentally orchestrated, but painstakingly counted and traced in real-life situations.9 The data points that allow for the counting depend on the availability of test kits and laboratory supplies, skilled personnel and the readiness of people to undergo testing. One dire problem has been how to count those who have no or only mild symptoms.

Then, there is the tracing, which requires detective work. Is the outbreak among the members of a choir due to their singing, or does a thorough investigation reveal that all those infected gathered together in a small corridor for coffee after rehearsal?

Possible, probable and actual transmission routes are different phenomena and hence different objects to research. Even so, they share something in common: they are all transmission routes. Studying them helps to shape the hygienic measures that seek to prevent the virus from reaching its human hosts. Researchers taking their cues from immunology do not invest in transmission routes, but foreground the hosts.10 For them, COVID-19 is an infectious disease that stimulates immune systems in intriguingly diverse ways. They underline that some people, once infected, are affected far less than others, and wonder to which extent this the preparedness of their immune system may be involved in this. It might seem as if this question is adjacent to questions about transmission and only becomes relevant once hygiene has failed. But it is not that simple.11

The complexity becomes apparent in evaluations of the population-wide use of face masks. Within the logic of hygiene, face masks are meant to prevent the transmission of virus. Accordingly, evaluating their efficacy is a matter of comparing the number of positive tests between regions where face masks are worn and regions where they are not.12 Within an immunological logic, by contrast, the most significant characteristic of face masks is not necessarily that they block the transmission of the virus, but that they might lower the transmitted dose. This would be interesting if a small dose of SARS-CoV-2 were to trigger an immune response without developing into a full-blown disease. In that case, small doses could serve as inoculations—at least for some people and for some time.13 The parameter of success for this particular use of face masks would not be fewer positive tests; there might even be more positive tests than in populations not wearing face masks. The parameter of success, in this case, would be the elicitation of a protective immune response, resulting in fewer cases of severe disease and fewer deaths.

The clash that so far has gained most public attention is that between the hygienic blocking of viral flows by means of lockdowns and the hampering of economic flows that results from them.14 If lockdowns are imposed, people—insofar as they have access to food and their housing is adequate—are supposed to come out on the other end intact and healthy. Blocking economic flows, by contrast, is not similarly reversible, as it creates a downward spiral. Once businesses have gone bankrupt and jobs are lost, it is not obvious how to revitalise economies. For economics, COVID-19 is a threat to the economy as measures to block flows of the virus also block monetary flows. This discipline does not disaggregate biological events from societal responses to it, as these jointly affect the economy. Moreover, the threat COVID-19 poses is worse in societies without a properly functioning welfare state, for when people without jobs have no money to spend, they cannot, once a lockdown ends, pay for the goods and services that might allow others to resume working and once more earn their keep.

However, while this vicious circle is often flagged as a straightforward argument against lockdowns, things are—again—not so simple. Hygiene and economics have different unities of calculation, which are graphed along different x-axes and y-axes, with recommendations that point in different directions—however, instead of simply clashing, they are also interdependent. After all, when too many people become seriously ill or even die, this, too, disrupts the social fabric and pushes the economy into decline. Hence, just as successful lockdowns depend on people having sufficient food and appropriate housing, a vigorous economy depends on a sufficiently healthy population.

One last example. As it is, most epidemiologists attempt to comprehend the pandemic by developing explanatory models. Using as their input all kinds of data that impress them as suitable, they hope to model the most likely routes according to which COVID-19 spreads through human populations.1 Above, we signalled that this probabilistic approach is in tension with the studies into possible transmission routes that physicists conduct. Here, we want to make a further point. Similarly to research by physicists, epidemiological models aim for generality. These models are abstracted from single instances, so that they may travel unhindered around the globe. This approach conflicts with the investment in specificities current in anthropology and other social sciences, where ‘human populations’ stand out as an undue abstraction. Which populations, when, where and under which circumstances?16 17 While models envision a generalised human, for social scientists, COVID-19 is a multifaceted problem faced by particular people, living under specific social and material conditions. This means that, even if, thanks to WHO coordination, COVID-19 has the same name across the globe, it is not the same reality everywhere.18 Living with this disease is a different plight in Brazil, Germany, China, Uganda, the USA, the Czech Republic, the Netherlands, Bangladesh and so on—and in each of these countries it is different for those with and without steady incomes, housing, gardens, parks, families or what have you.¹⁹

Social scientists share this investment in specificity with clinicians, who likewise take heed of the specificities of this singular patient in the here and now. But while clinicians in intensive care units prioritise such variables as oxygen saturation and blood levels of bradykinin, social scientists investigate such issues as overburdening due to double duties, suffering from loneliness, increases in domestic violence and deepening inequalities due to lack of schooling.20 The list is open ended, see box 1.