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Covid19 – another update

This is a good time to re-examine how well, or how badly, the UK has done, and some of the factors involved.

1. Number of deaths.

Data from https://www.worldometers.info/coronavirus/#countries [accessed 28-3-21]

We are frequently told that USA and Brazil have suffered greatly – and in terms of total deaths (562k, 310k respectively) that is true. But their population is much larger than that of the UK, and that has to be taken into account, by looking at the deaths per 100k population. If we do this for a selection of countries, we see the following table

CountryDeaths per 100k
UK186
Italy178
USA169
Spain160
Brazil145
France145
Germany91

I should add the caveat that the method of counting deaths varies from one country to another (even with the UK figures we get a different number from different sources), so the comparison is not absolutely reliable. It is also worth noting that some of the other countries have been catching up with us – the same comparison a month or two ago would have shown us to be further ‘ahead’. But it is quite clear that we have nothing to be proud of in the way we have dealt with the pandemic.

2. What could we have done better?

i) Lockdown and other controls. Obviously we were very slow to respond at the start; the Government delayed its response inexcusably. Would it have made any difference?

If we cast our minds back to January/February 2020, nobody knew when vaccines would become available, nor even whether effective vaccines would be possible. In the absence of a vaccine, all that can be achieved by lockdown (and other control measures such as border controls), would be a delay in the spread of the virus. It would not reduce the number of cases or deaths ultimately. The only factor that would eventually control the infection (in the absence of a vaccine) would be the much maligned concept of ‘herd immunity’ – eventually the number of people who had been infected (and hence became immune) would reach a level where further spread of the disease stopped. I should make it clear that this does not constitute advocating that as a policy; it is simply stating a fact.

That doesn’t mean that those control measures were pointless. Delaying the spread, or ‘smoothing the curve’, has a value. Spreading out the number of cases over time reduces the risk that hospitals would become overwhelmed. It also buys time for the development of a vaccine – and as it turns out that was critical. If our earlier control measures had been more effective, some of the people who died would now be available for vaccination.

ii) Border controls. Some countries have achieved a remarkable level of success by using border controls, coupled with rigorous lockdown measures. We are often told about New Zealand, Iceland, and Taiwan. for example. NZ and Iceland are much smaller countries, and much more isolated than the UK. Even Taiwan (which was cited as an example in a recent Guardian article) is only 1/3 of the size of the UK, and although it has frequent flights from China, it is more isolated than the UK. Although Britain is also an island, would it really be feasible to cut ourselves off from everywhere else in the way those other countries have done? All those ferries – and the Channel Tunnel – and including all the crews of the ferries, and the lorry drivers. To say nothing of the likelihood of informal passage from the continent. You can easily sail a small boat across the Channel, but I don’t fancy your chances of doing that to Iceland, or Taiwan; you would certainly need to know what you were doing. The experience of the Isle of Man is instructive here – they thought they had it sorted, and re-opened pubs etc. But it couldn’t be maintained, and now they have problems.

In the absence of a vaccine, such a policy would have to be continued until the disease was eliminated throughout the world.

3. We could have been better prepared.

i) General health. Many of the Covid-related deaths have been in ‘high-risk’ groups of people. Of these, I want to single out two factors: obesity and pre-existing respiratory conditions (for which air pollution is a major contributing factor). The Government has prevaricated for years over taking effective action to counter either of these problems. This is a major reason why we have done so badly in the current pandemic.

ii) The health service. The Government has treated the health service as a business, like selling soap. It’s not efficient to keep large reserve stocks of soap. You can predict how much soap people will buy, and if more is needed, you can get more supplies – ‘just in time’. That doesn’t work with the health service. Up to a point, you can predict how much spare capacity will be needed in an average winter, but that falls down when faced with an unexpected demand such a  pandemic. As we found out, it is not easy to suddenly buy in large supplies of PPE or respirators, when other countries are trying to do the same. And worse than that, you cannot suddenly increase the numbers of trained doctors and nurses. So the Government built all those Nightingale hospitals, forgetting that there were not enough staff available to run them – so they have been largely unused.

Several previous exercises had demonstrated that the health service was ill-equipped to deal with a pandemic – but these were ignored.

iii) Test and trace. We used to have a system where most hospitals had their own diagnostic laboratory, backed up by a network of laboratories run by the Public Health Laboratory Service. So samples could be taken locally (either in hospitals or by GPs), and tested locally. Hence people ddn’t have to travel long distances to get a test, and the results were available very quickly (often the same day). If contact tracing was required, that was also done locally, under the auspices of the local authority. That system could have been used to run test and trace, but much of it had been gradually eroded, by merging laboratories (so they are less local), abolishing the PHLS (the remnants being formed into the Health Protection Agency, HPA), and slashing local authority budgets, so the contact tracing teams are now a shadow of their former selves. The Government seemed to decide that was left of the system was not capable of doing the job, so they outsourced it, ending up with a system that was not fit for purpose, and was a gross waste of public funds.

Although I am cross about the waste of money, I’m not sure that it made any difference to the pandemic. Contact tracing is crucial in the control of some infectious diseases – tuberculosis and sexually transmitted diseases being two prime examples. In both cases, these are long-term infections, where the person concerned will go on infecting others for ages, so you not only have an opportunity to prevent further transmission, but you can also do contact tracing backwards – find out where they might have caught the disease, and deal with that as well. These diseases also highlight the value of having a team of trained, experienced contact tracers. It requires a good deal of tact and professionalism to ask someone where they might have contracted a sexually transmitted disease. Plus local knowledge as well. Someone with an hour or two of training, working from a call centre, is not going to get far.

The main problem with contact tracing for Covid comes down to timing. If you consider someone who is infected on day 0, then suppose they become infectious on day 4 (but not yet symptomatic). So they have started spreading it to others. They develop symptoms on, say, day 6. On day 7, they think “I’m ill, I must do something”. So they book a test, which is done on day 8. On day 9 they get the results and are told to isolate. On day 10, the contact tracers have talked to the identified contacts. But those who were infected on day 4 have now been infected for 6 days, and have started to spread it to others. I admit that the timings I have used are guesswork, but the general message holds – it is very difficult to get through the process quickly enough to interrupt transmission effectively.

4. Vaccine

Here, at last, we come to an area where the Government has done some things right. First of all, they seem to have got ahead of the curve in placing advance orders for large quantities of several potential vaccines, at a time when it was still uncertain whether any of them would work. We should also give credit to the UK’s regulator, MHRA, in giving speedy assent (on an emergency basis) to the vaccines. It is rather cheeky of the Government to claim credit for the development of the Oxford/AstraZeneca vaccine; the work of the Oxford Vaccine Group was largely based on blue-skies research in developing their vaccine delivery system.

The Government also made a good decision over vaccine delivery. They decided to keep their hands off! – and especially in not out-sourcing it. They just let the NHS get on with it, with the result that groups of GPs, community organisations, and many others moved very quickly to set up an impressive network of vaccination centres, including taking the vaccination out to the people who needed it.

But what about the variants? Are they going to compromise the success of the vaccines? The first thing to make clear is that variation is nothing new. Almost certainly, the flu pandemics that we have had from time to time will have been influenced by the occurrence of variants of the flu virus – indeed there is some retrospective evidence that this happened. And flu viruses seem to be more variable than coronaviruses. This is largely responsible for the repeated outbreaks of seasonal flu (the flu pandemics are caused by a more radical reshuffling of genes between human and animal strains). What is new about Covid-19 is that for the first time we have been able to follow the emergence of these variants as they happen.

Secondly, there are severe limitations on the extent to which the spike protein can vary. It has to be able to recognise a specific receptor on human cells. If it varies too much, it won’t interact effectively with that receptor and will lose infectivity. So the virus has to tread a narrow line between escaping immunity due to the vaccine (or prior infection) while still retaining infectivity. Furthermore, we cannot assume that a variant that becomes predominant, displacing a previous strain, is inherently more infectious. A variant that causes less severe disease can have an advantage, as those infected will be less ill, and therefore less likely to self-isolate. It has been suggested that the emergence of such a partially attenuated variant was responsible for the ending of the 1918-19 flu pandemic. In addition, our immune system is very complex. Each of us will produce a unique mixture of antibodies in response to the vaccine, or to infection; some of these antibodies will be very specific, and will fail to recognise the new variant, while other antibodies are less specific and will recognise a wide variety of related strains. So some people will be fully protected; others, perhaps less so. That’s one of the reasons why, when we get a bad year for seasonal flu, some get infected while others do not. So, there’s no need to panic – but it is sensible for the vaccine companies to make new versions of their vaccines – which they are doing, as it is relatively straightforward to do (and is already done for flu vaccines as new variants emerge).

5. What of the future?

It is certain that there will be future pandemics. We are better prepared for flu than we were for the pandemics in 1918, or even 1957 or 1968 – not only in the ability to produce new vaccines quickly but also because of the availability of antiviral agents that can be used for treatment of influenza. SARS-CoV2 is likely to remain with us after the current pandemic is over, perhaps producing seasonal outbreaks. We don’t yet have antiviral agents that can be used against coronaviruses, but they will come – there are many candidates being investigated.

But what about further novel pathogens? We have to recognise that in a sense we have been lucky over the last century or two. Influenza and coronaviruses are both only moderately transmissible and moderately pathogenic. After the experience of the last 12 months, that may sound a surprising statement. But an Ro value of 2-4 (for Covid) looks small compared to measles (Ro 15-20). And the case-fatality rate CFR (the chance of dying if you have been infected) of perhaps 1% for Covid is low compared to that for plague or smallpox (about 50%), or HIV/AIDS (where, before the advent of anti-retroviral therapy, it was effectively 100%). If you want a sleepless night, try imagining a pandemic caused by a pathogen with the infectivity of measles and the CFR of HIV.

Jeremy Dale

29/3/21

The ‘Red Wall’

The ‘Red Wall’

Something of a myth has arisen about the 2019  General Election,  that Labour lost because Jeremy Corbyn was unpopular, and the so-called ‘red wall’ seats turned suddenly away from Labour as a result.

In order to examine this, and why I regard it as a myth, it is necessary to look at the results in a collection of such seats, over a number of elections. This is not a scientific sample. But all the seats I have chosen are ones which used to have sizeable Labour majorities, and remained in Labour hands right through the period (apart from NE Derbyshire which changed hands in 2017). Not all of them were lost in 2019. The sample includes seats from NE England, Yorkshire, Lancashire, and Derbyshire (using old-style geographical designations). I am not going to consider the reasons behind any trends, which would involve speculation, but confine myself to the facts.

The first set of data shows the number of Labour votes cast in each seat. It is immediately apparent that in most cases the Labour vote held up well from 1974 up to 1997, irrespective of the overall outcome of the election. After 1997, the Labour vote declined in all of them – in some cases (e.g., Hartlepool, Bishop Auckland), a marked and steady decline; in other cases, rather more bumpy. In 2017, the decline was either arrested or reversed. There was clearly a marked drop in the Labour vote between 2017 and 2019, which gives the anti-Labour swing that the analysts focus on, but in many cases the 2019 result was comparable, or at least not markedly worse than the 2010 or 2015 results, and is generally consistent with the post-1997 trend.

Much the same story, although rather less marked, is apparent from considering Labour’s share of the vote in these seats, with a decline starting in 1997 and continuing through to 2019, with an upwards blip in 2017. Again, this does not support the concept that these seats suddenly turned away from Labour in 2019, but that this was, at least in part, a continuation of a longer term process.

However, there is no getting away from the fact that the 2019 result was a bad one for Labour. But how bad was it really? If we look at the number of Labour votes cast, we see the rather surprising result that there were more Labour votes in 2019, in England, than in 6 of the previous years examined. This includes 2001 and 2005 – in both of which Labour was the overall winner. If we take into account the size of the electorate and the turnout, by looking at Labour’s share of the vote, it was still higher than 1983, 1987, 2010, and 2015 (and the same as 1992) – and not far short of 2005. .But the distribution of those votes was somewhat less favourable in 2019 – so the number of Labour seats in England was rather less than in 2010 or 2015 – but still higher than 1983 or 1987. What made the 2019 result so much worse overall than in the years up to 2010 was the collapse of the Labour vote in Scotland, and, to a lesser extent, in Wales. In 2010, Labour won 41 seats in Scotland; in 2015, it was down to 1. After a small resurgence in 2017 (7 seats) it was back down to 1 again in 2019. In Wales, it reduced from 34 seats in 2001 to 25 in 205 and 22 in 2019.

The end result was that the number of Labour seats over the whole UK was the lowest for many years (although not far short of that in 1983) – but it is more complicated than just saying the ‘red wall’ turned against Jeremy Corbyn.

The Untied Kingdom

Highways England recently announced a plan to rename itself National Highways. Apart from the fact that it is going to cost £7 million, only a few years after spending millions on the previous re-branding, it sets me (and many in the rest of the UK other than England) wondering which nation the new name refers to. This is of course not a new problem. For example in Wales you have the National Gallery of Wales, in Scotland you have the National Gallery of Scotland. In England, it’s called the National Gallery.

If it was just a question of names, it would be merely annoying. But its symptomatic of a problem with deeper roots; all too often the terms England, Britain, and the United Kingdom are used interchangeably. It must be even more confusing for foreigners, (I expect some people in the Netherlands also get upset when we refer to their country as ‘Holland’)

A brief refresher course

The UK is made up of four ‘nations’: England, Wales, Scotland, and Northern Ireland. Note that NI is not the same as Ulster; when Ireland was partitioned, 3 counties (Donegal, Cavan, Monaghan) of the historic province of Ulster were excluded from NI.

Wales was legally part of England until the mid twentieth century (the Welsh Office was created in 1965 and gradually acquired more powers until devolution in 1999). For some purposes the entity known as England and Wales still exists – for example the Office for National Statistics (!) collects the census for England and Wales, and some of the COVID data they produce gives figures on that basis.

Britain, or Great Britain, is a geographical entity with little or no legal or constitutional identity. On a strict definition, it just refers to the main island, but it is more usual to include the adjoining islands from the Scillies to Shetland (but not the Isle of Man or the Channel Islands; they are not part of the UK; they are self-governing Crown Dependencies). There was at one time a Kingdom of Great Britain, formed in 1706 by the Treaty of Union between Scotland and England (which included Wales!), but that became obsolete in 1801 with the union with Ireland.

Northern Ireland is not part of Great Britain, despite the UK Olympic team being referred to as TeamGB. Presumably they thought calling it ‘TeamUK’ might be unfortunate (‘Tea Muck’?). NI and the Republic of Ireland have separate soccer teams, but a joint rugby team. People in NI can get an Irish passport.

There is no totally acceptable term for the whole archipelago. ‘British Isles’ is often used, but many in Ireland object to the colonial implications, and some use ‘these islands’ instead. ‘Britain and Ireland’ is clumsy.

An added difficulty is the absence of an adjective derived from UK, and hence no simple term for a citizen of that country – since NI is not part of Britain, ‘British’ is not strictly accurate. I can’t go around saying I am a citizen of the United Kingdom of Great Britain and Northern Ireland (which is what my passport says). Are there any other countries that don’t have a simple, accurate title for their citizens? The USA of course is even worse, as they are only the United States of part of America; Canadians, for example, could also claim to be ‘American’ (although I guess they wouldn’t want to!).

Confused? You may well be. Add devolution into the mess  – three of the four ‘nations’ have their own elected parliament/assembly, with different levels of devolved power. One of the ‘nations’ does not. England is run by the UK Government. The fault lines in this system are exposed by the COVID crisis, on an almost daily basis. Each of the devolved administrations makes decisions affecting their part, while the UK Government makes decisions sometimes on behalf of England and sometimes for the whole UK, and it is often not clear which.

One significant ‘fault line’ was exposed by the refusal of the UK/English Government to prohibit movement of people out of high risk areas of England, although Wales had already banned movement between parts of Wales; this created the paradoxical situation where someone could be fined for travelling between adjacent parts of Wales but someone from a high risk area of England could go where they liked. So the Welsh Government acted to ban such movement; although they denied that they were creating a border, it represents a step in that direction.

This comes on top of the Brexit debacle. Although Wales voted narrowly (52-48%) in favour, Scotland and NI voted heavily for Remain (62%, 56% respectively). Scottish resentment at being dragged out of the EU by England still rankles, and in NI the problem of what will become a land border with the EU is still unresolved.

So both COVID and Brexit are potentially driving the UK in the direction of either more complete devolution or complete disintegration of the UK. If the latter is to be avoided, it would be as well to consider what shape might hold the UK together.

The first task is to tackle the lopsided nature of devolution, by establishing an English government, separate from the UK one. This implies some form of federal structure. It is often argued that this is not possible for the UK because of the highly unequal size of the constituent nations – so England would still dominate everything (although the existing situation didn’t give Scotland any protection in the Brexit vote). But look at the USA. Compare the sizes of New York state, or California, with Rhode Island, for example. The structure of the Senate gives the smaller states greater influence. That’s not to say we should blindly follow that example in detail, but it shows that it is possible.

However, there is a further problem with England. Many people feel that London has too great an influence at present, and we should take the opportunity to address that as well. My suggestion is that London should be separated from the rest of England, to form a fifth ‘state’. Actually that’s not such a radical idea. In the USA, Washington is separate (as the District of Columbia) and in Australia, Canberra forms the Australian Capital Territory.

Doing that would necessitate an English ‘capital’ located somewhere other than London (say Manchester or Leeds), which would automatically tend to make the English government more responsive to the interests of the other parts of the nation.

An alternative, often canvassed. way of tackling the ‘English problem’ is regionalisation. But this always runs into the intractable problem of how you define the regions. Few, if any, parts of England form clear unambiguous regions, and the current regions are full of anomalies. Glossop is only 10 miles out of Manchester, but is part of the East Midlands region, with its ‘capital’ in Leicester. Yorkshire? Looks neat on a map, until you look more closely. Drawing the northern boundary along the Tees separates Middlesbrough from Stockton.

It would be better to abandon the regions, and devolve more power to local authorities at a lower level.

So, let’s say we have 5 ‘states’ – London, England, Scotland, Wales, and Northern Ireland – in a federal structure. To do the job properly, we need to consider the electoral system as well. The existing devolved nations each have some form of quasi-proportional representation, and the same should apply to the devolved ‘English’ government (leaving open exactly what form that should be). As for the UK government, this would be the time to get rid of the House of Lords completely, and replace it by a second chamber that would be elected on a balanced basis by each of the five ‘states’, again using some form of proportional representation.

Just some food for thought – it makes a change from posts about COVID-19 anyway.

Jeremy Dale

24/11/20

Herd Immunity Revisited – an update

Herd Immunity Revisited – an update

There have been a number of responses to my previous post, most of which have missed the point. Perhaps I didn’t put it clearly enough. So let’s try to clarify it.

The main point is that I am definitely not advocating withdrawal of any attempt to control the epidemic and relying solely on the development of natural herd immunity. It is highly probable that this would lead to hospitals being stretched beyond breaking point (remembering that the policy of this and previous Tory governments in systematically reducing the ability of the NHS to cope with unforeseen crises has played a major part). I say ‘highly probable’, because nothing is certain when it comes to COVID – I suspect the virus has more tricks up its sleeve yet.

I should also say that I am in no way associating myself with the so-called ‘Great Barrington declaration’. At the same time. it does not make sense to automatically reject everything someone says simply because that person has, or is associated with, some unsavoury political views. If Mussolini made the trains run on time (whether that’s true or not), that doesn’t make it a bad idea. Nor does it mean that anyone advocating railway punctuality must be a fascist.

My central point is that lockdown and test-and-trace procedures will not by themselves permanently eradicate the virus. Textbook models of epidemics say that if you get R below 1 and keep it there, the disease will disappear. But one of the central assumptions of that model is that you are dealing with an isolated community. In the absence of herd immunity, the population is still largely susceptible, and any movement of people risks re-introducing the infection.

New Zealand can be considered as an ‘isolated community’, and they seem to have achieved that position – but at the cost of rigorous quarantining of all entrants to the country. A few other islands have done so too. The Isle of Man is making a valiant attempt to do it. Of course Britain is an island as well. But can we consider quarantine for all who come to Britain? Not just asking them to self-isolate, but putting them all into dedicated quarantine hostels for 1-2 weeks? Can you imagine that? It would have to include those coming from Northern Ireland too, which would cause a political storm.

In my view, the real purpose of the current restrictions is, or should be, to slow down the epidemic so that the NHS can continue to cope. And it buys time in the hope that an effective vaccine will become available. In the absence of a vaccine, where will it end? If the restrictions succeed in bringing the 2nd wave under control, my guess is that we would ultimately get a 3rd wave, a 4th wave and so on, until eventually enough people have been infected and we reach the unmentionable herd immunity. In that situation, we would end up with having had the same number of cases, and (unless we get more effective treatment) the same number of deaths. Those taking decisions about the nature and extent of the lockdowns need to balance those objectives against the economic, social, and psychological costs of the lockdowns.

Jeremy Dale

21/10/2020

Herd Immunity Revisited

Herd Immunity revisited

At the start of the pandemic, there was much discussion about the possibility of letting it run its course until ‘Herd Immunity’ was reached. This option was rejected as it was projected to involve perhaps 350,000 deaths and a crisis in hospital admissions. Now, with deaths probably over 50,000, and a ‘second wave’ starting, the option of aiming for herd immunity has resurfaced – more precisely, aiming for herd immunity in the younger age-groups, combined with protection for the most vulnerable sectors of the population. So it seems a good time to have another look at the question.

Background

Statistical models of epidemics predict that, in the absence of any control measures, after an initial exponential rise in the number of cases, the epidemic will start to slow down as the proportion of the population who have already had the disease (and are presumed to be immune) rises, and hence the proportion who are still sensitive declines. Eventually it grinds to a halt because there are no longer enough non-immune people to sustain it. This point is known (rather unfortunately) as herd immunity.

It all hinges on the value of the now infamous parameter called R. For COVID-19, R is thought to be somewhere between 3 and 4, in a wholly susceptible population, in a country like the UK. That is, one infectious individual will, on average, infect 3-4 others. The point at which herd immunity kicks in (the Herd Immunity Threshold, HIT) can be estimated from the initial value of R, so if R=3, then HIT is about 67% (or 2/3). That’s about 40 million cases.

To calculate the number of expected deaths, we need to know how many of those will die – the case fatality rate. That is commonly put at about 1% (on average). 1% of 40 million is 400,000 (which is more or less where that 350,000 figure comes from).

The value of R is not just down to the nature of the virus. It is also influenced by the probability of making an ‘effective contact’ – that is a contact between an infectious person and a non-immune one, which is in turn affected by a number of factors such as how long you remain infectious, as well as how many people you come into contact with while you are infectious. This will depend on where you live; someone living in a remote area will contact very few people compared to one in a big city. A national value of R is a very rough measure of progress as it is an average value over areas with widely different real values.

The likelihood of an effective contact will also depend on your personal behaviour, especially the extent to which you go and mix with others. This is where the lockdown measures come in. They are an attempt to alter people’s behaviour so they will contact fewer people, and hence drive down the value of R.

So what?

Suppose the restrictions succeed in driving down the value of R to below 1, and keeping it there, the model tells us that each infectious person is infecting less than one other person, and hence the disease will die out, even without achieving herd immunity. And we’ll suppose that at this point, say 20% of the population have been infected (and hence are assumed immune). We would now have no cases, but 80% of the population is still non-immune. Is that the end of the story?

If we were living in complete isolation from the rest of the world, it would be. But we are not. All it needs is for one infected person to enter the country from an area where the disease is still rampant and away we go again. New Zealand is in just this situation, and they are attempting to keep it out by quarantining all those entering the country (which must devastate their tourism industry). But it is unimaginable for the UK to attempt to do this.

Furthermore, although after the first wave of infections there was a very substantial drop in the number of cases (presumably due to the restrictions, or some of them anyway), the disease did not disappear completely. There were enough cases continuing to be able to re-seed the epidemic once the brakes were taken off, so the second wave was inevitable. If the new restrictions now coming in succeed in controlling the second wave, we can confidently assume the same will happen again.

What this tells us is that if we don’t achieve herd immunity, we will have to carry on with some form of lockdown indefinitely (at least until a reasonably effective vaccine is available).

So we need to look again at the herd immunity strategy, and the assumptions that led us to reject it initially. In particular, how far have we already gone in that direction – in other words how many people have actually been infected? The limitations of testing means that it doesn’t tell us that. One way to estimate it is by looking at the number of deaths. Let’s call that 60,000 (a bit higher than the data from death certificates). If the case fatality rate is 1%, that implies a total of 6 million infections so far; in other words, about 10% of the population have now been infected at some stage. If the fatality rate is lower than that (I have seen estimates from elsewhere that put it as low as 0.3%), then the number of infections could be much higher, possibly up to 30% of the population. If you were to do this calculation in earnest, you would need to allow for the number of deaths in the elderly or other highly vulnerable groups (with a much higher fatality rate).

Alternatively, a more direct way, is to assess the frequency of SARS-CoV-2 antibodies in the population. ONS do sample surveys to measure this, and the latest figures I’ve seen put it at about 6%. However, this does assume that everyone who had been infected at some stage produces enough antibody to be detected by the test.

If we take somewhere in the region of 10% as the proportion who have been infected, that is still way short of the 67% that we think is needed for herd immunity. However, we’re looking at overall figures for the whole country, while COVID has affected some places much more than others. Trying to unravel that gets complicated, especially as those places with more cases have a higher initial value of R, and hence require a higher level of herd immunity. But it is tempting to wonder why London has not seen anything like the same level of 2nd wave (as yet).

However, although we may still have a way to go before getting herd immunity, is there any alternative? Of course, if a vaccine emerges (even a partially effective one), it would change the situation drastically. Without that, are we faced with having restrictions indefinitely? It may be that all that would achieve is to prolong the epidemic, but smoothing it out so that the NHS doesn’t get overwhelmed. In other words, we would get the same number of cases, and deaths, but over a longer time.

One alternative that is being canvassed is to withdraw restrictions and allow the epidemic to run its course, while, at the same time, providing better protection for those more vulnerable, especially in care homes. In that way, we could build up herd immunity in those who are very much less likely to suffer serious effects, which in turn would protect the most vulnerable. This is often caricatured as locking away all the elderly and sick people and throwing away the key. But it doesn’t have to mean that. We could, for example, provide much better support for care homes – not just PPE for the staff (important that it is) but also in installing facilities, such as screens, that would allow safe visiting. And we would need to make sure that those who were isolating at home would also receive better support, not just in providing food parcels, but again devising ways in which they could safely receive visitors.

The final verdict must be that unless and until we get a vaccine, herd immunity (however it is achieved) is the only way in which this epidemic will cease.

COVID-19 – a bit of perspective: update

An update

According to ONS, in the week up to Sept 11th, there were 9,215 deaths from all causes in England. Of these, COVID-19 accounted for 97 deaths – that is about 1% of the total. Of course, we would expect that figure to rise as the number of cases increases. For the whole period of the epidemic (up to Sept 11), COVID deaths (52,482) account for about 12% of the total number of deaths (434,618) in England and Wales..

If we assume a case fatality rate (the number of deaths as a percentage of the number of cases) of 1%, this means that just under 9% of the population have been infected.  But we don’t know the case fatality rate for sure; I have seen estimates that put it as low as 0.3%. If that is true, then the number who have been infected (England and Wales) would be as high as 17.5 million, or 29% of the population.  That would mean, given the highly uneven spread of cases, that there would be some areas that would, at some point during the ‘second wave’, approach the level required for herd immunity to kick in (usually taken as about 60%).

Jeremy Dale 25/9/20

COVID-19 – a bit of perspective

Every death is a tragedy for those affected. Especially so for COVID, where someone may die in isolation, unable to see, or be seen by,  their loved ones. In no sense do I want to diminish that – and if you have been affected by the virus you may not want to read on. But in the midst of all the publicity about COVID, I feel it is necessary to try to put it into perspective.

First of all, let’s look at the data for COVID deaths. This is very confusing. The Government dashboard (1 August) puts it at 46,193 in the UK. This is the number who have died having had a positive test result. This has been much criticised, as it would seem to mean that even if you get run over by the proverbial bus, having been tested positive months ago, you are still counted as a COVID-related death. On the other hand, if you die from COVID but have never been tested (or the test didn’t work), you wouldn’t be counted.

If you look at the data from the Office of National Statistics (ONS), you get a different figure,  50.800, in England and Wales only. This comes from death certificates, and is the number of times COVID was mentioned (even if other causes such as pneumonia were also mentioned). I’ll stick with the ONS figure, mainly because I want to compare it with other data from ONS.

So, 50,000 deaths. That’s a lot of tragedies. But death is a part of life. During the period of the epidemic, 245,000 people have died from all causes – so that’s getting on for 200,000 people have died from something other than COVID. And during each of the last five weeks, more people have died from what is recorded as Influenza/pneumonia than from COVID.

Another way of looking at the impact of COVID is to consider the excess deaths – that is the number of people who have died from any cause, compared to the average number who died in the same period over the last five years. This shows that since the epidemic started there have been over 53,000 excess deaths. That measure includes the possible indirect effects of COVID, e.g., people who didn’t get appropriate treatment in time. If we look at the weekly breakdown of excess deaths, we see that during the last five weeks it has been negative – that is, fewer people are dying than expected. The likely reason for this is that one effect of COVID has been to cause the death of some people who would otherwise have died soon anyway.

Historical comparisons

The current crisis has highlighted the fact that we are no longer used to people dying in large numbers from infective diseases. Medical advances, including antibiotics and vaccines, coupled with improvements in nutrition, housing, public health and other environmental issues, have in general made such diseases of historic interest only, at least in countries like the UK. (This is not of course true for most of the world, where diseases such as malaria and tuberculosis are causing death and suffering on a large scale – in low income countries, communicable diseases represent 5 of the top 10 causes of death).

A look at the death statistics (from ONS) for 100 years ago (1915) illustrates the point. In that year, there were 66k deaths from pneumonia/bronchitis and 39k deaths from tuberculosis. We can add others – 13k deaths from measles. 5k each from diphtheria and flu (not an epidemic year), 4k from whooping cough and nearly 2k from scarlet fever.

In the more distant past, there are numerous examples of devastating infections. The Black Death (1381) is thought to have killed a third of the population. In the nineteenth century, there were repeated epidemics of cholera, with tens of thousands of deaths, and tuberculosis was rampant (at its height, causing a third of all deaths).

In more recent times, the best comparison is with pandemics of influenza. (Technical note: Influenza viruses are classified by their H and A antigens, the most common type being H1N1. Various H1N1 strains are similar but not identical in both, so you get a degree of cross-immunity, while another type say H2N2 differs in both and there is no cross-immunity between them. Major pandemics usually occur with a virus that has ‘shifted’ to different H and N types)

In 1957-58 there was a pandemic of so-called ‘Asian flu’ (H2N2), which caused some 20-30k deaths in the UK. Then in 1968-69, we had an H3N2 strain (labelled ‘Hong Kong’ flu) for which the estimates of the number of UK deaths go up to 80k. In neither case was the official response anything like what we are currently seeing with COVID-19. And the media managed to find plenty of other news to cover.

More recently, there was some concern about ‘swine flu’ (2009). The incidence rose to about 110k cases per week in July, before dropping off, and then re-emerging in the autumn to about 84k cases per week in October. However, mortality was low (<1,000 deaths in UK), probably because this was an H1N1 strain, and older people had already encountered H1N1 strains and so had significant immunity to it.

Why all the fuss?

Why is it that fifty years ago we could face a disease that caused up to 80k deaths, not exactly with equanimity but at least without the massive sacrifices that we are currently making for a disease of (apparently) similar magnitude? Of course, we have to recognise that without the control measures it might have been much worse. Based on what was known about the disease, the initial assessment was that, if left unchecked, the disease would spread until Herd Immunity was achieved, and that would happen when about 60% of the population had been infected. Assuming a case fatality rate of 1%, that implied something like 350,000 deaths, which was deemed unacceptable. Of course we will never know if that would have happened, but a comparison with other countries is interesting. We hear a lot about the numbers of deaths in the USA and Brazil, but if we look at the numbers of deaths per million population, we are still some way ahead of either of them (UK 680, USA 477, Brazil 440) – although I am well aware of the dangers of reading too much into such comparisons, given the different methods and reliability of reporting deaths. But superficially, it could mean that our lockdown didn’t have much effect, and the original estimate of 350,000 deaths was over the top.

I’m not saying that we should all ignore the advice, and go out and party. But let’s keep a sense of perspective. At the individual level, unless you are in an extremely vulnerable category, there are plenty of other ways of dying that we don’t bother too much about. But collectively, we still have a duty to try to limit transmission so as to protect those who are more vulnerable. Above all, don’t panic!

Jeremy Dale

2 August 2020

Moonshine Project

Is it a good idea to regularly test the whole population for infection with SARS-CoV-2?

Superficially, you might well say the answer is ‘Yes, obviously’. But I want to look at it in more depth.

First of all, obviously, there are the practical considerations. The current system, fragmented as it is (some would say deliberately fragmented between the private and public sector), is proving to be quite unable to cope with testing those who really need it. And the tracing aspect is even worse. Remember when you hear the figures quoted, e.g., 70% of infections are detected, and 70% of contacts are traced – that is 70% of 70%, or 49%. So even with the Government’s claims, only about half of potential contacts are traced. And it is far too slow – several days to get the test result, and several more days (often longer) to reach the contacts, who thus may have been spreading the disease for days before being told to isolate,

Secondly, it depends on technology that doesn’t yet exist. There is much talk about rapid tests that are being introduced. These are antibody tests, which only tell you whether someone has been infected at some time in the past, not whether they are currently infected, Antibody tests don’t give a positive result until the infection is, in most cases, over.

Leaving the practicality aside, let’s assume that somehow we do have a test that can be easily and rapidly done for vast numbers of people. Would it be a good idea then, to screen the whole population?

To answer that question, we need to look at some concepts related to the test. I should clarify that what I mean by ‘test’ is what happens in the laboratory with the sample you have provided. The other parts of the process – taking the sample, transmitting it to the lab, and reporting the results – all have their problems, but I’m not considering those.

No laboratory diagnostic test is perfect. Biological systems are very complex, and all sorts of things can lead to a ‘wrong’ result. This can mean that someone who is infected gives a negative result (a ‘false negative’). For example, there might be something in the sample that interferes with the test process. The ability of the test to detect real positives is referred to as the sensitivity, which is defined as the number of positives detected divided by the number of true positives.

The other side of the coin is the specificity, which roughly means the ability of the test to correctly identify someone who is not infected. This is defined as the number correctly identified as negative divided by the number who are really not infected. This gives us a measure of how often we would get a false positive – i.e., a positive test result for someone who does not have the disease.

Now we can look at what this means in reality. Let’s assume we have a test that is 99% sensitive and 99% specific. That would be regarded as a really good test. And let’s assume we have a prevalence of 1 in 1,000. So, in a population of 100,000, there would be 100 cases, and the test would detect 99 of them. That’s not bad. The crunch comes with the specificity. In this situation, the test would return a positive result for 999 people who do not have the disease (false positives). In other words, there would be about 10 false positives for every correctly identified positive. If we scale that up to 60 million people, there would be nearly 600,000 people who would be told they were infected when they weren’t. Would they all have to isolate themselves? And even thinking about contact tracing on that scale gives me a headache.

These considerations apply to all occasions when you are screening random samples for some relatively rare event, whether it’s screening donated blood for an infectious agent such as HIV, or mass screening for cancer. The standard way of dealing with it is to use two independent tests. So, you take all the samples that gave a positive result in the first test and re-test them, with a different test. (It has to be a different test as the reason for the ‘wrong; result might be inherent in the sample). If you did that, with the above example, then after re-testing all the positives from the first test, you would find that fewer than 10% of the positives would now be false positives.

In effect this is what happens when you use a test to confirm a clinical diagnosis, or if you are applying a COVID-19 test to people who have symptoms. The clinical picture is the first test, giving a group of people who are much more likely to have the disease than the general population is.

Is a two-step procedure feasible? It could be argued that the first step could use the hitherto unknown and entirely conjectural rapid test, and the positive samples submitted to the existing PCR-based test – but only if this hypothetical new test was something entirely different. And it would still demand adding an additional 600,000 samples to the existing testing workload. Since that system is currently unable to meet the present demands, this seems unlikely.

If you would like to see the calculations I have used, and play around with them, send me an email and I’ll send you the spreadsheet.

Jeremy Dale

20 Sept 2020

COVID-19 – a bit of perspective

An update

According to ONS, in the week up to Sept 11th, there were 9,215 deaths from all causes in England. Of these, COVID-19 accounted for 97 deaths – that is about 1% of the total. Of course, we would expect that figure to rise as the number of cases increases. For the whole period of the epidemic (up to Sept 11), COVID deaths (52,482) account for about 12% of the total number of deaths (434,618) in England and Wales..

If we assume a case fatality rate (the number of deaths as a percentage of the number of cases) of 1%, this means that just under 9% of the population have been infected.  But we don’t know the case fatality rate for sure; I have seen estimates that put it as low as 0.3%. If that is true, then the number who have been infected (England and Wales) would be as high as 17.5 million, or 29% of the population.  That would mean, given the highly uneven spread of cases, that there would be some areas that would, at some point during the ‘second wave’, approach the level required for herd immunity to kick in (usually taken as about 60%).

Jeremy Dale 25/9/20

COVID-19 – a bit of perspective

Every death is a tragedy for those affected. Especially so for COVID, where someone may die in isolation, unable to see, or be seen by,  their loved ones.

In no sense do I want to diminish that – and if you have been affected by the virus you may not want to read on.

But in the midst of all the publicity about COVID, I feel it is necessary to try to put it into perspective.

First of all, let’s look at the data for COVID deaths. This is very confusing. The Government dashboard (1 August) puts it at 46,193 in the UK. This is the number who have died having had a positive test result. This has been much criticised, as it would seem to mean that even if you get run over by the proverbial bus, having been tested positive months ago, you are still counted as a COVID-related death. On the other hand, if you die from COVID but have never been tested (or the test didn’t work), you wouldn’t be counted.

If you look at the data from the Office of National Statistics (ONS), you get a different figure,  50.800, in England and Wales only. This comes from death certificates, and is the number of times COVID was mentioned (even if other causes such as pneumonia were also mentioned). I’ll stick with the ONS figure, mainly because I want to compare it with other data from ONS.

So, 50,000 deaths. That’s a lot of tragedies. But death is a part of life. During the period of the epidemic, 245,000 people have died from all causes – so that’s getting on for 200,000 people have died from something other than COVID. And during each of the last five weeks, more people have died from what is recorded as Influenza/pneumonia than from COVID.

Another way of looking at the impact of COVID is to consider the excess deaths – that is the number of people who have died from any cause, compared to the average number who died in the same period over the last five years. This shows that since the epidemic started there have been over 53,000 excess deaths. That measure includes the possible indirect effects of COVID, e.g., people who didn’t get appropriate treatment in time. If we look at the weekly breakdown of excess deaths, we see that during the last five weeks it has been negative – that is, fewer people are dying than expected. The likely reason for this is that one effect of COVID has been to cause the death of some people who would otherwise have died soon anyway.

Historical comparisons

The current crisis has highlighted the fact that we are no longer used to people dying in large numbers from infective diseases. Medical advances, including antibiotics and vaccines, coupled with improvements in nutrition, housing, public health and other environmental issues, have in general made such diseases of historic interest only, at least in countries like the UK. (This is not of course true for most of the world, where diseases such as malaria and tuberculosis are causing death and suffering on a large scale – in low income countries, communicable diseases represent 5 of the top 10 causes of death).

A look at the death statistics (from ONS) for 100 years ago (1915) illustrates the point. In that year, there were 66k deaths from pneumonia/bronchitis and 39k deaths from tuberculosis. We can add others – 13k deaths from measles. 5k each from diphtheria and flu (not an epidemic year), 4k from whooping cough and nearly 2k from scarlet fever.

In the more distant past, there are numerous examples of devastating infections. The Black Death (1381) is thought to have killed a third of the population. In the nineteenth century, there were repeated epidemics of cholera, with tens of thousands of deaths, and tuberculosis was rampant (at its height, causing a third of all deaths).

In more recent times, the best comparison is with pandemics of influenza. (Technical note: Influenza viruses are classified by their H and A antigens, the most common type being H1N1. Various H1N1 strains are similar but not identical in both, so you get a degree of cross-immunity, while another type say H2N2 differs in both and there is no cross-immunity between them. Major pandemics usually occur with a virus that has ‘shifted’ to different H and N types)

In 1957-58 there was a pandemic of so-called ‘Asian flu’ (H2N2), which caused some 20-30k deaths in the UK. Then in 1968-69, we had an H3N2 strain (labelled ‘Hong Kong’ flu) for which the estimates of the number of UK deaths go up to 80k. In neither case was the official response anything like what we are currently seeing with COVID-19. And the media managed to find plenty of other news to cover.

More recently, there was some concern about ‘swine flu’ (2009). The incidence rose to about 110k cases per week in July, before dropping off, and then re-emerging in the autumn to about 84k cases per week in October. However, mortality was low (<1,000 deaths in UK), probably because this was an H1N1 strain, and older people had already encountered H1N1 strains and so had significant immunity to it.

Why all the fuss?

Why is it that fifty years ago we could face a disease that caused up to 80k deaths, not exactly with equanimity but at least without the massive sacrifices that we are currently making for a disease of (apparently) similar magnitude? Of course, we have to recognise that without the control measures it might have been much worse. Based on what was known about the disease, the initial assessment was that, if left unchecked, the disease would spread until Herd Immunity was achieved, and that would happen when about 60% of the population had been infected. Assuming a case fatality rate of 1%, that implied something like 350,000 deaths, which was deemed unacceptable. Of course we will never know if that would have happened, but a comparison with other countries is interesting. We hear a lot about the numbers of deaths in the USA and Brazil, but if we look at the numbers of deaths per million population, we are still some way ahead of either of them (UK 680, USA 477, Brazil 440) – although I am well aware of the dangers of reading too much into such comparisons, given the different methods and reliability of reporting deaths. But superficially, it could mean that our lockdown didn’t have much effect, and the original estimate of 350,000 deaths was over the top.

I’m not saying that we should all ignore the advice, and go out and party. But let’s keep a sense of perspective. At the individual level, unless you are in an extremely vulnerable category, there are plenty of other ways of dying that we don’t bother too much about. But collectively, we still have a duty to try to limit transmission so as to protect those who are more vulnerable. Above all, don’t panic!

Jeremy Dale

2 August 2020

 

COVID-19: Airborne transmission?

COVID-19: Airborne transmission?

Some of you may have been as confused as I was by the recent reports suggesting that the possibility of airborne transmission of SARS-CoV2 has been neglected. You would be forgiven for thinking that the airborne route is what we’ve been talking about all along, and that it is the main route of transmission. That’s what masks and distancing are all about. This is an attempt to straighten out the issues.

Basic principles

When we cough or sneeze, or, to a lesser extent, talk or even just breathe, we eject small droplets of saliva and mucus. A sneeze may produce thousands of these, while a cough may yield only a few hundred. For talking, or singing, it will depend on the consonants – f, b, p, t and s are especially good at producing droplets (I am indebted to Cedric Mims in The Pathogenesis of Infectious Disease for the observation that most abusive words in English start with one of these consonants!). If we are infected with a respiratory tract pathogen, such as SARS-CoV2, then some of these droplets may contain virus particles. I’ll come back to that later.

What happens to those droplets? That depends on their size. The largest ones (1mm or more) will fall to the ground (or some other surface) within a few metres or less. With the smaller ones, because they have a large surface area relative to their volume, the water content will evaporate rapidly, resulting in tiny particles (‘droplet nuclei’) less than 5 micrometres in size (a micrometre is a millionth of a metre, or a thousandth of a millimetre). These can remain airborne virtually indefinitely. It is the potential of these particles to transmit the disease that is the focus of the current discussion. This is sometimes referred to as ‘aerosol transmission’ to distinguish it from transmission by large droplets.

Some unanswered questions

In order to assess the significance of the potential risk posed by these tiny particles, we need to consider the following factors:

– the likelihood that they carry the virus

– how many virus particles they carry

– how long will the virus remain able to establish infection

– how are they distributed in the air

– How many virus particles are needed to cause an infection (the infective dose).

Most of these are unknown; we’re just guessing, partly based on experience with other viruses. Let’s fill in some details.

Will the particles contain virus particles, and how many?

This depends on another unknown, the viral load, or more specifically the number of virus particles shed by someone infected. One of the main factors limiting our knowledge here, and elsewhere, is that almost exclusively the assays are based on detection of viral RNA rather than viable virus particles (which are much more difficult to measure).

Leaving that question on one side, it is intuitively obvious (and probably true) that the larger droplets are more likely to contain virus particles than smaller ones, and similarly are likely to have more virus in them. That’s just on a statistical basis. You should also consider the size of the virus. A single coronavirus, including the spikes, is about 130 nanometres (nm) in diameter (one nanometre being a thousandth of a micrometre). So if you put 7 or so viruses side by side, that would span the diameter of a one micrometre droplet. Without doing the detailed calculation, it can be estimated that the maximum capacity of the largest of these persistent airborne droplets (say 5 micrometres) might be of the order of 100 virus particles, if they can be tightly packed. And many of the droplets will be much smaller, containing no more than a few viruses. This will be relevant when we look at the infectious dose later.

How long does the virus remain infectious in small droplets?

Another unknown, and here the RNA assay is of no help at all. RNA will remain long after the virus itself is ‘dead’. But it is likely that it will be of limited duration due to drying – and, especially in the open air, the effect of UV light.

How are the droplets distributed?

This is a bit easier to answer. For the larger droplets, which are essentially transmitted directly from the source to the subject, the likelihood is dependent on the distance separating them, and more or less to the square of that distance (as it can go to either side of you). If the smaller droplets are distributed throughout the air-space, it will be related to the size of the room you are in. If you have a lot of people in a small, low ceilinged, room, then the risk may be considerable. If the room is larger it will be much less so, especially if the room is well ventilated. And of course if you are outside, the risk virtually disappears.

How likely are you to be infected?

This depends on the biggest unknown of them all, the infectious dose (i.e., how many virus particles do you need to inhale in order to catch the disease?). This varies a lot from one disease to another, from a few hundred up to millions. Because we have a variety of non-specific mechanisms protecting us against invading microbes, very few diseases have infectious doses less than a few hundred – it is often said that tuberculosis can arise from a single bacterium penetrating as far as the lungs, but that is exceptional (and a bit dubious!). For the original SARS virus, the infectious dose has been estimated as a few hundred (although this is not much more than a guess, and it may be higher), so it is often assumed that this will apply to SARS-CoV2 as well. If we combine that estimate with the previous discussion, recognising that each of these tiny droplets is likely to contain only a small number of virus particles, we would have to inhale dozens or hundreds of such particles. Potentially, this could happen in a small, ill-ventilated room if there was someone shedding large numbers of virus, but my conclusion is that this is likely to have a comparatively small effect on the overall transmission of the virus, compared to the risk of more direct transmission by larger droplets.

Jeremy Dale

10 July 2020

World-beating?

World-beating?

Johnson likes to talk up the UK performance in dealing with COVID-19. But strangely he doesn’t consider one statistic that shows the UK competing strongly for the ‘world-beating’ title. If we ignore San Marino, that title goes to Belgium, but with the UK in second place (here I ignore Andorra, with my apologies to both countries) – and closing.

We hear a lot about the numbers of deaths in various countries, and how USA and Brazil are leading the field- but to get a true picture we need to relate this to the population size, as deaths per million inhabitants, a parameter known to epidemiologists as the ‘death rate’. Let’s look at some data (as at 13 June).

Belgium has recorded 841 deaths per million. For the UK the figure is 621.

Spain and Italy are close behind (581, 566 respectively).

Some others for comparison: Sweden 482, France 452, Ireland 354, USA 352, Brazil 204, Germany 106. Of these, USA and Brazil are both likely to move up the list.

I should add that all of these figures are somewhat suspect, some more so than others, as practices vary between countries, for example in whether they are COVID-confirmed or merely suspected, and how assiduous they are in ascertaining COVID-related deaths in the community.

How did we get to the unenviable position of being (almost) world-beating?

The UK Government has done a lot of things wrong (or failed to do the right things). I’m not going to attempt a complete list, but a few examples will suffice.

It starts several years ago. There were warnings from at least two ‘exercises’ that we were ill-prepared for a pandemic – notably, but not solely, in the inadequacy of the stockpiles of PPE. These warnings were not acted upon. I suspect that the government was influenced by the ‘just in time’ business model, which holds that stockpiles are inefficient. This model failed spectacularly as it doesn’t deal with a situation when circumstances change suddenly (as supermarkets also found out).

Other problems arose from the repeated reorganisation of the infection control systems. At one time, each hospital had its own diagnostic lab, and each local authority had well-organised arrangements for monitoring and dealing with outbreaks of infectious diseases, including experienced teams of contact tracers. Much of this was dismantled and centralised, and what was left has been largely ignored by the government. Hence people having to travel considerable distances to be tested and it taking several days to get the results back.

Then we come to the lack of action at the early stages of the pandemic. Warnings were there in January, becoming more serious in February. The government did nothing until well into March. No controls on passengers coming to the UK, not even temperature checks. Now we hear that there were at least 1300 separate introductions of the virus to the UK.

They also failed at that stage to ramp up the provision for testing and contact tracing, so that it quickly became overwhelmed when the outbreak started in earnest, and had to be abandoned. It could have made a vital difference at that stage.

They were very slow to stop large gatherings of people – including the rugby international at Twickenham (7 March), the Cheltenham Races (10-13 March) and the Atletico Madrid match at Anfield (11 March). They maintain that the scientific advice was that these events were low risk – and it could be that while people were sitting in the stands watching, the risk was less than for people in a crowded pub. But what about travel to get there? What about the bars at the event? And in the pubs afterwards?

Even after those events, with the warnings becoming clearer and clearer, it took them another two weeks to impose a lockdown.

A large part of the blame must lie with Johnson himself – first of all his refusal to engage with the issue during January and February, and then, well I can’t blame him for being ill, but he seems to have established a cabinet without anyone able to take charge in his absence. And to cap it all, his failure to deal with Cummings after his flagrant flouting of the lockdown has created a situation where large sections of the populace no longer have the respect for the advice that is necessary for maintaining control during the easing of the lockdown.

I could go on – the refusal to co-operate with the EU over the supply of PPE and ventilators (was this a dogmatic antagonism to anything ‘European’?), the hesitation and vacillation over any changes, and then imposing them suddenly without warning, and without consultation with those who would be most affected – notably the fiasco over the re-opening of the schools, plus the multitude of ever-changing ‘guidance notes’, and the proposal to change the distancing rules – will they, won’t they? Who knows? But enough is enough.

 

Jeremy Dale

15/6/20