The Hart Group briefing paper on asymptomatic spread of COVID, by pathologist Dr John Lee, shows how the whole edifice of COVID restrictions is predicated on asymptomatic spread, yet how the scientific foundation for its very existence is shaky, or frankly spurious. But there is one potential fly in the ointment.
Lee rightly distinguishes asymptomatic spread (probably non-existent) from presymptomatic spread, which he says is uncommon, accounting (he says) for only around 7% of infections. In support of that figure, he cites this paper from Singapore, 2020.
The practical problem this raises, in the context of trying to persuade society, or individual institutions like churches, or simply the multitude of scared folks, is that 7% is still a significant figure. It would seem arguable that during any particular social interaction, one cannot tell the difference between asymptomatic carriers of the virus (see Lee’s categories for this, which is very much an artifact of PCR testing) and potentially dangerous pre-symptomatic “spreaders.” And therefore, the argument would run, one ought to keep all the social distancing, handwashing, tracing and testing and masks in place.
I guess in the end one must concede the existence of some risk once one admits that presymptomatic spread is even possible, even though it is said to occur only for around 48 hours before symptoms develop.
As a matter of proportionality, though, this does not really run. For example, during the various periods my church has been allowed to meet, all the rules have been pretty carefully followed, to the massive detriment of our mission and our people’s well-being. But as far as I know there has not been a single clinically confirmed case of COVID amongst us, whether in those who have attended or those who have stayed away. And therefore, as a matter of fact, there can have been no presymptomatic carriers in our midst, and ergo all the damaging precautions have been for nothing. There is surely a point, long since passed, where such precautions are excessive when applied across whole countries.
A related issue is that the research in the Singapore all relates to the early, exponential phase of the pandemic. At this stage the virus is at its most virulent, and the population at its most susceptible. Viral loads in the presymptomatically infected are going to be at their maximum. It is extremely unlikely that, granted the truth of the 7% figure in that paper, the same metric applies for a virus that is becoming endemic in a population with high rates of natural or vaccine immunity. As time goes by the risk becomes increasingly trivial.
It seems probable then that, to catch enough virus to get sick, most people are going to need prolonged exposure to someone shedding enough virus to make them obviously sick. And we know now that care homes, hospitals and families, where viral aerosols can build up, account for the lion’s share of infections – though the UK government appears not to recognise this as it is taking no obvious measures to equip and man dedicated infectious disease units despite their predictions of more infection catastrophes come the winter. That suggests that the predictable winter overload is being fostered, not prevented.
In any case, I’m also somewhat suspicious of accepting that 7% of cases figure for presymptomatic infections, based on the actual clusters of cases used in the Singapore article, and what we now know about COVID’s spread (by airborne aerosols, not droplets or fomites or hands) and its incubation period. Once you know that aerosols build up in any closed space where infected individuals remain for a while, contact tracing becomes very much less dependable, even in Singapore. How can you be sure that the church service a presymptomatic sufferer attended was the source of the infection in the next pew, rather than the shop or bus the second victim was in the previous day?
Here are a few examples (which you can check out in the paper). “Cluster A” involved a couple of Chinese tourists from Wuhan, who developed symptoms 3 and 5 days after visiting a church. Three other churchgoers subsequently developed COVID, but at rather odd intervals: the first 4 days later, the second a week after that, and a third a whole 15 days after the service. The last was found to have occupied the “infectors'” seat only later in the day.
But we know now that in practice infection doesn’t spread from contaminated surfaces, so we are asked to accept that a SARS-CoV-2 aerosol hovered over a particular pew as worshippers (apparently) came and went during the day, yet took over a fortnight to make the victim ill (whereas someone else became ill simultaneously with the original pair who had caught it back in Wuhan, just 4 days later). I’m inclined to doubt the adequacy of the contact tracing process more than I believe the cluster was the result of presymptomatic spread.
Cluster B involved a woman who developed symptoms 11 days after having dinner with a confirmed case. A couple of days before she did, she attended a choir, and another singer developed symptoms 5 days later. So it’s a possible – but had the second singer not also visited shops or been on public transport in the week before? Maybe she too had been incubating it for as long as a fortnight, and one occupies many potentially infectious spaces during that time.
Clusters C, D and E all involve possible presymptomatic infection of spouses or housemates, which given the now known high rate of mutual infection of spouses (around 40%) is somewhat plausible, but of no relevance to less intimate socialisation. Yet in all three clusters, the supposed presymptomatic infector and the supposed infected developed their symptoms on the same day. One would have expected several days’ difference – unless, in reality, both had been infected at the same time in some un-recorded setting.
Cluster F is another church example, where a woman supposedly infected two people sitting behind her two days before developing symptoms herself. Once again, the story becomes more suspect when you realise that one of the “victims” developed symptoms the very same day as the alleged source, and the second just two days after that.
The last cluster (G) involved a man probably giving COVID to a younger woman he “met” whilst travelling in Indonesia the day before he himself got symptoms, and four days before she did. It would, of course, be instructive to know what kind of meeting they had – if she was a prostitute, for example, the implications for presymptomatic spread are rather different from her sitting behind him in church.
So all in all, these cases (on which John Lee, it seems, bases his aside about presymptomatic spread) seem a shaky edifice on which to say that presymptomatic spread is significant, let alone to quantify it. Other explanations seem possible in each case.
But Dr Mike Yeadon is right to point out the case against presymptomatic infection, based on the entire experience of other viruses, including Coronoaviruses. This is that viruses cause respiratory infections in order that the infected (and hence symptomatic) tissues can spread enough virus particles into the air to give other people the same advantageous (to the virus) symptoms. In other words, “Coughs and Sneezes Spread Diseases,” though primarily, we have now discovered, by dispersing them as aerosols in enclosed spaces rather than by passing droplets between people. SARS-Cov-2 may well have been manufactured in a laboratory, but it is still dependent on the same biology as every other Coronavirus.
Hence we instinctively avoid ill-looking people through deep-seated cultural norms, and possibly even by biological instinct, and we are also programmed to avoid others if we ourselves get ill. We may not do quite so well with enclosed spaces, because draught-free rooms are a relatively recent comfort.
In conclusion, the case for presymptomatic spread being an Achilles heel in the “abandon lockdowns” argument has, I think, still to be demonstrated.