Why has coronavirus fled London?

30 May 2020

9:00 AM

30 May 2020

9:00 AM

My partner, Julian, hovered at my shoulder on Friday as I tapped out my Times Saturday column (about travel quarantine). I’d slipped in a paragraph with my own thoughts about the transmission of Covid-19. ‘Cut the lot,’ he said. ‘You’re not an epidemiologist. Nobody’s interested in your theories.’ This was probably good advice so I put my own thoughts on hold.

Until now. Because something’s still nagging me. I know I’m not an epidemiologist, but silences speak loud in science, and from those experts put up for media interview I notice a curious silence — a silence on what feels like a most important report and, from their interviewers, a timidity about pressing them.

The question the experts should be asked is about London. Why has coronavirus fled the capital?

London is now recording only a handful of new cases every day, while infections across the rest of the country are dropping far more slowly. It’s not as if there’s nobody left in London to infect: from a population of about nine million, two recent estimates of how many Londoners have developed antibodies put the proportion presumed immune at between 17 and 20 per cent.

That figure, of about one in five, interests me more and more. I first noticed it in reports of the proportion of cruise passengers infected on the Diamond Princess in February. Apparently just under 20 per cent had been infected; and on another cruise ship, the Grand Princess, some 16 per cent had the antibodies. In Stockholm (where restrictions have been lighter than in Britain), Sweden’s chief state epidemiologist believes around 20 per cent will have the antibodies, leaving 80 per cent theoretically vulnerable — but the infection rate there has been falling for more than a month. Governor Andrew Cuomo (headlines the New York Times) ‘says 21 per cent of those tested in NYC had virus antibodies’. Yet the city is beginning to unlock as the infection rate falls fast.

There are outliers to this cluster of ‘one-in-five infected’ reports but the clustering is hard to ignore. There is no such cluster at the bottom of the scale, where, among regions and nations, the lower infection rates differ wildly and appear best explained by the promptitude, skill and severity of the lockdowns applied. Timelines do determine when cities like London attain that 20 per cent, but once reached, the rate of new infections hits some kind of ceiling, and begins to fall quite rapidly. In London the R number is 0.4, way below the rest of the country.

Imagine yourself an ambitious Covid-19 virus. The conclusion you’d draw is that a rich harvest of infectables awaits you wherever (a) there is no sharp lockdown; and (b) the proportion of humans with the Covid antibodies — the susceptibles — is still in lowish single figures. But (c) that the going gets tough for you as the percentage testing positive for antibodies moves into double figures, and really tough as it moves above about 20 per cent in conurbations and perhaps lower outside them. Our ambitious virus could be forgiven for concluding that ‘herd immunity’ among its human host is approached at somewhere near that point.

This needs explaining, because at the outset of this crisis there appeared to be near-consensus among experts that herd immunity is reached around or perhaps above a 60 per cent infected figure. London and New York suggest that cannot be right — unless (and I can’t rule this out) 20 per cent represents herd immunity under lockdown conditions because transmission is then more difficult.

If so, we should very soon be seeing a surge of new infections as lockdown is loosened, because if the 20 per cent antibody positive figure is right, and all the rest are susceptible, then the remaining 80 per cent (about seven million Londoners) are waiting out there to be infected.

In short, if you believe herd immunity is only reached at 60 per cent, you should be terrified at any loosening of lockdown. If you don’t, then you must reconcile antibody testing that says 80 per cent are still susceptible with the difficulty the virus seems to encounter in marching very far past 20 percent of the population.

That is the reconciliation my hypothesis achieves. I propose that there may exist forms of human resistance to this virus that don’t show up in Covid-19 antibody tests.

I say ‘resistance’ rather than ‘immunity’ because I know no reason to assume the body’s defences to Covid-19 must be all or nothing: a binary division between those who have and those who lack immunity. Should we perhaps be looking at the population as a continuum ranging from the totally immune (those with the Covid-19-specific antibodies) to the totally susceptible?

Take, for example, the common cold, some variants of which are also Covid-related. So far as I know, there’s nobody who has never had a cold, or anybody who has one all the time. You develop some resistance while you have the cold or you wouldn’t recover but does it later desert you altogether? There may be such a thing as patchy, background, lingering or incomplete resistance. Discussing this, I was directed to recent comments on Twitter by Philipp Koellinger, an economist and behavioural geneticist at Vrije Universiteit Amsterdam. Koellinger notes that: ‘A wet lab study from Germany suggests that some degree of limited background immunity against Covid-19 may exist in the population (~1/3 of their healthy donor sample) due to previous infections with other “common cold” coronaviruses.’

I’m in no position to appraise the research Koellinger cites and will try to be very cautious in what I hypothesise. It’s this. That there could be some varying measure of resistance to Covid-19 among many who may not test positive for the Covid-19–specific antibodies; and in focusing on that Covid antibody test alone as indicating a pass-or-fail immunity, we could be overlooking important ways in which humans may be endowed with, or acquire, other kinds of resistance. If this is true, then ‘herd immunity’ may be a more complicated threshold than we have realised — and easier to reach.

There you are, Julian. But, as you say, who cares what I think?

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