(Image: Private Media/Tom Red)

People may well throw things at me at what I’m about to say, or would do if anyone in Melbourne was allowed to go anywhere or do anything, but it may be that COVID-19 is, for humanity, a piece of great good luck. Indeed the disease seems almost providential. It’s lethal enough to get our attention, but not so greatly as to tear society apart.

It takes the very old, cruelly, but almost no children, which would be a raw tragedy of another order entirely. It has been slow enough in its spread to allow us to catch up, even with criminally negligent efforts such as that of the Morrison government. 

Will we be willing to be lucky and use this opportunity to thoroughly reconstruct our institutions and planning for a world that has just reminded us that our control of nature is more apparent than real? It would seem not. The deep-seated human tendency to see any given level of misfortune as as bad as it’s going to get has been a strong undercurrent throughout the pandemic.

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The “once-in-a-century” rhetoric — for the third global SARS outbreak in 20 years — has been used to reassure ourselves that we will simply return to life as it was. 

Crucially, this seems to have centred on a presumed relationship between COVID’s rapid and universal spread and its relatively low lethality compared with horror viruses such as Ebola and HIV. That has been reinforced by the claimed lowered mortality rates for the Delta variant, which spreads faster. Many of us have become pretty shoddy amateur epidemiologists in the past year or so, projecting on to the disease the assumption that COVID makes a “trade-off” between rapidity of spread and mortality.

Well, epidemiologists do talk of trade-offs in viruses, but sadly there’s no hard and fast relationship between lethality and COVID’s “R-nought” number (its basic reproduction rate). R-nought has to be above one (each person infects one other) for the disease to spread in its early stages. Assessments of COVID have ranged from 2.8 to 5.7, significantly higher than influenza or rhinovirus (the common cold). In fact, there’s no hard and fast inverse relationship between R0 and lethality. Influenza has a lower R0 than Ebola, the common cold a higher one. Smallpox was both more lethal and more infectious than COVID.

The “trade-offs” that epidemiologists speak of are more complex than this and, of course, consider only the virus’ strategy for maximum replication, not any irrational sense of fairness. Viruses “trade-off” between internal host spread, and external spread — i.e. replicating furiously in a body, or getting to the next one — and it is the rate of internal host spread that is at the root of lethality.

In the case of COVID, this is often through provoking an immune reaction that kills the patient/host through inflammation. Indeed for a few decades it was thought that the rate of infectiousness and lethality were positively related, internal host spread being the motor of both (more viruses inside, more tissue damage, and more exits). 

It gets still more complicated than that, but the upshot is that any sense of comfort we might get from some assessment of virus-level trade-off is illusory. It demonstrates how difficult it is to think in a fully Darwinian way, when language is so deeply structured with notions of intent and purpose. There is no trade-off that matches our priorities, or even that of the virus as a species — the very notion of species is a “real abstraction”. There are trillions of replicating machines, throwing off mutations, changing every possible aspect of this virus’ functioning. 

What we’re getting wrong at the moment is any sense of relief, or content, in COVID’s limited lethality, and its particular form. COVID’s dirty little trick — purpose creeps back in — is its asymptomatic period, because asymptomatic spread allows a virus to be super-lethal without the penalisation of taking the host out of circulation. The prime example of this is HIV/AIDS, with a years-long gap between host infection and sickness and death. Could COVID evolve strains that take advantage of its asymptomatic lag time? Something like a supercharged MERS, the forgotten SARS, that had a lethality rate of 30%-50% in 2010 (but had a low R0? Or something simply new to the big time, such as the Nipah virus, to which there has been an unsettling turn of attention by virologists.

If the viral dice game comes up with something that combines an R0 of greater than one, an asymptomatic lag, and the cellular ferocity of MERS, then this pandemic will look like the dry run we wasted — perhaps with disastrous consequences. You wouldn’t need the lethality rate of an airborne virus to go up by much, or to spread more evenly, for breakdown to loom, and a total social reorganisation be required. 

What we need, and maybe we have, buried deep in government (though I doubt it) is a catastrophe plan. Maybe that’s what the sudden appointment of an army type to run the response was for, rather than just a pre-election khaki flash. If so, the only democratic way to do it would be to make it clear that that’s what’s being done. 

The public conversation has to be had at some point. The only rational course of action coming out of this pandemic would be global commitment to an international permanent vaccine development fund, capable of mobilising science on a scale well beyond the ad hoc process that occurred this time, and with an eye to increasing development speed beyond anything contemplated; together with a catastrophe plan, elements of which are public, and would allow for some debate about response, reorganisation, and — pretty dark stuff — what sort of social triage would take place. 

This virus came for the very old, and for the younger, chronically ill (who got little consideration). The next one may not. If it “turns its attention” elsewhere, our refusal to take nature’s hint this time round will be revealed as a collective failure, moral and of the will, with few precedents in human history. 

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Peter Fray
Peter Fray
Editor-in-chief of Crikey
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