A late autumn surge in reported Covid infections is underway in Europe, with spikes in Austria, Netherlands, Denmark, Germany, Switzerland and Norway, and the possible beginnings of one in France, Portugal and Italy. This is despite high vaccine coverage and the heavy use of vaccine passports in most of these countries including Germany, Netherlands, Austria, Switzerland, Italy and France.
Some of this is at least partly a result of ramping up testing, especially in Austria and Denmark.
Denmark’s positive test rate is currently flat (see below). This is despite the country declaring the pandemic over and abandoning vaccine passports in September. However, due to the climbing reported infection rate, the country’s Parliament is now said to be preparing to return to a state of emergency and reactivate the vaccine pass scheme, despite the rise being so far largely an artefact of increased testing.
Elsewhere, however, the positive rate is also rising, suggesting real Covid and not just a testing artefact.
In recent posts I’ve been exploring the question of why COVID-19 (much like other seasonal viruses) has a Jekyll and Hyde-like nature, being puny for much of the year then exploding in short, sharp outbreaks for a few weeks at a time, usually though not exclusively in the winter. I argued in a post last week that seasonality appears to be driven largely by cycles in the human immune system (though there may be environmental factors such as UV radiation, temperature and humidity as well). The trigger for the somewhat irregular (and not necessarily winter) outbreaks appears to be the appearance of a new variant (or virus) that is able to infect slightly more people, amounting to just one in 18 additional people when estimated from the secondary attack rate. The end of the outbreaks then corresponds to the exhaustion of the small pool of newly susceptible people and the restoration of the temporarily disturbed herd immunity.
I noted that the difference between a surge and a decline amounted only to a small absolute change in the R growth rate, from 1.3 during a surge to 0.8 during a decline, and that the shift between these rates often occurs very abruptly. This means that infected people quite suddenly start infecting 1.3 other people before, around three and a half weeks later, just as suddenly switching back to infecting just 0.8 people. This change in R is reflected in a similar change in the secondary attack rate (the proportion of contacts an infected person infects), which varies between around 15% during surges to around 10% outside of them. I observed that this difference is small enough to be explained by a slightly increased susceptibility to a new variant and a subsequent restoration of herd immunity a short time later.
After writing this it occurred to me that with such a subtle trigger it would seem that outbreaks should be highly sensitive to the amount of social contact people have with one another, and thus to the imposing and lifting of restrictions (or to voluntary social distancing). Indeed, it is logic like this which presumably explains why SAGE members and other scientists persist in believing in the efficacy of lockdowns regardless of how much data emerges showing they don’t make any significant impact on the infection or death rate.
A recent set of SAGE minutes explains the logic of restrictions:
I wanted to come back to the question of what causes COVID-19 occasionally to have explosive outbreaks. We’ve had two in England so far. Using the graph below (produced by Imperial’s REACT study using symptom-onset reports from their antibody survey, so no PCR tests involved) we can see when they occurred. The first occurred from around February 25th to March 19th 2020, ending after about three and a half weeks, as abruptly as it began. The second got going around December 2nd, and ended – once again abruptly after three and a half weeks – on December 25th. As the lines below indicate, these starts and stops bear no relation to when lockdowns were imposed or lifted (the red and blue lines respectively).
Given that (as we can see) Covid was around in England throughout the winter of 2019-20 (arriving in November according to this graph) and was also simmering away in the autumn of 2020 without taking off, a key question is what triggers the beginning and end of the more explosive outbreaks?
Another way of putting the same question is: why does COVID-19 occasionally, Jekyll and Hyde-like, transform from a relatively gentle, not very infectious disease into a super-infectious disease for a few weeks, before suddenly returning once more to its largely benign form?
Perhaps surprisingly, Covid in England has only been in ‘Hyde’ form for about seven weeks in total so far, with the R rate (the speed at which the epidemic is growing) only going significantly above one (indicating an exponentially growing epidemic) for around three and a half weeks in February/March 2020 and three and a half weeks in December 2020. The rest of the time it’s been up and down in different regions, particularly in the autumn, but there’s been no nationwide surge. What, then, on those two occasions triggered the disease to become briefly so much more infectious across the country?
We’re publishing an original piece today by a retired Professor of Forensic Science and Biological Anthropology and an epidemiologist with a PhD from a Russell Group university asking whether the recent rise in infections from the Delta variant invalidates the hypotheses that SARS-CoV-2 is a seasonal virus. After all, if it was, you’d expect it to be declining in the U.K. and across other northern latitudes. But they suspect infections have peaked and are about to start falling. Here is an extract:
Does the recent rise in infections in the U.K. – despite mass vaccination and Non-Pharmaceutical Interventions (NPIs) – presage a substantial third wave in the summer? Does this rise effectively falsify the seasonality hypothesis?
Well, according to the Government’s own data, percent positivity in England is reported at 2.7 for the most recent available day (June 15th), having more than doubled from 1.3 on June 15th. Infections – number of positive tests reported – present a more complicated picture. They leapt to around 9,000 per day in England from 17th to June 18th, having almost plateaued at about 6,500 the week before. However, this jump occurred after the Government’s announcement of June 14th and may already be about to decline. The percentage change in the 7-day case rate has shown a steady fall since June 7th.
The issue of COVID-19’s seasonality has been covered extensively on Lockdown Sceptics. Back in February, Glen Bishop noted that a model developed by Imperial College researchers – which predicted there would be an additional 130,000 deaths this summer – assumed that transmission does not vary by season.
In a follow-up article, I reviewed eight separate studies that found evidence for the seasonality of COVID-19. Indeed, it would be rather surprising if COVID-19 wasn’t seasonal given what we know about other human coronaviruses, i.e., that they are – in the words of one recent study – “sharply seasonal”.
However, doubts have been expressed about whether COVID-19 is in fact a seasonal disease. Such doubts are based on the observation that countries like Chile and South Africa saw epidemics burgeon during their summer months, and that Britain itself is now seeing a rise in cases.
But as the biologist Francois Balloux notes in a recent Twitter thread, the fact that some countries have seen infections rise during the summer is not inconsistent with seasonal factors playing a role in transmission. It just means they aren’t the only factors involved. (One also has to consider viral evolution, population immunity and human behaviour.)
A new study by researchers from Yale and Columbia (which was published in the journal Nature Communications) offers particularly strong evidence for the seasonality of COVID-19. The authors looked at the relationship between seasonal factors and the R number across US counties between March and December of last year.
They ran a statistical model of the R number, with temperature, specific humidity and UV radiation as predictors. The model controlled for a range of other factors, including spatial, demographic and socio-economic variables.
The authors found that each of the three seasonal factors was independently associated with R. They then calculated the fraction of R that was attributable to seasonality, and obtained a value of 17.5%. Interestingly, specific humidity was the most important of the three, contributing 9.4%.
The authors’ findings indicate that “that cold and dry weather and low levels of UV radiation are moderately associated with increased SARS-CoV-2 transmissibility”. However, they were unable to examine possible differences in seasonality across different variants, leaving this as a topic for future research.
Overall, their study provides some of the best evidence yet for seasonality. And it gives one more reason to be sceptical that the current rise in cases here in Britain portends a major epidemic.
It’s well-known that flu-like illnesses are seasonal, and COVID-19 seems no different.
What is not well understood is what drives the seasonality. The flu season is in the winter months so the obvious candidate is temperature. However, closer analyses have tended to rule out a simple role for temperature, not least because seasonality occurs in places with very different climates.
Other potential candidates are sunlight (including UV radiation) and humidity. None is completely convincing, though sunlight has been shown to have a direct role in stimulating the immune system.
Now there’s a new kid on the block: pollen.
Martijn Hoogeveen is an independent researcher who has been exploring the role of pollen in driving seasonality. Pollen is known to be triggered or inhibited by meteorological factors. Hoogeveen explains:
Meteorological variables, such as increased solar radiation and temperature – among others the absence of frost – not only trigger flowering and pollen maturation, they also affect the pollen bio-aerosol formation: dry and warm conditions stimulate pollen to become airborne. Rain, in contrast, makes pollen less airborne, and cools the bio-aerosol down. Very high humidity levels (RH 98%) are even detrimental to pollen (Guarnieri et al., 2006).
The main idea is that the pollen plays a further, significant role in stimulating the immune system (such as when it causes hay fever), which has a strongly inhibiting effect on flu-like viruses. A further, more speculative idea is that “anti-viral phytochemicals in pollen” could directly inhibit viral aerosols in the air.
Last week, the UK’s sports bodies wrote a joint letter to the leaders of the main political parties. It warned that the return of some spectators from May 17th will be “insufficient to end sport’s Covid financial crisis” because attendance will be capped at 25% of capacity in larger venues.
“Looking ahead to June 21,” the letter went on, “we support the Government’s ambition to secure the full return of fans, without restrictions if possible.” However, it also said, “All of our sports can see the benefit that a Covid certification process offers in getting more fans safely back to their sport as quickly as possible.”
In other words: the sports bodies want to get fans back into bleachers as soon as possible, preferably without restrictions, but if using vaccine passports is what it takes, then so be it.
However, my reading of the evidence is that vaccine passports would provide little benefit at outdoor sports events (which I assume covers most such events). And given objections that have been raised on grounds of privacy and non-discrimination, mandating them for all sports events seems like a very unwise idea.
To begin with, the percentage of people with COVID-19 antibodies is now well above 50% in England and Wales, as this chart from the ONS indicates:
The percentage will be even higher by May 17th, when spectators can finally return to stadiums. And it will be higher still when the next football season begins in August. Due to the seasonality of COVID-19, transmission is likely to be low over the summer, so by the time restrictions might be needed in September, a very large percentage of people will have some form of immunity.
What’s more, evidence suggests that the vast majority of infections occur indoors. This is because wind quickly disperses the virus in outdoor environments, and viral particles degrade more quickly when exposed to sunlight.
In Ireland, only 0.1% of infections could be traced to outdoor activities (though this doesn’t include all the associated indoor activities, such as travel to and from events). And despite England’s packed beaches last summer, the epidemiologist (and SAGE member) Mark Woolhouse told MPs there were “no outbreaks” linked to beaches.
A systematic review of five studies published in The Journal of Infectious Diseases found that less than 10% of infections occurred outdoors. And a recent study published in Environmental Research concluded that “the probability of airborne transmission due to respiratory aerosol is very low in outdoor conditions”.
Chris Whitty has said, “The evidence is very clear that outdoor spaces are safer than indoors.” And a paper by the PHE Transmission group notes, “Evidence continues to suggest that the vast majority of transmission happens in indoor spaces.”
Before the UK’s hugely successful vaccine rollout, the risk of outdoor transmission was low. By the time sports venues re-open on May 17th, the risk will be even lower. While there are some circumstances where Covid certification makes sense (like visiting relatives in care homes), attending outdoor sports events is not one of them. Instead of spending more time checking fans at the entrance, venues would be better off improving ventilation in high-risk spaces.
It’s time to get fans back into stadiums – but they should only have to show a ticket on their way in.