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Oxford AstraZeneca Data, Again

We have some more data to mull over with the Oxford/AstraZeneca vaccine. The situation so far has been pretty confused, with various efficacy numbers appearing from different people in different venues. It’s fair to say that the rollout of the clinical data has not gone smoothly, and that it’s done the effort no favors. As many will recall, the current big questions are whether a lower first dose of the two-dose protocol is more effective (as appeared from some of the earlier data) and what the interval between the two doses (lower dose or standard dose) should be, since the UK government has been looking at getting a higher percentage of the population vaccinated with the first shot by delaying the second.

The earlier report showed 54.9% efficacy in the group that got two standard doses four weeks apart (95% confidence interval of 32.7% to 69.7%). That number improved to 66.7% when the low dose/standard dose cohort was added in, because that smaller group itself showed 90% efficacy (95% CI of 67% to 97%). This new preprint reports on 1293 participants who had a 12-week interval between two standard doses. Efficacy in this group was 82.4% (95% CI of 62.7% to 91.7%), which would seem to be a notable improvement. That’s not a very large sample, and the confidence intervals between the four-week and the twelve-week group still overlap in the 60% efficacy range, but you can make a case (and AstraZeneca certainly is) that this shows better overall effects.

Another key piece of data is the efficacy seen during that 12-week period: 76% (95% CI of 59% to 86%), which is basically the same as when analyzed after the second dose. The preprint makes the point (and I agree with them) that the second dose is likely to be needed for longer-lasting protection, because it really does raise antibody titers significantly, but it certainly looks like the protection from a single dose with a longer delay is worthwhile, and that the delay will not hurt things (and may well make the overall efficacy higher).

Why should this be? The answer is “immunology”, and that’s not just the last refuge of scoundrels. Historically, it appears that longer delays in a two-dose regime can make things better, make them worse, or not make much difference, and the only way to be sure is to go out and get the clinical data. So even though this is not a large 12-week data set, I’m glad to see it. I think that the UK’s move to get as many first doses into the population as they can was the right one, and it’s good to see some data that at least don’t undermine it.

What about the low-dose/standard dose business, though? This preprint offers a possible explanation: it turns out that the cohort that got the lower dose at first also had a longer delay before getting the second dose. So it’s possible that the apparent increase in efficacy was driven less by the lower first dose than by the longer gap between the doses. We can’t rule out an effect from both, though – the data are just not in a shape to do that. Overall, the complaints that I (and many others!) have had about the data collection and rollout for this vaccine are still valid: we’re learning what could be important things about this candidate from analysis of small subgroups, some of which were themselves the results of mistakes and miscommunication during the trials. And the release of that data has been just as patchy and noisy – you really would have expected better from AstraZeneca.

But there is something good to say about their data collection: since the UK study that’s included in these numbers tested its subjects by nasal swab every week, regardless of any symptoms, we can actually get a read on something that everyone’s been wondering about: transmission. It’s become clear from all the successful trials that vaccination (whether by mRNA, the several different viral vectors, or recombinant protein) is extremely effective at keeping people out of the hospital and at preventing people from dying from the coronavirus. This is very good news, and it deserves to be highlighted. But are those severe cases just being converted to lesser ones, with other lesser cases then being converted to asymptomatic ones, and in that case has the number of people walking around shedding infectious virus really changed?

The swab data say that it has. It appears that the vaccine reduced the number of people showing PCR positivity by 50 to 70%. The actual numbers were -67% after the first dose and -54% overall, but I wouldn’t read anything into that difference, because the confidence intervals for those two measurements completely overlap. So it looks like everything is shifted: hospitalized cases end up being able to stay at home with more moderate symptoms, people who would have had moderate symptoms end up asymptomatic, and people who would have been asymptomatic end up not testing positive at all. Oh, and people who would have died stayed alive. There’s that, too.

If you just look at efficacy in preventing asymptomatic infection, you get a really low number (16% efficacy, confidence interval banging into the zero baseline). But my interpretation of that is that the overall number of asymptomatic patients didn’t change too much, because as just mentioned, the “would have been asymptomatic” group is not showing infection at all, and their numbers have been replaced by people from the “would have been showing symptoms” cohort, who are now just asymptomatic. And since transmission would seem to depend on viral load (among other factors), reducing viral load across the population (as shown by the significant decrease in PCR positivity) would certainly be expected to slow transmission. As Eric Topol noted at the time, this same effect had been noticed in the Moderna data in December. So with the numbers we have now, I feel pretty confident that yes, as one would have hoped, these vaccines also reduce transmission of the virus in the population. I believe that we should soon see this in a large real-world way in the Israeli data, where a significant part of the population has now been vaccinated.

137 comments on “Oxford AstraZeneca Data, Again”

  1. Adrian says:

    My impression is that from March last year symptomatic spread is no longer a major factor, asymptomatic and presymptomatic spread are the real problems.

    So no reduction in asymptomatic infections are a problem.
    And lack of symptomatic cases removes the visible tip of the iceberg that previously led to discovery and isolation of clusters.

    It feels as if these vaccinations will be the first step, followed by immunity created by COVID-19 running unimpeded through the whole population.

    1. Kebar says:

      “My impression is that from March last year symptomatic spread is no longer a major factor, asymptomatic and presymptomatic spread are the real problems.”
      There are still a lot of people who cannot afford to miss work, even if they have symptoms.
      So I am pretty sure we still have sysmptomatic people taking trains/buses/underground to commute to work.

    2. Marko says:

      “The swab data say that it has. It appears that the vaccine reduced the number of people showing PCR positivity by 50 to 70%.”

      That directly translates to a reduction in transmission rates, full stop. People who don’t become PCR+ don’t transmit to a measurable degree. If you try to culture from their swabs, you fail.

      I’ve been chastised by the vocabulary police for suggesting that this represents “sterilizing” immunity, of perhaps limited duration. I’m not wed to that word, but we should have a term for what this represents. I floated “pasteurizing”, but that didn’t catch on. How about “sanitizing” immunity?

      I’d much prefer to be sanitized than sterilized anyway. 121°C @ 15 psi steam-baths are not my idea of fun.

      1. DataWatcher says:

        . . . and, of course, to coin a cliche, if it can’t spread, it can’t mutate. Possibly the most encouraging aspect of these new observations . . .

        1. Adrian says:

          This would only be true if social distancing is maintained indefinitely and President Biden takes back his dangerous promise to reopen schools within 100 days.

          Only 50% to 70% reduction in transmission alone is not sufficient to get R below 1 even if 100% of the population (including all children) was vaccinated. Not for the legacy variant of SARS-CoV-2, and even less for the improved variants of SARS-CoV-2 that increase transmissibility even more.

          It is not feasible to enforce social distancing in a vaccinated population, vaccinations will give the virus the opportunity to spread and mutate through 100% of the population.

          1. confused says:

            But if post-vaccination it’s “just a cold” (IE no severe illness), why would mutations then be more dangerous than in any of the other circulating respiratory viruses? We don’t worry about transmission of those…

            Not a rhetorical question, I am really unclear on why this is emphasized so much.

            (Or, perhaps another way to ask possibly the same question – is there reason to believe that SARS-COV-2 is *inherently, in terms of the virus itself* more dangerous than other currently circulating respiratory viruses rather than simply being more dangerous *because the human population is mostly currently immunologically naive to it*?)

            I mean, if no one had ever had either influenza (any type) or a flu shot, would it be less dangerous than COVID is now?

          2. Adrian says:

            Depends on the exact influenza virus.
            H5N1 is a real killer – literally. If you catch that one, there’s a 50% chance you will die.

            In an unvaccinated population one would expect the virus to become more transmissible and less harmful over time. The “less harmful” was for example very visible when HIV adapted better to humans. It will be an interesting experiment to see a virus running through populations with non-sterilizing immunity where the immunity might also vanish after some time.

          3. confused says:

            I meant ordinary, circulating seasonal influenza. If no one had ever been exposed to any strain of influenza, or had a flu shot, would we see COVID-comparable or higher death rates?

            And I’m not talking about *the virus* evolving to be less harmful, I’m talking about the same virus being more deadly in an immunologically-naive population but much less so in a non-naive population.

            For example, IIRC, historically measles had very high death rates when first introduced to (Polynesian?) islands, with almost entire age cohorts dying, but vastly lower death rates in European, non-naive populations.

            That was a difference of several orders of magnitude, whereas one order of magnitude would be sufficient to drop COVID IFR (maybe 0.6% or so) below that of seasonal flu (maybe 0.1% or a bit less).

          4. confused says:

            Also, would we really expect immunity to “vanish” over time? Diminish, sure, but hasn’t there been evidence posted on this blog before that memory B cells etc. will persist for a long, long time?

            We don’t really “need” sterilizing immunity, just enough immunity to reduce SARS-COV-2 to the fifth “common cold” coronavirus.

          5. DataWatcher says:

            . . . although, just to play devil’s advocate, measles may have a much higher R0 than COVID (so far), but the mutation problem isn’t severe at all. I still think that’s the wild care in terms of ongoing vaccine efficacy and concomitant reduction in serious cases, if mutants continue to become both more vaccine-resistant, contagious, and virulent, none of which appear to have been the case with measles.

          6. confused says:

            Is the mutation problem severe with any “long-term-in-humans” virus? Seems like every high-impact “new” virus jumps from animal->human rather than being a mutations of an already-circulating-in-humans-but-not-severe virus.

            Even with influenza, which causes pandemics pretty regularly, those are “new” animal->human jumps, right? (Usually birds or swine…)

            If we don’t worry about new immune-evading variants popping up with RSV or the four common-cold coronaviruses or parainfluenza or…

            I still feel like I’m missing something here. Is there a counterexample?

          7. Chris Phillips says:

            I really wish I could understand why some people think immunity acquired from vaccination is so dangerous and immunity acquired from infection is not.

            Please can someone explain?

          8. Adrian says:

            COVID-19 starts as a pretty deadly disease, which might be due to using ACE2 for cell entry.
            The human coronaviruses that are part of the common cold are not known to have ever caused something like that on a larger scale.

            The main reason why measles were less deadly for Europeans is not immunity acquired during the lifetime, the main reason is that the first waves of the measles likely wiped out large parts of our ancestors leaving only the most resilient ones alive to pass their resilient genes to us.

          9. Chris Phillips says:


            “The human coronaviruses that are part of the common cold are not known to have ever caused something like that on a larger scale.”

            Not known to have done do, but you surely know that it has been proposed that they all did so when they first crossed into humans. In particular, it’s been suggested that OC43 caused the so-called “Russian flu” pandemic of 1888-1889.

            On genetic grounds the others are believed to have crossed centuries earlier, so that any records are likely to be very incomplete.

          10. Marko says:

            “COVID-19 starts as a pretty deadly disease, which might be due to using ACE2 for cell entry.”

            NL63, a common cold coronavirus, also targets ACE2 :


          11. Roland says:

            @confused “Is the mutation problem severe with any “long-term-in-humans” virus? Seems like every high-impact “new” virus jumps from animal->human rather than being a mutations of an already-circulating-in-humans-but-not-severe virus.

            Even with influenza, which causes pandemics pretty regularly, those are “new” animal->human jumps, right? (Usually birds or swine…)”

            I agree the simple mutation risk seems to be overstated. We should expect a novel virus to adapt to it’s new human host in the beginning so these new advantageous mutations (at least D614G, N501Y, K417N, E484K) are not that surprising – some were even predicted – but that doesn’t mean we’ll keep seeing 4-5 equally bad mutations every year and constant immune evasion.

            When it comes to immune evasion once the virus is backed into a local optimum on the mutational landscape it might for example only be able to gain new immune evasion by becoming better adapted to upper respiratory infection and less virulent. That might sound wishful thinking but it has some logic behind it. We seem less good at raising IgA antibodies by vaccination, and IgA antibodies waning may be much more significant than general immunity waning, so clinging on in our noses and causing reinfections every few seasons seems a good move for the virus. A less symptomatic infection would give it a transmissibility advantage too.

            Influenza A is really a unique beast because it infects so many different animals, which causes many strains to be circulating, which leads to reassortment events when two strains merge to produce dramatic changes. That can be human+animal combination in the more serious cases, but I believe the evidence points to seasonal changes frequently being driven by human+human strain reassortments. Influenza is really good at reassortment because it’s multi-stranded.

            Covid-19 seems to have some decent reassortment capability despite being single stranded but probably significantly less than Flu? It also mutates more slowly. However it has been shown to infect humans, cats, dogs, bigger cats, mink, ferrets, bats, and surely others, some of which could turn out to be significant. It’s more likely to jump species if two similar strains capable of combining are already present in both species. There’s also the pretty scary prospect of a MERS/SARS-CoV-2 recombination event.

            So it has some of the risk factors for being a constant nuisance, but lacks others. Some people argue all Influenza A in humans derives from the 1918 pandemic and that’s been a pain in the butt since. On the other-hand HCoV-OC43 is hypothesised to come from the 1889/90 pandemic and only exists in 3(?) types causing relatively few cases of severe illness with a non-dramatic reassortment identified about 15 years ago.

            Incidentally even measles seems to be trying to evade vaccine immunity, just really slowly:

        2. ScientistSailor says:

          @datawatcher…Actually the virus can mutate w/o spreading, it just has to last long enough in a single patient to replicate and battle some selection pressure. We think this is where the UK variant came from, because it showed up out of nowhere with >10 mutations. You’d usually expect to see mutations accumulate 1-2 at a time.
          Mutations arise in bacteria all the time without spreading…

      2. Navin R. says:

        “That directly translates to a reduction in transmission rates, full stop. People who don’t become PCR+ don’t transmit to a measurable degree”
        Not sure if this is absolutely certain. Airborne transmission could lead to inoculation in lungs and this could precede PCR positivity in pharynx. If aerosol is generated in lungs, then perhaps even superspreading could occur when still PCR negative.
        Maybe I’m being pedantic but I’m not sure… Is there evidence that refutes such a model?

        (though I doubt this would be an issue post-vaccination.)

        1. Marko says:

          “Not sure if this is absolutely certain. ”

          I said it’s not happening to a measurable degree. If it happens once in a blue moon, who cares? Transmission from a person who consistently and repeatedly tested negative by PCR has never been reported to my knowledge, and I’d bet good money it never will be.

          “Airborne transmission could lead to inoculation in lungs and this could precede PCR positivity in pharynx. If aerosol is generated in lungs, then perhaps even superspreading could occur when still PCR negative.”

          Yes, but the weekly testing done in this case rules that example out. Those PCR negative potential superspreaders would have subsequently been detected as PCR+.

          C’mon , this ain’t hard. PCR is widely recognized as being overly sensitive for contact tracing purposes because it detects even people with trivial viral loads who are not likely to be infectious. We turn loose everyone who repeatedly tests PCR negative because we know they can’t transmit.

          The people at STAT and others bashing this result are doing it because it’s a favorable result for Oxford that hasn’t been demonstrated for the US vaccines. And, BTW, where are those comparable studies from Moderna and Pfizer? We were supposed to have the results by now. The lame excuse that’s circulating is that there was “no funding” for the studies. Meanwhile, Pfizer is touting the $15 billion they’ll rake in selling vaccine this year. Which makes perfect sense, actually.

  2. Ozgood says:

    On the Lancet article confirming the efficacy of the Russian vaccine, Sputnik V:

    I am long retired from the field. When the first reports of the Russian vaccine came out, I did about ten minutes of Googling. It was obvious that the two lead scientists were major figures in the field and that the Gamaleya Institute is also well respected. Their vaccine should be taken seriously.

    What did we hear from the mainstream and much of the tech media? Russia Bad.

    1. Julia says:

      I’m not in the field, but I’m from Russia and two things are true:
      – there are many excellent scientists in Russia
      – there also may be a lot of political pressure to cut corners, and political pressure is a lot harder to withstand in Russia than in the U.S.

      1. Marko says:

        I’m not in the field, but I’m from the U.S. and two things are true:
        – there are many excellent scientists in the U.S.
        – there also may be a lot of pressure from industry to maximize profits, and pressure from industry is a lot harder to withstand in the U.S. than in Russia

        Six of one, half-dozen of the other….

    2. Anonymous says:

      It’s wonderful that the Russian vaccine is effective, and of course their are great scientists and a superb scientific tradition in Russia. But launching a vaccine with the level of review that Sputnik 5 underwent was a gamble, as has been discussed on this blog.

    3. Lappan says:

      When those first laudatory reports of Sputnik hit the headlines it was with accompanying glibness about the level of testing, which it rapidly emerged amounted to phase-1, or “it didn’t promptly kill the sample population”. Of course this engendered a hostile reception since it looked at best naive and more likely snake-oil-salesmanship. The fact that the developers disavowed the claims was only partially reassuring, since it served to confirm that they weren’t in the driving seat.

      1. confused says:

        I have to say I’m unconvinced that was the wrong approach during a pandemic, though. I certainly would have taken the vaccine as soon as I saw data that it produced an antibody response as good or better than natural infection.

        If we’d started giving vaccines to nursing-home residents (wouldn’t even take mass production since they’re not that numerous) after Phase II, before the fall/winter surge, we could have prevented a *ton* of deaths – and the death rate in that population is so high that side effects are basically irrelevant (hard to find really good numbers, but something like 5%-10% of that subpopulation appears to have died in the US).

    4. Johnathan Hughes says:

      I feel that you misrepresent things a little.

      No, we didn’t hear “Russia bad.”

      We heard “Russia have acted prematurely in approving the use of their vaccine.”

      And you know what? They had. Thankfully it looks like it has worked out (and Derek said on this very blog that as far as he could tell it was a perfectly reasonable approach to making a vaccine, if unusual, so that might not be a surprise), but at the time that it was approved they had done so with far too little data.

      1. Watson Ladd says:

        The worst case is it doesn’t work and they need to vaccinate everyone again. Shots in arms are good actually.

        1. metaphysician says:

          No, the worst case is some mix of the following:

          1. It sickens and kills people, just at a rate low enough to not be detected by a Phase 1 trial

          2. It doesn’t do a damn thing about Covid, but it takes forever to actually prove this and end its usage, because nobody wants to be told “your miracle cure is worthless”

          3. Its deployment hinders and delays the development of actual useful vaccines

          4. Its approval sets a precedent that makes it easier to deploy untested, unproven snake oil in the future

          1. Not-an-epidemiologist says:

            After the combined Phase I/II trials, we knew that the vaccine generated an excellent immune response with neutralising antibodies.

            At that point, you have to calculate the risk of action vs. the risk of inaction. All of your points are valid, but by the end of Phase II, unlikely. (Let’s pause for a second, and note that not a single vaccine candidate that has progressed to Phase III trials for this disease has so far failed.) The risk of inaction during a second wave hopefully needs no explanation — just take a look around.

            If there wasn’t a raging pandemic, early vaccination prior to Phase III results would be completely immoral and insane — very few if any would dispute that. But we’re not living in that world. And while vaccine production capacity has been an issue all along, we had the ability to protect vulnerable populations significantly earlier than what we did. Our inaction has led to a large number of unnecessary deaths (and will continue to do so for some time to come yet).

            If saving lives is the goal here, then we failed. And if it’s not, then what the hell are we even doing?

            (It’s worth noting that the decision by various counties to use a delayed second dose for Pfizer and AZ was made on exactly these lines. Our perspective on risk has shifted, and I wonder what would happen if we were placed in this scenario again in the future. My guess is that we would see earlier emergency authorisation of vaccines.)

    5. Klimax says:

      One needs to be bit careful, apparently there are some anomalies and missing stuff:

      Might cause problem with approvals.

      1. Chris Phillips says:

        Just to be clear, that thread is about the Sputnik vaccine, not the Oxford one.

  3. Adrian says:

    All these numbers are for the current vaccines against the legacy variant of SARS-CoV-2.

    Based on the limited information available, the current vaccines seem to be less effective against the improved British/Brazilian/South African variants of SARS-CoV-2 that are about to become the dominant variants everywhere.

  4. A Nonny Mouse says:

    I think the comments about Astra Zeneca are a bit harsh; they came quite late to the party after the government had rejected Merck as the partner and a lot of the work had already been done by Oxford (there’s a good BBC programme following the development if people have access).

    Really a bit like asking for directions with the classic “well I wouldn’t start from here”!

    If there were more time, I am sure that AZ would have started all over again.

    1. Ted A Bateman says:

      What is the program called? Would like to watch it. Will search.

    2. Nathan says:

      Vaccine development Monday-morning-quarterbacking is peak internet.

  5. Michael Loewinger says:

    Yes. We’ll the Russians issued press releases saying the vaccines were ready to use after phase 1 and phase of testing. That did not inspire confidence. Now with current data of course looks much better.

  6. Terence Gordon says:

    Astra-Zeneca results seem to apply only to younger populations. Public heath officials in BC have determined that age is the single greatest risk factor for severe outcomes from COVID-19 infection. That, coupled with growing EU restrictions on the age groups that will receive the vaccine are worrisome to at least one 80 year old.

    1. Eric says:

      There is strong secondary evidence to suggest it will work as well on over 65s as under 65s. There are probably age groups that other vaccines haven’t been tested on extensively either (over 90s?) but no one’s saying you wouldn’t give people of that age the other vaccines.

    2. dearieme says:

      I’m not in the field, but I’m a European. and two things are true:
      – there are many excellent scientists in Europe
      – there also is a lot of pressure from the EU Commission and national governments to save face, and pressure from them is a lot harder to withstand in Europe than in Utopia.

      1. AngularMan says:

        The swiss medical regulator rejected to authorize the use of the AstraZeneca vaccine as well. For lack of trial data … and what are their political reasons?

        Moreover, there really is no urgency for the EMA to approve the vaccine for older people. There are enough high priority targets in the lower age bracket and AstraZeneca won’t be able to deliver large quantities to the EU over the next weeks anyway. So why not wait for better trial data?

        1. Stuck in Zurich says:

          They haven’t rejected it outright, they have further delayed and dithered and continue searching for the perfect paperwork solution as is the Swiss way (from

          The medical watchdog agency, Swissmedic, on Wednesday announced that it had asked for additional information from the Swedish/British company AstraZeneca about the Oxford/AstraZeneca vaccine before considering giving its approval.

    3. Thomas says:

      Prefereable, Pfizer or Moderna vaccines are used for those above the age of 65. That is not worrying, though a case can be made to use AZ’s for that age group as well. Perhaps no proven efficacy in that age group, but get the jab sooner.

      1. DataWatcher says:

        This is probably a different discussion, but once again the idea is being floated that since the vast majority of infections are being spread by people between the ages of 29 – 49, perhaps a focus on this population for vaccination might not be a bad idea.

        1. Marko says:

          I think the data from Israel will blow that idea out of the water in fairly short order. I hope so, anyway.

      2. A Nonny Mouse says:

        Well, there are 8 million in the UK who are over 70 who have had the AZ jab so it appears that we have wasted a lot of money, time and effort!

        1. DataWatcher says:

          Does it have to be “either”/”or”?

          1. Marko says:

            either/or what?

          2. DataWatcher says:

            “Either” the elderly “or” the younger group. A tiered expansion of eligibility to begin to include some younger cohorts, I think, could have positive results. This, of course, will have to wait until the rollout truly starts “rolling,” which hasn’t quite happened yet. Israel has a well-managed public health system (four govt.-run HMOs) , which we don’t. I think that, even more than the worrisome appearance of the new mutants, probably even more than vaccine resistance, is our main Achilles’ heel.

          3. Marko says:

            OK, so I see you responded to the wrong comment, as I suspected.

            Yes, it is most definitely either/or. In a time of vaccine scarcity you better make the right decision on who to protect first – those at high risk of hospitalization and death or younger , less at-risk cohorts because you think they may transmit more. As I said, I hope the Israel data keeps us from making a blunder here.

            The pandemic can rage to its heart’s content if nobody is getting seriously ill, as far as I’m concerned.

          4. DataWatcher says:

            Actually, I pretty much agree with that (even if “seriously ill” can be a somewhat dodgy concept to define). But it would take a significant paradigm shift on the part of our policy makers to change from focusing on case-positivity rates to seriousness of cases. I realize that hospitalizations and deaths are also part of their equation right now, but numbers of cases also still remain paramount. I don’t think it’s being discussed what should be done, in terms of everything from re-opening economies to eventually loosening things like masking and “distancing” mandates, if hospitalizations/deaths go down to diminishingly low levels while case-positivity rates remain relatively high.

          5. Marko says:

            “I don’t think it’s being discussed what should be done, in terms of everything from re-opening economies to eventually loosening things like masking and “distancing” mandates, if hospitalizations/deaths go down to diminishingly low levels while case-positivity rates remain relatively high.”

            There’s no discussion to be had. If hospitalizations and deaths disappear, you better watch carefully or you’ll get stampeded by the rush to normalcy.

          6. confused says:

            Yeah, right now we care about cases/positivity because it is a leading indicator of future hospitalizations/deaths. If COVID severity drops to “regular respiratory virus” levels after the population’s no longer immuno-naive, there’d be no justifications for any more measures than we use against “regular respiratory virus” (ie, effectively none).

          7. Some idiot says:

            Marko, I get the feeling that you and the chief medical officer here in Denmark would get on well (and I reckon he has been doing a bloody good job, too). Every time the question has come up, he said that the priority was to reduce serious illness and death. Full stop. And that is the criteria used to prioritise vaccinations. First priority is nursing home residents and employees, plus health workers with patient contact. These have now almost completely had their second dose. Next on the list are the oldest, and then at some stage those with other health risk factors.
            Again, he has emphasised all the way through that hospitalisations was the most important number, with infections “interesting” due to their predictive power for hospitalisations. (Again, more or less what you have said…! 😉 ).
            Will be very interesting to follow how the distribution of hospitalisations changes over the next two months. I would guess that by the end of April there will be far fewer older people (as a proportion) hospitalised.
            Incidentally, on Monday, students in 0 to 4th will be going back to school. The State Serum Institute (SSI) released the modelling that this decision was based upon. What I found interesting was the ranges they used for the increased infectivity of the UK variant, which were 40-55-70%, so looks like they reckon it is going to end up on around 50% (in their estimate).

          8. Marko says:

            Denmark has been doing a good job overall vs CoV2 , and their sequencing rate has been phenomenal, especially compared to the paltry rate in the US. I think they’re sequencing virtually every PCR+ now.

            If there are any Danish families out there looking to adopt, I’m available!

          9. Some idiot says:

            Yep, the info on the sequencing said that they would be sequencing every PCR positive “as long as there is material enough” (I have absolutely no idea how high that % would be). But they also now have PCR primers for a number of other point mutations of interest, and are running all PCR positive samples through those as well.

            I’m still keeping an eye out for the next update on their estimate for how much more infective the UK variant is… Hopefully it will be soon…

          10. Chris Phillips says:

            “3.5m doses begged from the EU to give second doses to those that had already had the Pfizer vaccine
            Total number of over 70 to be vaccinated is about 13m
            This means most of the rest will have to use the AZ vaccine as there isn’t anything else at the moment”

            Absurd misinformation.

            In fact Pfizer is under contract to supply 40 million doses to the UK. As I’ve already pointed out, the EU has said it won’t interfere with the fulfilment of existing contracts. Perhaps you are thinking the EU’s word isn’t worth much – with some justification – but after the mess they got themselves into last week I think they will be hesitant to have a second attempt to achieve international pariah status.

          11. JS says:

            “Yep, the info on the sequencing said that they would be sequencing every PCR positive “as long as there is material enough” (I have absolutely no idea how high that % would be).”

            Latest estimate of R from SSI is here:
            They estimate that roughly 70% of samples will be good enough for sequencing.

            For week 3 they have sequenced just over 60% of samples. Click on “Virusvarianter” on top of for daily updates. B.1.1.7 prevalence is steadily increasing.

            A side effect of the large fraction of samples that are sequenced is that in case of apparent reinfections, it will be possibly to compare the original and new sequence on the spot. Many samples are also saved, which may further improve the statistics.

          12. Marko says:

            I’d like to see the Danes start a big matched-cohort prospective study following PCR positives’ clinical outcomes to pin down the mortality increase, if any, due to the UK variant. Right now, when they’re at about 50/50 variant/WT, would be a good time to do it. The UK has so few WT cases left that they can only look retrospectively. It would be harder to get the numbers needed in Denmark than in the UK, of course , with their much lower daily deaths/capita.

            Basically, I’d just like to see some confirmatory data on the mortality increase from somewhere else. It shouldn’t be unique to the UK, barring some subtle differences in the variant.

          13. DataWatcher says:

            Meanwhile, though, predictions continue to look grim — over 630,00 deaths by June, with upwards of 700,000 possible if the new variants become more dominant. A lot of people poo-pooh’d the predictions of upwards of 400,000 by January, but those turned out to be spot-on, so . . .


        2. Bob the (molecule) Builder says:

          I’ve been looking for data on who is getting what in the UK. By age would be great. Where did you get the data from?

          1. A Nonny Mouse says:

            If you were asking on numbers of UK people getting the vaccine, I estimated based on
            0.5m had 2 doses of the Pfizer vaccine so far
            3.5m doses begged from the EU to give second doses to those that had already had the Pfizer vaccine
            Total number of over 70 to be vaccinated is about 13m
            This means most of the rest will have to use the AZ vaccine as there isn’t anything else at the moment; I am sure that this is why they are looking at mixing vaccines.

            My neighbours in their 80s have both had it; one got the Pfizer as she was able to got to our local GP which is one of 6 centres in the local borough. The husband, who cannot leave the house, had the AZ vaccine due to the transportation issues.

          2. JonathanN says:

            A Nonny Mouse appears to be correct. A friend went to a centre and got the Pfizer one, while I had mine at home with my 83-year old mother and it was AZ. She had no adverse reaction to it apart from a sore arm, while I was as sick as a dog for a few days, and had a sore arm. I’m 56.

          3. A Nonny Mouse says:

            It seems that the Pfizer vaccine has been given to 7m in the UK, not the 4 million that I had estimated. 143 deaths, which was about expected given the age of the people.

      3. Jonathan says:

        AZ may have “no proven efficacy” in over-65s, but only in the sense the numbers in the trial weren’t enough to meet statistical confidence on their own. There wasn’t evidence they did worse.

        The reason was the urgency of starting clinical trials, the Oxford lab didn’t want to delay by needing to justify a trial in older individuals to the regulators. They were added later, but by then in smaller numbers.

        However in earlier trials they previously published data showing that there wasn’t a worse antibody response in over-65s. And the current pre-print, while messy in its sub-groups, does include an analysis indicating that clinical efficacy correlates with antibody response. So in that sense it confirms the previous presumption the vaccine will work OK in over-65s.

      4. Ian Malone says:

        The Pfizer vaccine submission had only about 4% of subjects over 75 and doesn’t conclusively show efficacy in that group either. yet people don’t seem to question giving it to over 75s.

        1. Chris Phillips says:

          I think the reason there was a focus on the age question was initially a rather naive speculation that this could be the reason for the apparently increased efficacy of the accidental low dose/standard dose regimen. I say naive because while errors have clearly been made, I don’t think the people analysing the data are so stupid that they would have missed something so obvious.

          Over the past week or two unscrupulous EU politicians trying to divert attention from their own incompetence have taken up the ball and run with it. So now here we are with a lot of people believing something for which there is no strong evidence, only an absence of evidence to the contrary.

      5. A Nonny Mouse says:

        Seeing as the EU is now blocking exports of the Pfizer/Biontec vaccine to non-EU countries (UK included though it seems that Switzerland and Iceland are still token EU countries- Japan has also been hit by this) the UK will have to use the AZ vaccine almost exclusively once the 3.5 million second doses of P/B which have been agreed are received.

        1. Chris Phillips says:

          I don’t think it’s correct that the EU will be blocking exports. They have said they will not prevent contracts being fulfilled. Of course, whether the EU can be trusted in the light of recent events is another matter.

          1. A Nonny Mouse says:

            We have been allowed the 3.5m doses to give a second jab to those who have already had it; after that, who knows. I saw a report that the EU’s decision had lead to problems in Japan as it seems that the EU was supplying them.

          2. A Nonny Mouse says:

            The European Commission has confirmed that it has received and approved one vaccine export request to the UK and two to Canada, since introducing controls.

            Today’s news. I am assuming that this is part of the 3.5m doses agreed.

          3. Chris Phillips says:

            “A Nonny Mouse”

            So the EU has said it will not interfere with contractual obligations, and sure enough it has been approving exports.

            That being the case, what’s the basis for your claim that the EU is going to block the remainder of the vaccines that Pfizer/BioNTech is contracted to provide?

            Sorry, but I don’t feel very tolerant about silly, misleading claims in the situation we’re in now. The EU centrally and some of the governments have been coming out with some almighty crap about vaccines recently. Surely that’s bad enough.

          4. Antibody says:

            @Chris Phillips

            Whoa just one minute. If anyone is “blocking exports” it’s the UK. Supplies of the AZ vaccine made in the UK are not leaving the country, presumably because that’s what the UK government insisted on in the contract. Good job for us that the EU were more generous and didn’t sign contracts with Pfizer insisting the EU got priority for Belgian-made vaccines. Don’t you agree? Sickening vaccine nationalism has been on full display in Blighty this week.

          5. Adam says:

            The EU was sluggish and the UK booked manufacturing capacity. How can you block something that doesn’t have an order or contract?

          6. Chris Phillips says:


            “Whoa just one minute. If anyone is “blocking exports” it’s the UK. Supplies of the AZ vaccine made in the UK are not leaving the country, presumably because that’s what the UK government insisted on in the contract. Good job for us that the EU were more generous and didn’t sign contracts with Pfizer insisting the EU got priority for Belgian-made vaccines. Don’t you agree? Sickening vaccine nationalism has been on full display in Blighty this week.”

            Sorry, but that’s absolutely nonsense. You need to learn what the facts are.

            The UK isn’t blocking exports of anything. The EU is unhappy that AstraZeneca isn’t able to supply what they were contracted to use “reasonable best efforts” to supply from sites within the EU. The contract allowed AZ to supply from elsewhere, though the EU evidently wasn’t keen on that because AZ were obliged to supply from within the EU if possible. But the contract laid no obligation on AZ to supply from outside the EU. Any dispute the EU has is with AZ, not with the UK government, which has taken no action in the matter.

            But the response from the EU has been – if not to block exports – to give itself the wherewithal to block them.

            And the EU has made so many factually false claims about this that people really should be more sceptical about swallowing their propaganda. Fortunately they were stupid enough to publish the contract themselves, which exposed their falsehoods.

            People should be sceptical about incompetent politicians who have screwed up and are trying to divert attention from their own failings. It’s hardly a new phenomenon!

  7. Daniel Barkalow says:

    There’s the possibility on the weekly swab data that it doesn’t reduce the chance of getting infected, but it does mean that people don’t stay infected nearly as long, and that they don’t produce as much virus while they’re infected. I’d think of this less as an N% chance to not get infected as an N% reduction in R.

    1. Chris Phillips says:

      If I understand correctly the typical duration of testing positive is about three weeks, so a reduction in duration shouldn’t mean that weekly swabs miss infections altogether, unless the reduction is really dramatic.

      I think any reduction in duration of infectiousness should be an added bonus on top of the 50-70% reduction in numbers testing positive.

      This should show up in their data (unless people are told to stop swabbing after they have tested positive), but I can’t see any mention of the possibility.

  8. DataWatcher says:

    “I’d think of this less as an N% chance to not get infected as an N% reduction in R.”

    . . . which, especially since the symptoms will almost certainly be much milder, is at least as important, right?

  9. Doug H MD says:

    “So with the numbers we have now, I feel pretty confident that yes, as one would have hoped, these vaccines also reduce transmission of the virus in the population.”
    I don’t think a reduction was ever seriously in doubt, the real question in my mind was do we get sterilizing immunity and the answer to that is certainly not. And so people need to be told to maintain all caution imo

  10. Doug H MD says:

    Meanwhile the data coming out of Israel is open to a variety of interpretations. It seems pretty clear that these vaccines don completely eliminate deaths at least not in the period of time a week or two after the second dose.

    1. Quin says:

      Analysis of Israeli data – preprint just released:

      “While our study cannot accurately estimate the effectiveness of the Pfizer-Biontech vaccine, it suggests that the effectiveness is greater than 50% and that there is a considerable level of prevention of transmission following vaccinations.

    2. Quin says:

      Another Israeli data analysis:

      Bottom line Pfizer real world effectiveness estimate: 66-85% for infection, 87-96% for severe disease.

      1. Marko says:

        A good visualization by the FT showing the impact of the vaccine on the over-60 numbers in Israel :

        1. Marko says:

          Given the high proportion of deaths that occur in the over-60 age group, and the nearly-complete vaccine coverage in that group, the overall death numbers should continue to plummet in Israel. I’d be worried if they fail to do so. I’d be less worried if case counts don’t respond as dramatically, as that could be driven by the under-60s, where vaccine coverage is progressing much more slowly.

  11. Vivaldo says:

    Dear readers, which vaccine would you chose – AZ or J&J and why?

    1. Brian says:

      Given the current supply constraints, I would take whichever one I could get. A pretty good vaccine right now is “almost” certainly better than a somewhat better vaccine two or three months from now. National Public Radio has a pretty good story on their website that touches on that question among other things. See the link for details:

      1. confused says:

        Yeah. They all seem to be extremely good at preventing *severe* illness which is what concerns me, if I get cold/mild flu symptoms well that’s unpleasant for a week and then it’s over.

        However, I might have stronger feelings about getting one of the mRNA ones with higher nominal effectiveness if I were, say, 85 years old.

        1. debinski says:

          Interestingly, Pfizer has among the lowest efficacy rate for severe disease (or possibly the lowest, I don’t have all the numbers). In their efficacy evaluable population, the efficacy rate against severe disease was 66.4% and did not meet their predefined success criterion. Moderna’s was 100%. However, Pfizer only had 4 reported cases of severe COVID in the interim analysis, so this could easily be a fluke. Moderna had 11.

          1. DataWatcher says:

            Any idea why this is so? The two vaccines seem so similar in virtually every other way . . .

          2. Chris Phillips says:

            Doesn’t that just mean that Pfizer had one severe case in the vaccine arm and three in the placebo arm? I don’t believe you can get a meaningful estimate of efficacy from such small numbers.

          3. DataWatcher says:

            Yes, I had the same thought. Very small numbers. That’s part of why I asked — can we trust these data? (Also, self-interest — I’m due for my second Pfizer jab this next Thursday!)

          4. debinski says:

            As mentioned earlier, it is most probably a fluke due to small numbers. No reason to believe Pfizer would have less effect than others (especially Moderna) on serious disease – as far as I know. But it’s all we have right now. I just think it’s interesting that everyone seems to view Pfizer as the gold standard but the efficacy in serious disease has not yet been demonstrated. The 95% confidence interval on the 66.4% efficacy rate was (-124.8, 93.3).

          5. DataWatcher says:

            We’re still waiting for transmissibility data for Pfizer and Moderna, too, although if I’m not mistaken the early indications looked encouraging. I believe Novavax did achieve sterilizing immunity in the early non-human primate trials, while J&J did not. At least arguably, this will be more significant than ever, given the current situation with the proliferation of increasingly contagious, vaccine-resistant, and (probably) virulent mutant strains. For that matter, when/if the transmissibility issue with Oxford/AZ gets sorted out, that could be a major advantage for them, as well.

    2. dearieme says:

      My wife and I got the Pfizer jab because it was the one available virtually instantly.

  12. Marko says:

    With a seductive number, AstraZeneca study fueled hopes that eclipsed its data

    This is nothing more than vaccine-nationalism-inspired gaslighting. Sad to see.

    1. Chris Phillips says:

      Really strange that the article says the finding of a 67% reduction in cases for one dose but only a 49.5% reduction for two dose is “hard to explain”.

      “Biologically how do we explain that? Does that signal that those numbers can not be directly compared?” asked Natalie Dean, a biostatistician focused on vaccines at the University of Florida …

      In fact the numbers with their confidence intervals are 67% (49%, 78%) and 49.5% (37.7%, 59.0%), so probably not a statistically significant difference (particularly if allowance is made for the fact that it was a post hoc analysis).

      My impression is that it’s usually been reported as 50-70%, not just the higher figure.

      1. Marko says:

        Yes, amazing isn’t it?

        And from a biostatistician, yet!

      2. Chris Phillips says:

        But there is something I don’t understand about their analysis.

        For the single-dose group that produced the 67% efficacy figure (Table 2), it seems all the participants were swabbed, so they have simply added the symptomatic and asymptomatic case numbers together.

        But for the two-dose group that produced the lower figure (and actually it should be 54.1% (44.7%, 61.9%) overall for the two-dose group – the 49.5% figure was just for the standard-standard subgroup), only some of the participants were swabbed. In calculating the overall efficacy against infection for two doses, it looks as though they have somehow scaled up the asymptomatic figures to allow for that. I can’t work out how they have done it, and I can’t see any explanation of it. It doesn’t look like a simple overall multiplicative factor. Presumably it is different factors for different subgroups, so it may depend on some assumptions about the variation of efficacy with some other parameter(s).

        If a biostatistician were puzzled about the difference between the efficacies, I would also expect her to notice that there were some demographic differences between the one-dose and two-dose groups (Table S2). The two-dose group was older, more male and less white.

      3. egil says:

        Indeed, people often focus too much on the point or best estimate, but the CI’s will tell you much more. In this case, that there very likely is no difference.

  13. Bill says:

    Anything in this data relevant to the US hesitancy with OxAZ? Is the world being rash or are we sticking to our “tried and true” procedures regardless of cost in lives?

    1. sgcox says:

      As I said before, AZ/Oxford vaccine will not be approved and distributed in USA. It is at no profit during the pandemic phase (as defined by WHO) because of the conditions negotiated by Oxford with AZ. As a result, it is 5-10 times cheaper than current US vaccines and undermine the business model which claims only for-profit can produce efficient medicines. The hostile reception is not surprising. The EU attitude to AZ/Oxford vaccine is likely driven by other, more political reasons.

      1. Tom H says:

        If it will never be approved, why is AstraZeneca running a phase 3 trial in the US?

        1. sgcox says:

          Happy to be proven wrong.
          Plus of being pessimist – you are either proven to be right or get a pleasant surprise.

          1. Tom H says:

            Fair enough, it MAY NOT be approved in the US. I agree that there is a chance of that. It’s just not a done deal yet.

  14. Chris Phillips says:

    The UK has announced a trial to evaluate the efficacy of giving two doses of different vaccines, and varying the interval between them between 4 weeks and 12 weeks. Perm any combination of (1) first vaccine, (2) second vaccine and (3) interval between the doses, to get 8 eight arms. But only 800 participants in total. Beats me how they expect to get anything meaningful out of that:

    1. Marko says:

      I think the assumption there must be that we have the immune “correlates of protection” well in hand, so that smaller studies can give answers without the need for clinical outcomes

      1. Chris Phillips says:

        Yes – on reading it more carefully I see you are right – they are going to look at measured immune responses, not infection rates.

      2. stats guy says:

        On the 12 week vs 4 week results.

        Quoting the linked abstract “exploratory analyses of the impact on immunogenicity and efficacy of extending the interval between priming and booster doses.”

        The results on 12 week separation between doses vs 4 week are exploratory and post-hoc. Couldn’t get to the full article but we don’t know if there are differences in the 2 populations (12 week group vs 4 week group). As with any post-hoc analysis these should be viewed with caution. Needs to be confirmed in a much bigger study.

  15. Richard West says:

    Is not the slow vaccine rollout like taking half the bottle of antibiotic … leading to a stronger rebound of the virus with possible mutations? If they can’t roll it out fast enough, it would be better to pause now and wait until they can vaccinate everyone together or as close as possible … no?

    1. Some idiot says:

      My take on that (out of my field, but just thoughts from listening to experts) is that roll it out as fast as you can, but fully vaccinate the elderly and health workers ASAP. Reducing serious illness and death is the most important, and that all the statistics show that serious illness and death from COVID19 is primarily amongst the elderly. So protect them ASAP in order to reduce the overall severity of the pandemic on society.

      The question as to whether or not that would tend to increase mutations is one I will duck (due to ignorance), but my guess is the answer would be No.

    2. Chris Phillips says:

      I’ll keep asking, then. Why do people think that immunity acquired by vaccination is more likely to encourage mutations than immunity acquired by infection (if that is what they think)?

      1. Darby says:

        It might be that the vaccine presents just one antigen (the spike) that gets targeted, while infection targets multiple ones.

        1. Chris Phillips says:

          Thanks for replying, but why should that in itself be worse? I’m still having trouble understanding the basis of what aspect of less-than-100% immunity is considered to be bad. Particularly given that people seem to have different opinions about which of the two – immunity acquired from vaccines or immunity acquired from infection – approaches 100% more nearly.

    3. AVS-600 says:

      A reasonable concern on its face, but vaccines have two big differences from antibiotics:

      1. The vaccine can be given prophylactically in a way that specifically treats one disease.
      2. Immune escape isn’t something a disease does in response to a vaccine, per se, it’s something a disease does in response to your immune system’s actions.

      The first point means that dosing everyone possible with the vaccine means slowing or halting the spread of the disease. In theory, if you could continually dose humans with a narrow-spectrum antibiotic, you might see the same effect. In practice, antibiotics are always going to cause too many side effects as well as potentially generating resistant strains of bacteria that you *aren’t* trying to target.

      The second point means that you don’t actually get much benefit from not vaccinating. If you vaccinate, the disease might escape from the immune system’s response to the vaccine. If you don’t vaccinate then it will escape in the same way from the immune system’s response to the real coronavirus.

      Overall, the most important factor in immune escape is how quickly the disease spreads and multiplies, because that determines the rate at which it mutates. There is a very good reason there are worrying variants from South Africa and Britain, but none from Australia or Vietnam. We don’t know for sure at this point exactly how much the vaccines will actually stop the transmission of the disease. It’s almost certainly not 100%, but it’s also almost certainly not 0%.

      1. JS says:

        It is not my area of research, but I recall two advantages of vaccines over antibiotics/antivirals:

        3. Vaccines attack the infection earlier, thereby reducing the number of bacteria or virus particles, which in turn means that fewer are able to mutate.

        4. Vaccines typically target multiple sites vs. typically a single site for antibiotics/antivirals. A mutation affecting one site is therefore less likely to propagate, as the other site(s) will still inhibit the replication. That is also the argument for the use of HAART antiviral therapy for HIV.

        “The second point means that you don’t actually get much benefit from not vaccinating. If you vaccinate, the disease might escape from the immune system’s response to the vaccine. If you don’t vaccinate then it will escape in the same way from the immune system’s response to the real coronavirus.”

        The vaccines using spike only may cover fewer sites than a natural infection. As I recall it neutralizing antibodies to the spike bind to only a couple of independent sites, while natural infections also elicit neutralizing antibodies to at least one site on the NTD. Combined with 4. above it might thus be expected that it is easier to escape immunity acquired from a spike-only vaccine than that from a natural infection.

        The scary part is that B.1.351 appears to have mutations close to the site of the NTD where the NTD antibody binds.

        Having said that, it is also possible to make arguments for why a vaccine will do better than natural infection.

        Either way, most of us would probably prefer getting vaccinated over getting infected.

        But as I say it is not my area of research, so take the above with a grain of salt.

        1. Trottelreiner says:

          Also, whatever log-term side effects you might get from the vaccine, like narcolepsy or ither auto-immune diseases due to molecular mimicry, you also get from the infection.

          Which in my book is another advantage of the spike vaccines, we only get antibodies to ONE protein, so the area of attack is smaller than with the full virus.

          Also, some of the spike protein during infection might have switched its configuration, so ADE.

          Please nite, only musings of an amateur virologist/immunologist, and my degree in molecular biology is quite old…

  16. egil says:

    The estimate for VE for asymptomatic cases all have CI’s running in the the negative, and even the estimates for >14 days after second dose and <8 weeks between first and second dose are negative (-11.4% for 11 weeks. All with wide CI’s. To me that indicates we shouldn’t put too much value on the actual estimates. The analysis of VE in asymptomatic cases similarly shows wide CI’s into the negatives. The overall estimate there was 16% for 22 to 90 days, but they have no data for 61-90 days, so they just assume 22-60 = 22-90, but they do give different estimates for 22-30 and 31-60? The 67% reduction you mention is for any PCR+, both symptomatic and asymptomatic. I would argue that data for reduction in asymptomatic cases is very flimsy at best.

  17. Marcus Theory says:

    “In Dr. Johnson’s famous dictionary patriotism is defined as the last resort of a scoundrel. With all due respect to an enlightened but inferior lexicographer I beg to submit it is the first.”
    –Ambrose Bierce, the Devil’s Dictionary

    So maybe immunology is the first resort of this particular scoundrel? 😀

  18. Marko says:

    New data on Oxford/AZ vaccine vs. S.Africa variant :

      1. Doug H MD says:

        smart of them’
        the data coming out of these trails is a complete mess.
        did you see the CIs?

        1. Marko says:

          Yes, it seems that the AZ vaccine doesn’t do much against mild/moderate disease , with no data on hosp/death. It sounds like they’ll use the J&J and Pfizer vaccines for HCWs and other high-risk workers and also do limited rollouts (~100k per) of several vaccines, including AZ, and potentially combos to try to sort out what works best at preventing severe disease vs the variant.

        2. Marko says:

          There’s a good summary of the various vaccine results in this video from ~01:01:00 to ~01:18:00 :

      2. Chris Phillips says:

        Reportedly they are putting it on hold rather than dropping it altogether.

        1. Marko says:

          Yes, they have plans to evaluate several vaccines in limited rollout studies, so AZ still has a shot. Also, I shouldn’t have said the AZ vaccine didn’t do much against mild/moderate disease, the fact is that the confidence intervals were so wide that it’s hard to say what the real effect might be.

          One thing disturbing about the SA video presentation was the mention that there may be a signal of increased disease severity with the SA variant, sounding eerily similar to the early chatter about the UK variant. I hope it’s a false alarm, in both cases.

          1. Chris Phillips says:

            It’s good to hear that there are still studies under way. It would be smart of the rest of the world to flood South Africa with enough vaccines of various kinds to enrol everyone there in the more vulnerable groups in a giant multi-vaccine trial to clarify the situation. The UK is fighting tooth and nail to try to stop transmission of the SA variant, but realistically that can be only a delaying tactic.

            But the world hasn’t shown very much smartness so far, and I don’t suppose it will happen.

      3. Chris Phillips says:

        Shabir Madhi of the University of Witwatersrand is quoted as saying that infections were 22% lower in the vaccinated group, which was not statistically significant.

        1. Chris Phillips says:

          But he seems to have told the BBC it’s only 10%.

          The quality of communication doesn’t seem to improve.

          1. Marko says:

            You can see where the two figures are coming from in this slide from yesterday’s presentation :


            The 22% measures efficacy against all strains, while the 10% refers only to events involving the variant. The difference is rather meaningless, given the wide CI ranges and the fact that only a few infections in the placebo arm involved non-variant strains. It’s too bad the trial wasn’t bigger in SA.

          2. Chris Phillips says:

            Thanks. That would explain it.

            It certainly doesn’t look good, though quoting these efficacy figures without a confidence interval is ridiculous. It seems the difference between 10% and 22% was down to just 5 participants out of about 1500, who were in the all-variants group but not the B1.351 group. (Though I don’t understand what that means. For the 3 extra ones in the vaccine group, who all got infected, presumably they couldn’t determine whether it was the new variant. But for the 2 in the placebo group?)

            The AstraZeneca data as a whole seem to be turning into an object lesson in how not to conduct and report clinical trials.

          3. Chris Phillips says:

            I should have said “but for the two in the placebo group, who didn’t get infected?”

            If they didn’t get infected, why doesn’t it also count as protection against the new variant specifically, and not just against COVID-19 in general?

  19. DataWatcher says:

    This is probably more appropriate for a different thread, but I’m wondering what people think about the two new therapeutics being tested in Israel right now: EXO-CD24 (currently in Phase 1 trials) and Allocetra (currently in Phase 2). Preliminary findings look encouraging, but of course it’s still really early in the game. Is there a possibility that one or both of these could prove to have actual game-changing potential? And if so, what might the timeline be?

    For all the hoopla over Aeronabs a few months ago, they seem to have faded from our radar screens, leaving one skeptical about breathless news reports of potential “miracle cures” like this. Nonetheless . . .

  20. michael888 says:

    Covid-19 is essentially a disease of the Elderly. Globally the median age of death is 82, which means that over half of deaths are in this age group. 95% of deaths are reportedly in those over age 60. Nature published end of the summer that if you are under age 50, even with co-morbidities, you have almost zero chance of dying from Covid-19. (The CDC’s numbers seem slightly different from the rest of the world, and the format of their demographics tables have changed since the Spring, as has their grouping of Covid-19, pneumonia and influenza data. Hard to believe 10,600 people work there).
    A major deficiency in all the studies is the relative lack of vulnerable populations. I vaguely remember the median age in Pfizer’s clinical trial being 52, exactly 30 years younger than the median age for Covid-19 victims. Frankly the only data that really matter are those from those over age 80 (half the vulnerable) and those over 60 (along with those with cancers and renal failure, most of the other 50%). Yet these data seem largely missing. (Also note that for Flu the Elderly receive quad doses; we have no idea if that is necessary for protection from Covid-19 in the Elderly). Having worked in Pharma, we know why. Studies on the young and healthy, not at risk from Covid-19, are not affected by deaths. Almost all the Covid-19 deaths (476,416 in the US today) are in the Elderly (95% of today’s total is over 450,000 of total deaths). The Elderly (over 65) die at the rate of 2.2 million per year, and of the present 450,000 Elderly dead almost all will be among the 6.6 million who will die over the next three years. When someone dies from Covid-19, that invariably pumps up and hypes the numbers; when the elderly die from a vaccination: “that is expected. These people are old”. These Vulnerable MIGHT get an extension of their lives with vaccinations, and the risk: benefit favors it for them. However it’s stupid for most non-vulnerable to be vaccinated.

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