This cacophony of almost random forecasts isn’t unique to public commentary on viruses – almost any area of national debate is drowning in confident predictions, very few of which have much value. Most of those you read suffer from one of two problems: the forecaster probably isn’t telling you what they really think, and even if they were, what they think might not be any good.

Accuracy, even among professional forecasters like intelligence analysts, has often been a target rather than an achievement. So anyone trying to work out who to listen to in order to understand the future always had their work cut out for them.

That’s why in 2011 the US Intelligence Advanced Research Projects Activity agency, IARPA, invested in a massive forecasting competition to try and make concrete improvements. Teams would compete to forecast hundreds of topics over four years, from a range of subjects in different countries, with the winning strategies studied and shared with the wider intelligence world.

The bestselling book Superforecasting went on to describe the techniques used by the winning team (of which I was a member) in that competition. We didn’t get everything right, but we learned that it’s possible to do a lot better than foreign policy experts by moving away from the traditional methods employed.

There were three key structural lessons from the competition:

1. Keep score
2. Identify the best forecasters
3. Work as a team

The most important item on this list is keep score. Most forecasts that we come across in the media are made by in-house pundits or people rung up by television stations or newspapers for a quote, and these aren’t scored – there’s no penalty for being wrong most of the time. Old articles are rarely revisited and if they are, the pundit can normally wave away criticism and continue along the same line. Some pundits have made a career out of political analysis despite consistently being wrong in their predictions.

If there’s no reward for getting things right, then accuracy will drop down the list of incentives behind the forecasts. Instead pundits will say what they think will cheer people up, what will promote their career via wacky, attention-grabbing predictions, what shows loyalty to their friends or signals political values and ideals to others — or any of the million other reasons someone might predict something without actually expecting it to happen.

It’s not just that pundits and others in the public eye are bad at predicting, they’re mostly not even trying to. And these predictions can influence politicians and decision makers.

The way to build a successful forecasting system is to reward people for accurate forecasts and disincentivise bad ones. Just that little step, of keeping score and letting everyone know at the start that what they say will matter, immediately changes everything. Now when someone is tempted to predict great success for a project led by their pal, they might think about how embarrassed they’ll be if it goes wrong, and drop their confidence.

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Once people are actually trying to predict accurately, you can move on to step two — feedback. Scorekeeping doesn’t just incentivise people to be honest, it also gives them the opportunity to improve. Once you know what you’ve got right and got wrong, you can go back and review. As forecasts resolve, people tend to get better calibrated – that is, there develops a closer relationship between their confidence in their forecast and the outcome.

And once you have a regular run of forecasts, you can take one of the most important steps — stop listening to people who can’t or won’t predict accurately, and pay attention to the most accurate team members, the “superforecasters”.

One of our most striking findings was that the ability to forecast is a skill in itself, independent from subject matter knowledge. Successful forecasters aren’t perfect, of course, but a good track record of predictions is a strong indicator of future performance. And with these skills, superforecasters work for banks, governments and other organisations providing probability estimates for all kinds of risks as well as training analysts in forecasting.

In a system where forecasters are punished for getting it wrong and rewarded for getting it right, the most accurate people float to the top, and when they work together on a team, they become even more accurate.

The forecasts

Last week we gathered a small group of well-calibrated forecasters with good track records to look at the UK’s pandemic outlook over the next few months. With Britain facing both the worst period of the crisis but also an exit strategy with the vaccine roll-out, “when will this end?” is the most urgent question everyone is asking right now.

We can’t promise clairvoyance, but we made the best use of our team’s skills and produced the following set of estimates on three topics:

• How bad the daily death toll will get
• How many vaccines we’ll have administered at the end of February
• When daily deaths will first fall below 100

Superforecasters cannot predict exactly when the pandemic will be over, but these three questions act as proxies for the questions of how bad it will get, how soon an individual is likely to get a vaccine, and when the pandemic will recede. A double-digit daily death toll does not mean the end of the nightmare, but with large-scale vaccinations taking place it will certainly mean is in sight.

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These forecasts are presented as the median estimate of the group; the principle of the “wisdom of crowds”, the idea first suggested by Francis Galton that the median of any large number of guesses will usually be fairly accurate, applies to experienced forecasters as much as anyone.

We also include our “80% confidence” interval as an expression of the uncertainty surrounding our forecast. For example, our central estimate that the death toll will peak at 1,278 with an 80% confidence interval of 892 to 5,750, means we think there’s only a 10% chance it’ll be less than 892 and only a 10% chance it’ll be greater than 5750. (The confidence intervals are represented by the blue rectangles, and the central estimates with the red lines.)

The worst of the pandemic

The median estimate of the group was for the 7-day average of daily deaths to peak at 1,278, but with an 80% confidence interval of 892 — 5,750

Alongside the predictions, we note down anonymous comments from the forecasters in the team to explain their reasoning. Among the notes accompanying this question, perhaps the most optimistic was that there is a “small chance we are at the peak now”.

On the other hand, the worst-case scenario is if the hospital system collapses and we are forced to “en mass palliate anyone over 60/65” and the most pessimistic predicted 5,000 deaths a day. The big factors were new virus strains and “poorly managed vaccination centres causing infections among the most vulnerable and highest priority population”.

However, with 160,000 infections a day currently in the UK and a fatality rate just below 1%, 1,400 deaths a day seems likely.

Another forecaster also predicted that a third wave was “likely” once the current lockdown ended, “with quite possibly the highest caseload yet, but [was] unlikely to have as many fatalities due to prioritised vaccination of elderly and otherwise-vulnerable” individuals.

A lot of this depends on whether the vaccine protects against any new strains, and how quickly those vaccines are rolled out.

The February Vaccine Target 

Millions of people are currently waiting for a letter informing them of their vaccination appointment, a jab that will end a year of house arrest and often extreme anxiety. The Prime Minister has promised two million jabs a week, and tens of thousands of lives, and millions of livelihoods, depend on getting the jabs out as soon as possible.

We asked the team to forecast how many vaccine doses will have been administered in the UK by the end of February and the central estimate was 12 million, with an 80% confidence interval of 6 million to 20 million.

Among the big questions are the supply and how much political pressure there will be for the distribution network to move faster. Two more vaccines, by Novavax and Johnson & Johnson, are also expected to get approval next month and that will also increase supply.

One forecaster predicted that “Boris’s current target was 13 million for end of February: best guess is they undershoot that slightly and ramp-up only really gets going in March/April…. this has been the consistent pattern of undershooting a bit throughout the pandemic.”

So with a median estimate of 12 million, you can find out when you and your loved ones are likely to receive theirs here.

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In which month will deaths fall below 100 a day?

By estimating when deaths fall below 100 a day we can get some idea of when the virus is close to beaten.

Our group estimated April as the most likely month for daily deaths to fall below this level, with an 80% confidence interval of March to August.

Among the key unknowns are new strains, and also whether hospitals get overwhelmed “which results in cascading preventable deaths”. We can estimate when deaths will fall based on first wave patterns, when it took “two and a half months to get from 1k per day to below 100 in the March-July lockdown”, although the vaccination programme might accelerate that. Generally speaking, it takes about three weeks to half the deaths, and so following an expected peak in January, death rates will half four times by late April.

At this point, one forecaster suggests, the government will open up the economy and deaths will continue around 100 a day because this will be regarded as tolerable. Another believes this figure may continue until September, by which time a combination of vaccination and infection will have introduced herd immunity.

The most “optimistic” forecast suggested that we may have got deaths down by March but that might be because “we screw up” and “have killed everyone who could possibly die from it and therefore the virus has nowhere else to go”.

The most pessimistic suggested: “If there is a less successful vaccination programme, multiple policy errors such as keeping schools open once teachers have been vaccinated but not paying attention to cases/repeated attempted opening up, or mutations of the virus, then it might be December before deaths get below this level.”

But another thought that new drugs — the most recent breakthroughs came late last week — will have reduced the fatality rate fairly soon.

January and February 2021 are going to be very traumatic months for tens of thousands of people in the UK. But to be forewarned is to be forearmed, and if you’re worried about the next few weeks you might want to gain a better estimate of how bad it will get, when your vaccine will come, and most importantly when the nightmare will be over.

And perhaps next time that Britain faces a crisis of this magnitude, we’ll have systems in place that incentivise people to tell the truth, identifying those with strong track records of forecasting, rather than turning to those who tell us what we want to hear.

Forty years later, we have a new virus to contend with. Although it doesn’t have a truly terrifying 30% mortality rate like smallpox, the coronavirus SARS-CoV-2 is vicious enough to have killed 1.5 million people in less than a year, and has shut down economies worldwide. A major reason for those shutdowns, of course, was that we didn’t have a vaccine: there was no option but to attempt to stop people from spreading it by keeping them apart. But now we do have vaccines – several of them, and they’re accompanied by a much better understanding of how SARS-CoV-2 works. Imagine how satisfying it would be — after a 2020 filled with disease, death, lockdown, loneliness, bankruptcy and general misery — if we could eradicate this virus too. 

This might seem like we’re jumping the gun. After all, as we write this, nobody outside of clinical trials has actually been vaccinated against the coronavirus. But the most sophisticated vaccination programme in world history will begin within the next few days. How likely is it that we can get rid of this thing altogether?

First things first. Is eradicating our novel coronavirus even possible? This wouldn’t be the case for, say, the virus that causes influenza — mainly because there isn’t just one major flu strain, but many dozens, each of which is constantly and rapidly evolving. We have to come up with a new flu vaccine every year, and eradicating all the different strains just isn’t viable with our current technology. The Covid-19 coronavirus, on the other hand, evolves far more slowly, opening up the possibility that we could tamp it down with the right combination of vaccines and other measures.

Evolution is actually one of the prime reasons we should want to try to wipe out this new virus. Even though it might do so slowly, it’s still possible that it might evolve a new strain — one that’s deadlier and which the vaccines we’ve just developed don’t counter. This isn’t a far-fetched idea: the closely-related coronavirus that causes SARS has a fatality rate somewhere around 15%, and the even scarier one that causes MERS is worse than smallpox, killing around 34% of cases.

But even setting aside evolution, eradicating SARS-CoV-2 would have clear benefits. It would obviously reduce the suffering caused by the disease, and lessen the likelihood of flare-ups in specific parts of the world — most likely poorer countries where vaccines are harder to come by. It would also save us money in the long run. If the virus is always with us, we’ll always have to vaccinate against it: even if immunity from a vaccine is long term, it won’t be forever, and as populations grow, there will be more of us to vaccinate. Every penny not spent on regularly vaccinating people against COVID-19, after it’s no longer an issue, could be spent on improving health in other ways.

So there’s a clear rationale for eradicating the disease, and it might even be possible in theory. What about in practice?

To date, only two infectious diseases have ever been eradicated — the aforementioned smallpox, and also rinderpest, a particularly nasty cattle virus that can have a near-100% fatality rate, which was wiped out in 2011. That should tell us that removing a disease from circulation is an extraordinarily difficult task.

Smallpox had been endemic in Asia for perhaps 2,000 years. By the 18th century, it killed around 400,000 people in Europe annually. Wars, conquests and the slave trade introduced the disease into the Americas, South Africa and Australia, and records suggest that it destroyed entire tribes in what are now South Africa, Kenya and the Democratic Republic of the Congo in the 19th century, and killed huge swathes of people living in urban settlements.

In the years before a vaccine, authorities quarantined ships to prevent the disease from being introduced into disease-free ports; when that became unviable, some communities practised variolation — a risky procedure where people were deliberately exposed to weakened forms of the virus to protect them from the fatal strain. However, Edward Jenner’s invention of the smallpox vaccine in 1796 — the first ever vaccine, in fact — was a game-changer, leading to the first real reductions in the incidence of the disease. As time passed, techniques used to manufacture, store and administer vaccines improved tremendously, and states initiated vaccination programmes to inoculate their citizens from the deadly disease.

Although smallpox was eliminated in some regions in the early 20th century, the prospect that it could be eradicated across the world was met with widespread scepticism, and was not even considered a serious possibility until 1958, when the WHO resolved to guide a worldwide campaign. The operation was a decentralised undertaking, and it took decades to secure funding and political support for eradication everywhere — for many years, it was simply not seen as a priority, or even an interest, to many governments or community leaders. Where money was available, the strategy began with mass vaccination and shifted towards tracing and containment as cases declined. Eradication was finally achieved in 1980, 184 years after the vaccine was first invented.

The problems that beset the smallpox eradication programme — poverty and a lack of funding — are also major reasons that other diseases haven’t yet been beaten. For example, the Rockefeller Foundation’s early 20th-Century effort to wipe out hookworm, a parasite that can create a drag on children’s development, was very nearly successful, but it didn’t quite penetrate far enough into the world’s least developed places, where poor sanitation and infrastructure help the worms spread.

Hookworm has even come back in extremely deprived parts of the US, where it was thought to be eliminated. A similar story can be told for yaws, a bacterial disease that causes ulcers and physical deformities, and which keeps returning in the very poorest parts of the world.

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A more optimistic story concerning a parasitic infection is that of Guinea worm disease, where a worm grows in the host’s flesh and creates an extremely painful wound, stopping them from walking or working, and making them vulnerable to further bacterial infection. Since there’s no vaccine for a non-viral disease like this, education is the main way to prevent it: The Carter Centre, established by the former US president, has been showing people good ways to clean and filter drinking water, among other strategies, and has been the main cause of global disease cases declining from around a million in 1989 to double figures in recent years. We’re many years behind our elimination target, however: the disease remains in very poor countries in Africa, such as Chad and South Sudan.

Poverty has also frustrated attempts to eradicate polio, which infected millions across the 20th century, resulting in death, paralysis, skeletal deformity or confinement to a coffin-like iron lung for weeks, months or years. The plan was to eradicate the three different kinds of wild poliovirus by the year 2000, but it proved trickier than expected. Nevertheless, the virus’s days are numbered: India was declared polio-free in 2014, then Nigeria as recently as August 2020. Presently there remains only one wild type of poliovirus, and it remains endemic only to the neighbouring countries of Afghanistan and Pakistan. 

Other eradication attempts have run aground for other reasons. The effort begun in the late 1940s to rid the world of malaria, for instance, was a failure due not only to ballooning budgets, but to our old friend evolution: mosquitoes evolved resistance to DDT, the pesticide that had previously, and successfully, been used to exterminate them. Now, eradication is back on the table: in September 2019, a special commission put together by the medical journal The Lancet projected that with the right policies, we could still eradicate malaria within a generation.

So whereas there are reasons for hope about freeing the world from polio, Guinea worm and maybe even malaria, we haven’t finished the job on any of them yet, and we’re in some cases decades behind schedule. These are all reasons to temper our expectations about eradicating SARS-CoV-2. And we’re about to see another.

In a word, the problem is animals. The fact that other mammals can be infected with a virus makes it vastly more difficult to stamp out a disease, as the persistance of rabies shows. Vaccinating animals — especially wild and stray ones — is understandably far more difficult than vaccinating people. Indeed, the reason we can’t technically say that we eradicated the SARS or MERS viruses, despite their spread through humans being completely halted, is that they still circulate among non-human animals — and since there’s no vaccine for either disease, it’s quite possible that they’ll reappear in future. 

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We already know that the novel coronavirus can infect bats, cats (including lions and tigers), dogs, monkeys, ferrets, hamsters and shrews, among other species. In recent weeks, Denmark had to cull 17 million mink after outbreaks in humans were traced to infections among the animals on farms where they were bred for their fur (and in a rather grim sequel, thousands of them had to be dug back up again). 

Of course, the origin of the virus is bats — they’re one of the major non-human carriers (the technical term is “reservoirs”) of SARS coronaviruses. Virologists have for years made predictions that bats would be the source of new disease outbreaks: they carry a wide variety of coronaviruses, they’re widely dispersed around the world, often live near humans and can migrate easily, and the viruses they carry are likely to cause disease and jump to humans. That suggests that vaccinating just bats — and the particular species that carry human-infectious viruses, rather than all the other potentially-infected animals — would get us quite far.

When authorities began to control the spread of rinderpest, they did so by isolating infected farm animals and restricting their movement, culling them and disinfecting their habitats, all before a vaccine was developed. With COVID-19, we have a head start given we already have a vaccine — and it would be relatively straightforward to develop a bat-version. We could put oral vaccines in bait — a common strategy for controlling disease in wild animals.

There are also other ways to prevent SARS coronaviruses from jumping to humans once again. Most countries, for example, already mandate vaccinations and travel quarantines for animals entering the country. And we could focus on improving hygiene standards for handling wild animals — particularly of the flying mammal variety. In the future, it could even be the case that new vaccines will protect us against multiple strains of SARS coronaviruses at the same time.

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There are several other factors that affect whether a disease is eradicable. One is how easy it is to detect: if you can precisely pinpoint who has the virus, you can get them quarantined as soon as possible. That’s not really a check in favour of the eradication of Covid-19, since its symptoms — particularly the cough and the fever — can easily be confused with those of other viruses, such as the flu. On the other hand, better diagnostic tests are being developed all the time, and we might soon end up in a situation where super-rapid, super-accurate, super-cheap tests can help us rapidly isolate people carrying the virus.

Another factor is how easy the disease is to prevent. Although the initial evidence suggests that at least two of the vaccines for Covid-19 developed so far are extremely effective at preventing symptoms, we don’t really know yet whether they also prevent transmission of the virus, and indeed whether they prevent infection itself. Luckily, there are good scientific reasons to think this latter will be the case. We’re also getting better at preventing spread through non-pharmaceutical means: not just lockdowns, but less invasive interventions like masks, ventilation of rooms, social distancing, and contact tracing, all of which improve as we learn more about the mechanics of how the virus spreads. 

This is another area where technical advances will likely help us in future. At the moment, our vaccines are (literally) a shot in the arm. Nasal vaccines, which vaccinate the upper as well as the lower respiratory tract, are more likely to stop transmission as well as symptoms in the vaccinated person, and could well be developed in the months and years to come (we’ll also need an oral vaccine for those wild animals).

Ventilation technology will also probably improve, allowing us to spend more anxiety-free time indoors (as in so many things, hospitals in East Asia learned this lesson well after the original SARS outbreak in 2003). Even simpler technologies, like new types of masks that are more tolerable to wear and thus more likely to be effectively used, could help slow the spread.

Finally, is it possible to eliminate the virus in particular regions of the world? If so, it increases the plausibility of doing it on a wider scale. For COVID-19, the answer seems to be a cautious yes: there are regions that, right from the start of the pandemic, have had extremely low transmission thanks to effective tracing, quarantine and other policies.

For example, from the perspective of the UK, with our population of 67 million and 80,000 deaths, it seems unbelievable that Vietnam (population 96 million) has had a mere 1,358 confirmed cases and 35 deaths. That’s not full elimination by any means, but it — along with the extremely impressive performance of other Asian and Australasian countries, even without a vaccine — goes to show that good policy really can drive the virus down to near-negligible levels.

And that’s probably the best we can hope for: getting things to the point where, like SARS and MERS, the virus is effectively gone, even if not fully eradicated. The fact we have a vaccine means we’re already in a better position than for those two other coronaviruses; but that the virus is so contagious, and has already spread to every corner of the globe, makes things more difficult. The good thing is that the strategies mentioned above will all reduce the burden of disease, with all its associated costs to life and to our economies, even if they fail to completely extirpate the virus. For that reason, aiming for eradication is the smartest strategy.

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Even if we can’t win the peoples of the world their freedom from SARS-CoV-2, all our technological advances might render it far less risky to be infected. The model here is HIV: even though there’s no vaccine or cure, with the right drugs the virus is no longer a death sentence. We’ve already seen the novel coronavirus become less deadly as our medical treatments have improved; better steroids, anti-virals, and perhaps even synthetic antibodies could reduce the fatality rate even further.

The Covid-19 pandemic has given us plenty of reason to despair, but all the scientific progress we’ve made in a few short months gives us a lot to feel optimistic about, too. The urgency of the pandemic has meant that we’ve accelerated reviews by regulatory agencies, poured vast funding into research and development, and developed not one but multiple effective vaccines at an unprecedented speed. 

When all the world’s attention is focused in the right way, we’ve seen that the most vexing problems can suddenly become solvable. For millennia, humans had been unable to exterminate any infectious disease. And yet just in the last century, our technology and ambition allowed us to declare victory against two of them, and set us on track to defeat several more. Once the first wave of mass Covid vaccination begins, we shouldn’t rest on our laurels. We should do our very best to free ourselves of this virus forever.

This week, of course, it was the Oxford/AstraZeneca vaccine, one week after Moderna announced their results and two weeks after Pfizer’s. 

The headline efficacy results of the Oxford trial are lower than for the other two vaccines. But it’s still great news, and it may be the case that the headline result is not the thing we ought to be looking at. And, most important, the Oxford vaccine, compared to the other two, can be made in far larger quantities far more quickly, can be stored and distributed much more easily, and will be available at a fraction of the cost.

The team is submitting its data to a journal probably around the time you read this, and it will be in the public domain in a week or so. At the moment we have no real data to look at — and, in fact, even the scientists who worked on it have not had access to all of it. So I thought it might be useful to try to collate what we can know, so far.

First, that headline result. The Oxford vaccine is, apparently, 70% effective (the announced result is 70.4%), compared to the 90% or higher for Moderna and Pfizer’s offerings. Except it’s simply not.

There were two groups in the vaccine study: one of about 9,000 people who were given a standard dose and then a booster shot of the same volume a month later; and a second group of about 3,000 people who were given a half-sized dose, and then a standard-sized booster. We should note at this point that the plan to divide the trial like this was in the original trial protocol, so we can be pretty confident that they haven’t just chopped the data up after the fact to make things look good. (EDIT: Although it is all quite complicated; see here.) 

The vaccine appears to have been 62% effective in the first lot, and 90% effective in the second. But if you’re given the vaccine, it will be either a full-dose/full-dose regimen or a half-dose/full-dose one, not some average of the two. So it’ll either be about 62% effective or about 90% effective, assuming those numbers are accurate.

Of course, “assuming those numbers are accurate” is the key phrase. We know there were 131 cases in total in the trial, and we know that there were 100 cases in the control group, and 31 among people who had the real vaccine. But only about 30 or so were in the half-dose group, and the smaller sample size means greater uncertainty.

Incidentally, it’s not completely clear why the smaller dose first is more effective. Andrew Pollard, the chief investigator, speculated in a Science Media Centre briefing on Monday morning that the smaller dose may have “primed” the immune response in some way. I’ve seen other scientists wondering whether it’s because the larger dose pushes the body to develop an immunity to the genetically modified virus that’s used to deliver the antigen. The immune system is complicated; I imagine we’ll find out more about what’s going on in the coming weeks.

There’s another point, which is that the headline figure also doesn’t tell us the impact on asymptomatic cases. The Pfizer and Moderna trials only looked at symptomatic cases: the  Oxford trial, on the other hand, asks all its subjects to swab themselves in the throat and nose every week (I’m on it, so I can vouch for this particular unpleasant duty), so it should catch anyone who’s got the virus, symptoms or no. The results don’t affect the headline figures — those only refer to symptomatic cases — but they are used to establish the effect of the vaccine on transmission. 

It is theoretically possible (but not very likely) that a vaccine could stomp heavily on the symptoms of a disease, so almost no one gets sick, but not stop people from actually getting the virus. By regularly swabbing asymptomatic people the study can see whether that’s the case. All we know so far is that there is an impact on transmission, but until all the data has been released, we won’t know how big that effect is; again, even Prof Ewer of Oxford hadn’t seen those numbers, and nor had Pollard, when he spoke to the SMC briefing.

There’s another level, as well, which is that no one who had had the actual vaccine — whether they got the half-dose or the full-dose regimen — got a “severe” case of Covid. Admittedly “severe” is defined as requiring hospitalisation, and obviously you can have quite a nasty case of Covid without ending up in hospital; but given how lethal this disease can be, it is nonetheless good news that no one ended up dying or in the ICU.

You may rightly say that all this sounds a bit woolly, and it kind of is. Here’s what we know: the vaccine, if administered correctly, probably works about 90% of the time on symptomatic cases, but we can’t be all that sure; it has some effect on asymptomatic cases, but we don’t know what; and no one who took it ended up in hospital, although we don’t know yet whether that means everyone just had a mild case of the sniffles or something more. It’s all good news, but very vague good news.

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So here are some bits of good news that are not vague. First, several million doses of this vaccine — which, as we’ve seen, definitely works, by the targets set — have already been made, and there is lots and lots more on the way. According to Pam Cheng of AstraZeneca (again speaking on the SMC briefing), by the end of December there will be enough actual vaccine to make about 20 million doses for the UK alone, of which about 4 million will already be in vials, ready to go. She thinks there will be about 200 million doses’ worth of material ready worldwide by the same time.

By the end of the first quarter of next year — so the beginning of April — she says there will be enough material for about 700 million doses worldwide, and about 40 million doses ready to go in the UK. And by the end of the year, they expect to have made 3 billion doses. The Serum Institute in India, the world’s biggest vaccine manufacturer, has a licence to manufacture it, so that’s a plausible number. Ewer said that it is estimated that something like two-thirds of the world’s children have received a vaccine made by the Serum Institute: “They are manufacturing on an enormous scale,” she said. “This is exactly what they specialise in, and that’s why we worked so hard to get them on board, because they can do large-scale cheap manufacture.”

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Better still, if the half-dose/full-dose regimen gets licensed, then that means it takes 25% less vaccine per patient. So your 40 million doses would vaccinate about 26 million Britons, instead of 20 million. Your 3 billion doses at the end of 2020 would vaccinate 2 billion people worldwide, not 1.5 billion.

That’s nowhere near enough for herd immunity, especially if the efficacy is on the lower end of the estimate, but it’s enough to vaccinate a huge chunk of at-risk groups and essential workers such as healthcare staff. And AstraZeneca and the manufacturers it has licensed the vaccine to will continue to churn out hundreds of millions more a month.

On top of this the Oxford vaccine, as has been widely reported, can be stored at normal fridge temperatures — between 2° and 8°C. It’s not that it would have been impossible to get huge amounts of the Moderna and Pfizer vaccines to, say, rural Malawi, with their -20°C and -80°C storage requirements, but it will be a damn sight easier with this one.

And, perhaps best of all, the Oxford vaccine looks as though it will sell at something like £2-3 a dose, according to Ewer. Pfizer is expected to sell its vaccine at about £15 and Moderna at more like £25. It is simply much more plausible that this can be bought and distributed in the large numbers required for use in the developing world. This is, says Ewer, partly because the viral vector vaccine technology is older – Johnson & Johnson has one for Ebola which is already being used — so “all the background work on deployment has been done”, while the mRNA vaccines are entirely novel (if exciting).

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I don’t know what this will mean for Britain in the short term. I was speaking recently to a senior scientist who helps advise the government about the mass testing that’s been piloted in Liverpool, and he mentioned that one possibility is that people who test positive have to isolate for a week, but then get a six-month passport saying they’ve had the disease and are safe. He suggested that the same system could be used for vaccines; it sounds plausible to me, with caveats, but whether it actually happens is anyone’s guess.

But the takeaway is that this, like the Pfizer and Moderna announcements in previous weeks, is fantastic news. More vaccines will come, and may be better in various ways, but this is a mass-availability, cheap, effective, easily-stored candidate that does everything you want. It will form the backbone of Britain’s response, and the world’s, and I’m really excited by it.

Now, I just can’t wait to find out what we get next Vaccine Candidate Announcement Day. See you next Monday!