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Johnson and Johnson, SinoVac and More

We have some more data on the vaccine front that’s worth looking at. J&J has published a bit more on their trials of their adenovirus-vector candidate, with data on the immunogenicity of the vaccine in patients. They have several cohorts evaluated: a single shot of low dose, single shot of high dose, two shots of low dose and two shots of high dose. This article at STAT sums it up: it’s clear that the vaccine generates neutralizing antibodies at both low and high doses, that the higher doses do indeed tend to give higher antibody levels, that the two-dose regime leads to higher antibody titers overall, and that these titer rise over time (present at day 29 after injection and actually higher at day 57).

So far, so good. But what we still don’t know are the correlates of protection: which of these antibody levels are enough to keep a person from getting the coronavirus and to what extent? The same goes, of course, for the T-cell data. The paper shows levels of both CD4+ and CD8+ T cells after vaccination, but how these relate to protection is an open question. And for all of these, such numbers might be different in different patient groups (particularly older versus younger patients). Fortunately, we should soon (within two weeks, I’d say) be getting actual efficacy data from the single-dose trial, so I’m not going to spend much energy speculating.

There’s another thing to watch: the New York Times reported yesterday that J&J has told the US government that they might have fallen as much as two months behind on their production schedule for the vaccine. No word as to what the problem might be. Adenovirus vectors have vulnerabilities of their own, with a whole set of manufacturing steps that are distinct from the other types. What you gain in not having everything reliant on a single pathway, you can lose when unique problems crop up. But overall it’s still far better to have a diverse set of things under development than not.

Now for another vaccine candidate, the inactivated virus one from SinoVac. I discussed that one here after an earlier publication, and when last heard from there was an odd report from Turkey of 90% efficacy in a small trial with no data to back it up. Then just a few days ago there was a figure of 78% efficacy from the trial in Brazil, but that has now been revised to 50%. Meanwhile, Indonesia says that a preliminary analysis shows about 65% efficacy – the government there has approved the vaccine, but the rollout is apparently not going well. To be honest, these are about the efficacy numbers one could expect from an inactivated-virus vaccine. It’s an old technology, and it doesn’t always work that well. The chaotic release of these data (and the lack of comment from SinoVac themselves about any of these numbers) does not build confidence, with the consequences that you can see in that last link.

But that takes us back around to what the true efficacy of another vaccine is: the Oxford/AZ one. The statistics on that are a mess too, and their public presentation has been a mess, and we can only hope that things come into better focus when their US trial reports (other data are coming as well). But at the moment, I wouldn’t be prepared to put money on how much better it is than the SinoVac one. To be sure, a 50% or 60% effective vaccine (with a reasonable safety profile) is surely better than no vaccine at all. But it means that you have to vaccinate a lot more people before you start to make a dent in a pandemic like this one, which is a significant real-world limitation. Of course, here in the US we’re not doing that great a job in rolling out the 95% effective ones, either, if we want to talk real world effects!

Update: let’s compare these numbers with the immunity that a person can get from just being infected with the coronavirus itself. That’s been a matter for speculation, but we now have some numbers from the NHS in the UK. In their SIREN study they’ve been looking at a large cohort of health care workers, monitoring them for infections and antibodies. Out of over six thousand who have had the virus, there have been about 42 re-infections. Comparing that to the cohort of people who were never infected, that comes out to 83% efficacy. So there’s your comparison number – which means that being vaccinated with either of the mRNA agents provides better protection than being infected with the real coronavirus can.

164 comments on “Johnson and Johnson, SinoVac and More”

  1. Elliott says:

    I just tried posting this in an earlier discussion but it deserves repeating here. I subscribe to an expert-written newsletter (FDAMap) which reported today that the CanSino vaccine trial results are highly unreliable. The Chinese ran multiple independent trials with different agenda and got variable results. To quote the report: “The Chinese manufacturer seems to be constantly trying to control the interpretation of the data from its different partners and the result is a mishmash of irreconcilable reports.”

    The report concludes that the EU and US are unlikely to approve this vaccine. The 50.4% avg effectiveness number is probably rather dubious. Ouch.

  2. Adrian says:

    Derek, I am wondering how much of this is comparing apples with oranges.

    From the article you linked:
    ‘While officials had asserted last week that the vaccine provided absolute protection against moderate to severe symptoms, they had not disclosed another group who had “very mild” infections despite having been vaccinated.’

    It all depends on what “very mild” actually means.

    At the moment, I wouldn’t be prepared to put money on the vaccines already approved in the US to beat preventing 50% of all infections.

    And this New York Times article is clearly getting the facts wrong when citing the 95% efficacy of the vaccines approved in the US against severe COVID-19 in a section that talks about herd immunity.

    1. Adrian says:

      95% efficacy of the vaccines approved in the US against ***symptomatic*** COVID-19

    2. A Nonny Mouse says:

      Totally agree with you; I am trying to find an article that I read where many of the Moderna people had actually caught the virus but were asymptomatic and so weren’t actually counted.

      The A-Z people did a lot more PCR work and so caught the ones who were asymptomatic.

      1. cynical1 says:

        How do they know they caught the virus if they were not testing asymptomatic patients along the way in the trial? Did they later test the participants for nucleocapsid antibodies? (I’m guessing anybody in the vaccine group would test positive for the spike antibodies based on the mechanism of the vaccine.)

        1. debinski says:

          Both Moderna and Pfizer trials test periodically for nucleocapsid antibodies. “Asymptomatic COVID” is a tertiary endpoint of the trials. I don’t believe any of these data have been published yet and did not appear in the FDA briefing documents.

          1. WH says:

            I’m not sure how they’re controlling for it, but there’s a lot of cross-reactivity of anti-nucleocapsid antibodies across the seasonal coronaviruses and SARS-CoV-2.

      2. bamboozled says:

        in fact, the AZ trial may have biased against showing efficacy against “symptomatic” covid because participants were swabbed weekly and would often have known they were PCR positive (swab positives were asked to isolate by T&T) before developing symptoms. I guess you’re more likely to report a symptom if you already know you have covid. As far as I am aware, neither Pfizer nor moderna did this.

    3. ghyu says:

      Exactly. The director of the Brazilian study claimed that “Other studies did not include as a case [of infection] two days of a headache”.

      If you look at the Moderna protocol, you’ll find that he’s actually correct in making that assertion. In there it says:

      • The participant must have experienced at least TWO of the following systemic symptoms: Fever (≥ 38ºC), chills, myalgia, headache, sore throat, new olfactory and taste disorder(s), OR
      • The participant must have experienced at least ONE of the following respiratory signs/symptoms: cough, shortness of breath or difficulty breathing, OR clinical or radiographical evidence of pneumonia;

      So unless you believe the Butantan institute is lying (if they are, they’re doing it very badly!), someone with just a headache would be counted as a symptomatic case in their study but wouldn’t be counted in the Moderna study.

    4. Jen Herman says:

      Completely agree. We don’t have data regarding efficacy of the mRNA vaccines w/respect to reducing hospitalizations or mortality. The phase III trials were not designed to address most important questions. We should be more skeptical of 95% vs. 50% and yet…

  3. Philip says:

    Question to those that know more than I do. Given the choice would you get the SinoVac vaccine or just one dose of the Moderna vaccine with the second dose delayed six months?

    Keep in mind that the FDA briefing documents for the Moderna vaccine showed a 92.1% efficacy (95% CI: 68.8%-99.1%) for 14 days after one dose. I would go with the Moderna vaccine, but I am just a computer programmer, not a medical professional.

    1. Smokerr says:

      The medical professionals are disagreeing!

      I have a Naturopath (sp?) niece and she is anti vaccine though she hides it behind cherry picked data.

      We do the best we can with what we have.

      Amazingly our school district is running the best vaccine operation (Moderna) in the city or state. My wife and I got vaccinated today on a walk in basis (getting the appointment system to work was impossible which is in line with states dumping setup onto health care providers instead of one good functioning site you have hundreds that are crappy)

      We are per-scheduled for the next shot with cards to ensure that anyone knows what vaccine we got. If there is a shortage we can make a determination of what to do.

      Probably 50% were walk in, we got it via word of mouth and took a chance.

      My 90+ mother in another state and assisted living does not get her first one till next week, go figure.

    2. jim jeffery says:

      Hey Phillip, Similar to your comment, I am just a mathematician. I am also an 80 year old Covid survivor who thanks to Florida Governor de Santis pushing out the Moderna vaccine to all our PUBLIX Grocery chain’s Pharmacies, my wife and I were able to go on-line to register and received the first shot the next day! Mathematically, the 2 shot Moderna vaccine is by far the highest efficacy of all the vaccines currently available. It did cause shoulder soreness for both of us for a few days and Publix Pharmacy misread the CDC guidelines with regard to wait times before administering shots to Covid survivors and at first refused to give me my injection. I downloaded the official CDC guideline and proved to them that their 90 day wait time was in error. The actual wait time is only 14 days as it is defined as “following the completion of at-home quarantine period” which is 14 days! Even Fauci is giving out false info this morning apparently to encourage African patients to take the low efficacy Johnson/Johnson product!

  4. Dale says:

    Hey Derek,
    I know you’re busy but just a friendly reminder that I think a lot of folks would love any background info you could provide on vaccine approvals for pregnant women, children, etc. What that typically looks like… Thanks.

  5. GamingBuck says:

    Derek, minor typo. You’re missing an open paren in:
    “Fortunately, we should soon within two weeks, I’d say) “

  6. Ross Presser says:

    Is it conceivable that efficacy of a vaccine could vary significantly from one country to the next, due to varying populations? Could that ever be positively known without even more trials?

    1. Smokerr says:

      Possibly yes. Japan previously had an issue with a vaccine that was too strong for its smaller stature (generally) people and there were deaths.

      China vaccines could be two weak for some populations as well as possible ethnic variations and that does not cover the propaganda aspect.

      1. Differences in safety profile down to ethnic difference?- vaccines being “too strong” or “two weak” [sic]. Care to provide some evidence to back up this nonsense?

    2. aairfccha says:

      Efficiacy of BCG apparently goes down the closer you get to the equator, but to my knowledge the reason isn’t really known.

      1. Alexander Yule says:

        BCG efficacy (particularly in adults) is indeed highly variable between countries, but nothing to do with geography. Exposure to non-TB mycobacteria (the so-called “masking effect”) has been shown to compromise BCG efficacy. Not all BCG vaccines are the same with respect to the M.bovis strain and differences in the method of culture are thought to contribute to variability.

  7. Marko says:

    ” So there’s your comparison number – which means that being vaccinated with either of the mRNA agents provides better protection than being infected with the real coronavirus can.”

    You’re comparing apples and oranges , and with a very predictable bias. The reinfections in the UK study were detected by regular PCR and antibody assays, not by reporting of symptoms as was done in the vaccine studies. They could have been predominantly asymptomatic, for all we know. Additionally, the reinfections that were detected occurred after an average of 5 months, compared to the much shorter average period of protection that could be inferred from the mRNA vaccine studies.

    Taken together, my current bet would be that natural immunity provides better, not worse, protection than the vaccines. That could change as more long-term data accrues, of course.

    1. x says:

      Given how the immune system selects and develops antibodies, I don’t think you can say one way or the other whether natural immunity (which can target inappropriate epitopes) or vaccination with mRNA that just produces spike proteins will be more effective. Arguments could be made either way and, of course, individual outcomes would depend partly on individual variation (no two people get exactly the same “starter pack” of antibodies, nor will they necessarily develop the same variants).

      1. Tony M says:

        You may be interested in “Information for Healthcare Professionals on COVID-19 Vaccine AstraZeneca” Source:

        They present a table on “SARS CoV-2 S-binding antibody response to COVID-19 Vaccine AstraZeneca ”
        …………………………………………Level (GMT)
        Baseline ………………………………..57.18
        28 days after dose 1………………8,386.46
        28 days after dose 2……………..29,034.,74*

        * ranges from 22,222.74 for dose interval 12 weeks

        The interesting point is it then says that “In participants with serological evidence of prior SARS CoV 2 infection at baseline (GMT=13,137.97), S antibody titres peaked 28 days after dose 1 (GMT=175,120.84)”.

        I note: baseline SARS CoV-2 S-binding antibody response for prior infection was greater than the level achieved for no prior infection one dose but less than the level achieved for two doses. However, the level achieved by those who had prior infections 28 days after 1 dose was nearly 3 x higher than the highest achieved 28 days after 2 doses!

        I am not a medical professional but considered the above point may be note worthy.


        1. Tony M says:

          Should say:

          * ranges from 22,222.74 for dose interval less than 6 weeks to 63,181.59 for dose interval greater than 12 weeks”

          1. DJK says:

            This is very interesting. The numbers do not bode well for the J & J vaccine. The antibody levels for the Oxford vaccine seems stronger than the J& J. Would anyone with more expertise like to comment?

    2. Jim Ancona says:

      Yes, Derek you should really restate that last update paragraph. As I understand it, we have no information about whether the mRNA vaccines prevent asymptomatic infection or transmission. So using the SIREN study to compare “efficacy” is just wrong.

      While I’m at it, why is every expert talking about herd immunity using the vaccines? Herd immunity is only possible if they prevent infection or transmission, correct? I certainly hope they do at least reduce transmission enough to get R below 1, but until we know that the only benefit we can be sure of is the reduction in symptomatic and especially severe disease.

    3. Anon says:

      According to the UK SIREN study linked by Derek: “Of the 44 potential reinfections identified by the study, 2 were designated ‘probable’ and 42 ‘possible’, based on the amount of confirmatory evidence available. If all 44 cases were confirmed, it would represent an 83% rate of protection from reinfection, while if only the 2 ‘probable’ reinfections were confirmed, the rate would be 99%. Further research is ongoing to clarify this range.”

    4. Doug H MD says:

      what is that bet based on Marko?

      1. Marko says:

        It’s based on the limited data we have so far, as I said above. We don’t have a clue about vaccine efficacy from time points of 5-6 months post-vaccination like we do for natural infection/reinfection, for which we at least have this study and the earlier study in UK health care workers, both of which suggest the “efficacy” of natural infection could be comparable to the vaccines’ efficacy that was calculated over shorter time frames.

        Additionally we have the experience from MERS, SARS, and common cold coronavirues regarding longevity of immune response. For vaccines, all we have is the Moderna CEO bragging that his vaccine will last a year, without showing us the data. I’m just taking the safer bet at this moment. If new data so advises, I’ll change my bet.

        1. Marko says:

          BTW, on another bet I’d make right now, watch the data out of Israel in coming weeks. They’re measuring vaccine efficacy on-the-ground, among the general population, not among clinical trial participants. My bet is that the numbers come in at less than the 94% promised, perhaps substantially so.

    5. Mandark says:

      Marko, the “efficacy of infection” against symptomatic reinfection was also reported as 0.94 (strictly speaking, the adjusted OR of 0.06 was reported in the article linked below, but they calculate protection against reinfection as 1 minus OR). So the number itself is comparable with the efficacy RNA vaccines.

      What makes these values not comparable in my eyes is that the SIREN study used odds while the vaccine trials used rates. These two measures are very different.

      1. Marko says:

        Thanks, I hadn’t seen the BMJ piece.

        It’s funny. Before, people complained that there was too much breathless reporting in the medical and popular press based on preprints , which are not peer-reviewed. Now we’re getting breathless reporting based on rumors of not-yet-published preprints. Next, I suppose, the reporters will simply make up their own numbers – no peer-review, no preprint, no nothing.

  8. azt says:

    What plausible mechanism would there be for a vaccine being more effective at preventing the second infection than the virus? The viral infection must surely be more effective as the real virus has presented more proteins than just the spike vaccine.

    1. dr2chase says:

      My homeopathically-informed-opinion is that in a natural infection, which proteins end up on our immune-system’s no-fly list can vary; we might end up immune to proteins that are not as essential to the virus as the spike protein, or that might even cause ADE.

      1. Steph says:

        Great point–thank you for this. Still studying to decide whether or not to get vaccinated.

        1. dr2chase says:

          I cannot imagine why you would not get a vaccine. The vaccine risk is truly tiny (especially with mRNA vax — there are so few moving parts there, each has a particular purpose), Covid risk is not that tiny, and we have only a vague idea of the long-term effects of Covid infection.

          1. eyesoars says:

            We do have some knowledge, and they are not good. A large fraction of those hospitalized (more than 1/3) have clotting abnormalities, often with damage to the heart, lungs, brain, and kidneys. There are increased risks of stroke, heart-attack, etc.. Lung function/capacity is typically much reduced, often with considerable lung scarring, even in many who don’t report breathing issues.

    2. MP says:

      There are also great examples in which the virus actively works to subvert the immune response.

    3. Charles H. says:

      I can see two plausible mechanisms.
      1) The vaccine only creates immune reaction to one fraction of the virus, which under selection pressure evolves to be resistant. The virus induced immunity creates immune reaction to multiple parts of the virus, which is harder to evolve away from.
      2) The vaccine only stimulates certain parts of the immune system, which quickly forget the immunity when no longer threatened. The virus stimulates much more sections of the immune system, parts of which retain a memory.

      N.B.: Don’t believe either of those choices, but those are ways that the vaccine could create a weaker or more temporary immunity than an actual case of the virus. One could equivalently construct scenarios where the vaccine was more effective.

      1. Marko says:

        Agreed, and along the same lines, if you really wanted to fairly compare they respective immunities head-to-head, you’d compare the immunity conferred by a 2-dose vaccine to that conferred by a primary infection plus a reinfection, i.e. natural immunity with a “booster”.

  9. Anon says:

    Derek: We should also have a discussion on India’s Bharat Biotech vaccine (Covaxin) efforts that they claim shows good efficacy! But the numbers are all over and as such no one knows where this is headed. They claim that they have some initial scientific information out there, but these are as dubious as China’s SinoVac.

  10. Probable vs Possible? says:

    It mentions that 2 are “probable” and the rest are “possible.” Does anyone know what the difference is between the two?

    1. Marko says:

      None of the reinfections had been PCR tested for their first infection. They were detected upon recruitment for the study via seropositivity. The two “probable” cases were the ones that reported having COVID-consistent symptoms for their first infection, during the first wave in the UK.

      1. Mariner says:

        The question there is what the symptoms for the ‘possible’ infections actually were. If somebody had a regular cold symptoms/sore throat/runny nose, was this classified as a ‘possible’ infection? Difficult to say as the range of symptoms goes all the way from completely asymptomatic through to serious illness and death. I’d personally suspect that some of the ‘suspected’ cases might not have previously had Covid-19 which would improve the numbers somewhat, but who really knows at this point?

        The media in the UK, of course, is breathlessly reporting these results as absolute fact. Just as they do with every other story based on incomplete data.

      2. Chris Phillips says:

        Are you sure that’s the defining distinction? I don’t find the page Derek linked to very clear on that point. If the doubt related to whether those who tested positive for antibodies had really been infected previously, I don’t see why there should be such a large scope for uncertainty, unless there was a huge false positive rate in the antibody testing.

        1. Marko says:

          No , I’m not sure. That’s just the interpretation that makes a bit of sense to me. I agree that the PHE report is very fuzzy.

          I’d think the antibody seropositivity should be fairly definitive, if they required positives on both the spike and nucleocapsid assays, or even if only spike was positive as long as it was S1-specific. I hope the preprint, when published, clears things up.

          1. Marko says:

            Looked into this a little. Here’s what the preprint on the SIREN protocol says :

            “…At enrolment, all participants will have their serum re-tested by PHE for antibodies to SARS CoV-2, including the Roche Elecsys Anti-SARS-CoV-2 spike (S) and nucleocapsid (N)
            protein assays(16) and additional in-house assays to examine for neutralising antibody.
            Individuals will be classified as seropositive or seronegative based on PHE antibody testing
            for N and S. ”


            The Roche antibody assays have low false-positive rates, on the order of 1 or 2 per 1000, so I doubt the “probable” vs “possible” distinction is very significant.

  11. Steve Scott says:

    It should be noted that the initial J&J Phase III trial includes two different dose levels and one shot. However, J&J is conducting a parallel Phase III trial with two shots 57 days apart. Enrollment of 30,000 volunteers began Nov. 15.
    Interpret all this as you will.

  12. GD says:

    Sinopharm has 79% efficacy based on their release. Whilst it’s also an inactivated vaccine, does the fact that it’s been approved by the Chinese regulators (in addition to regulators in other countries) show that Sinovac’s lower efficacy isn’t necessarily because it uses the inactivated virus?

  13. Bill says:

    OxAZ has been given to millions of people now. I presume the majority are single dose, 2nd dose pending, as that was the UK plan. Does anyone track the ongoing apparent results? Have OxAZ+7-day people disappeared from the hospitals as was predicted?

    1. Adrian says:

      It is far too early for seeing any effects of that.

      It takes 1-2 weeks from infection to hospitalization, so any positive effect on hospitalizations of OxAZ+7-day people would start 1-2 weeks after OxAZ+7-day.

      That’s 2-3 weeks after the first shot.

      3 weeks ago (Christmas) no country had approved OxAZ.

      Any measurable effects of OxAZ (or any other vaccinations done in January) on hospitalizations and deaths would start in February/March.

      1. Bill says:

        Yeah, I don’t know what their mix of vaccines has been but Pfizer got it’s UK EUA on 2 December. So some people might be 5 to 6 weeks out. If they administered soon after EUA.

        1. Adrian says:

          You were talking about the Oxford vaccine, not the Pfitzer one.
          Different vaccines, with different protection.

          It is far too early for having any reliable data for the effects of the few vaccinations in December.
          This kind of data is similar to what the Phase III trials produced for two shot dosage.
          Sufficient data for publishing of Phase III data was available after 4-6 months, don’t expect a reliable answer to your question before Easter.

          1. Chris Phillips says:

            Or perhaps ever, given the difficulty of estimating efficacy without a randomised study with a control group.

            It strikes me that after the Phase III results we’re not much closer to being able to make a quantitative comparison between the efficacies of the different vaccines than we were after Phase II, because of the different criteria being used for infection/severity.

          2. Adrian says:

            On hospitalizations (and even more on ICU usage and deaths) all vaccines are having pretty strong numbers.

            If everyone 70+ in the UK had a first shot between December and February, the share of people of this age group in hospital and in the daily deaths for COVID-19 should be much lower around Easter than it is today.

          3. Bill says:

            Adrian, you take things pretty literally. AFAIK, all the current vaccines are believed (not proven) to largely eliminate hospitalizations after one dose…and appropriate activation time.

            Since many people have received one dose starting as long as 6 weeks ago, I want to know if anyone is following their response wrt hospitalizations? I believe all the trial results supported that, but I only saw second hand information. And I’ve heard nothing about early EUA vax results in that regard.

          4. Adrian says:

            > Adrian, you take things pretty literally. AFAIK, all the current vaccines are believed (not proven) to largely eliminate hospitalizations after one dose…and appropriate activation time.

            Bill, don’t assume that data from one vaccine would be applicable to other vaccines, and proving it for one vaccine would not automatically prove it for other vaccines.

            > Since many people have received one dose starting as long as 6 weeks ago

            It’s more like “few people” and “as short as”.
            The UK had only around 400k people vaccinated 3 weeks ago, these were staff and residents of care homes.

          5. Chris Phillips says:


            The figures were about double that – 633,000 by 20 December and 954,000 by 27 December. Also, it’s not correct that only residents and staff of care homes had been vaccinated three weeks ago. In fact I believe that – although care homes were meant to be top of the list – they initially prioritised other groups because of logistical issues. (I know one of my neighbours was vaccinated nearly four weeks ago.)

  14. Marko says:

    Prof Eleanor Riley, Professor of Immunology and Infectious Disease, University of Edinburgh, said:

    “The take home message from this study is that a primary infection with SARS-CoV-2 provides at least 94% protection against symptomatic reinfection for at least 5 months. This suggests that natural infection provides short term protection against Covid-19 that is very similar to that conferred by vaccination.

    “Importantly, natural infection induces approx. 75% protection against asymptomatic reinfection, suggesting that people who have recovered from SARS-Cov-2 infection are much less likely to transmit the virus to others….”

    Other “expert” takes at the link. The sense I get is that most everyone is confused as hell about what this study says regarding the relative protection provided by vaccines vs natural infection. The fact is, it’s too early, and we have too little data, to say so definitively.

  15. Ivan says:

    First things first, a non expert here, my field is far away from the discussions here.

    But this study here
    6-month SARS-CoV-2 antibody persistency in a Tyrolian COVID-19 cohort

    seems to me is in a bit of a contrast to one at the end of the text
    Past COVID-19 infection provides some immunity but people may still carry and transmit virus

    Here is an interview wit the author also

    The title reads (by Google translator)

    Corona antibody studies prove constant, stable immunity

    A study carried out at the Innsbruck University Clinic comes to the
    conclusion that those who have recovered from corona have stable long-term
    immunity. The results are consistent with international findings. Furthermore,
    there is no need to worry about repeated infection, mutations or transmission
    by the immune system, explained study leader Florian Deisenhammer in an APA


    Text in German:
    “Sinnvoll wäre es, wenn diejenigen, die sich impfen lassen wollen, zunächst
    auf bereits vorhandene Antikörper getestet werden”, stellte Deisenhammer klar,
    “in aller Regel ist die durchgemachte Erkrankung aus Immunisierungssicht viel
    wirksamer als eine Impfung”

    My translation to English

    Deisenhammer made it clear that “It would make sense to first test those who
    want to be vaccinated for existing antibodies”, “usually having already gone
    through the disease is much more effective than a vaccination from an immunization
    point of view”.

  16. Lorenzo Lucchini says:

    Any commentary on the adverse reactions encountered in J&J? I’ve seen there are a LOT of grade 3 reactions, especially in people under 55 taking the single-shot high-dose version (at 20%), but also at the lower dose (9%).

    This means 20% and 9% respectively had an adverse event bad enough to be hospitalized or to be disabling for an amount of time, isn’t that the definition?

    It seems like a lot unless I’m getting something wrong, both in terms of being just unacceptably too much, and in terms of being worse than the mRNA vaccines we have now…

    1. Roland says:

      The three most common grade 3 were:
      Fever ’39-40C / 102.1-104F’
      Headache ‘Significant; any use of narcotic pain reliever or prevents daily activity’
      Fatigue ‘Significant; prevents daily activity’

      Hospitalisation is grade 4 and there were none of those. (Actually one fever was hospitalised briefly but apparently not in the temp range for grade 4). Other serious adverse events were deemed unrelated to the vaccine.

    2. A Nonny Mouse says:

      My son (23) had the Pfizer dose and his arm was very bad for a day and he suffered fatigue.

      The younger immune response is the cause- plus, for him, he already had antibodies and suspects that he had already had it (fatigue for a day, about 2 days after I was the same).

    3. debinski says:

      J&J’s phase 3 protocols use the lower dose only (5×10^10 viral particles).

  17. Michael says:

    “Out of over six thousand who have had the virus, there have been about 42 re-infections. Comparing that to the cohort of people who were never infected, that comes out to 83% efficacy.”

    This is probably a bit pessimistic because it’s not independent and not blinded. E.g. people who are more prone to take risks were likely more prone to be exposed for both the first and the second infection… and if they took their past infected status as evidence they are now immune and took even more risk, then it’s even more skewed.

    1. A Nonny Mouse says:

      They are healthcare workers, so of course they are taking more risks. They ought, though, to have decent PPE.

  18. ghyu says:

    Are the numbers really comparable? The Brazilian institute studying the SinoVac vaccine complained that very light symptoms like headaches weren’t counted as cases in the Pfizer or Moderna trials. If you look at the definition of a covid19 case in the Moderna protocol it says that you need to have two mild symptoms for two days or one more severe symptom plus confirmation by a PCR test. The 78% efficacy for SinoVac was calculated excluding those with very mild symptoms, so this is the number that’s equivalent to Moderna’s 94%.

    1. Doug H MD says:

      exactly. apples to oranges. side by side trials alone would resolve this

  19. E Ray says:

    The data I’ve seen from J&J doesn’t look much better than the mRNA vaccines, so I wonder how it was always assumed that J&J’s could potentially be a 1-shot vaccine, while the mRNA vaccines were always assumed to be a 2-shot vaccine. One of the mRNA companies released a graph of total cases in placebo and vaccine arms, which steadily rises together until about a week after the first shot of the vaccine, at which point it mostly levels off, and no difference is observable after the 2nd shot 3 weeks later. So it would appear that the mRNA shots likely are quite effective after just one dose as well, but of course there is no full clinical study data to back that up…

    1. A Nonny Mouse says:

      Being conducted on the UK population as we speak!

  20. peter waldo says:

    Vaccine efficacy in the ‘real world’ may never be truly known or agreed upon given the hard to quantify & measure dynamics in a real life setting (i.e, “vaxed spreader” vs. previously infected/recovered & re-infected spreader w/o symptoms!). Unfortunately, lost in the “fog” of rollout are some concerning initial AE safety signals. Combining both mRNA vaccine treatment numbers (just to characterize based on the n we have with a new platform technology) you have a relative risk number of 6.9 for developing idiopathic Bell’s Palsy in the vaccine group. The AAO-HHS’s press statement in support of FDA emergency approval stated that since the overall idiopathic facial paralysis rate per 100,000 is around 15 – 30, the combined trials’ incidence of 17.7 was acceptable, thought the incidence was “greater than expected”, but not a causal relationship at this point and that the FDA “should do active surveillance with deployment of the vaccine into larger populations”. Ho hum.

    1. Sc says:

      I wonder where this weird FUD about mrna vaccines is coming from all of the sudden. Two brand new commenters just showing up out of the blue.

      1. Peter Waldo says:

        Instead of speaking to the substantive gaps, questions and concerns being raised you’re suddenly uncomfortable, reacting with an ad hominem, that’s from a place of fear and uncertainty? Let’s seek to gain clarity and answer meaningful, important questions, even if the answers may make us uncomfortable.

        1. Sc says:

          Trying to spin background rates of bell’s palsy into a “substantive concern” strains credulity IMO.

  21. Crni says:

    Can someone explain the math to me please? I just can’t get to the 83% number.

    If 20,787 healthcare workers were tested and 6,614 of these participants tested positive for COVID-19 antibodies upon recruitment, that is an attack rate of 32%. One would expect 2104 to get re-infected if there is no protection. Only 44 got re-infected. That’s 2% of the expected number so 98% protection no? What am I missing?

    1. Chris Phillips says:

      Actually, I can’t get to 83% either. I don’t think the government press release Derek linked to contains the data that would be needed to estimate an efficacy rate.

      But a Nature article on the same study entitled “COVID reinfections are unusual — but could still help the virus to spread” says there were 318 infections among the “14,000” (actually 14,173 by my reckoning) who were initially negative according to antibody tests. That is by comparison with 44 infections among the 6614 who initially tested positive for antibodies.

      That means an infection rate of 0.67% among those previously infected, and 2.24% among those not.

      Maybe I’m missing something. One report I saw said that these data had been published in a preprint, but I haven’t been able to find it. It would be nice to know!

      1. Chris Phillips says:

        I had the temerity to enquire to the press office about the calculation, and had a prompt response saying a preprint should appear at medRxiv in the next day or so, including a detailed explanation of the methodology.

  22. Jonas says:

    The Brazilian study is a joke. Two days of diarrhea are counted as a case. I’m no expert, but that doesn’t sound very scientific to me. I suppose the reason they used a very flexible case definition was to accelerate the study. Then you have the delaying of the results where they waited for an extra 13 cases after which they magically got to 50,4% efficacy… 0,4 percentage point above what is necessary for approval.

  23. DTX says:

    One thing that hasn’t been mentioned is the amazing strength of the nocebo effect in the Pfizer & Moderna studies, particularly in young people. Notably, in 18-64 year olds in the Monderna trial, 28.8% reported fatigue and 29% reported headache after receiving the PLACEBO.

    Even more surprising is that these and other “side effects” in the placebo groups were much less common in the older age cohort, i.e., 65 -85 yr olds. Only 22.7% reported fatigue and only 19.3% reported headaches.

    Considering that 65-85 yr olds are much more likely to experience fatigue & headaches than younger people, these results are even more amazing. The most likely explanation was that the younger participants were more susceptible to the power of suggestion (if you have another idea, please offer it).

    The study populations heard and/or read in the clinical briefing materials that the vaccine candidate could cause these effects, so they imagined they had them. This isn’t a new finding – many studies have shown the nocebo effect. However, I’ve not seen such a stark age difference like this before – with younger groups imagining far higher rates.

    Pfizer’s data showed a similar finding, i.e., the younger cohort reported (imagined) far higher rates (~33%) of side effects from the placebo.

    1. Irene says:

      Oddly enough, I have experienced fatigue and headache without any injections at all! Is that, too, a “nocebo”? People are under a lot of stress these days, and younger people are more likely to be wrangling a job, kids, etc.

      1. Chris Phillips says:

        Yes – to say it’s a nocebo effect, you’d really need a third arm of the study in which people received nothing at all, knew they’d received nothing at all, and were asked to report headaches etc.

      2. DTX says:

        Nocebo is when someone receives a placebo and reports a negative side effect (the placebo effect is when they report a positive effect). I’d like to think when I’m 65, 75 & 85 years old, I report much less fatigue than in my younger years, but this is highly doubtful.

        The 6 Feb 2020 of the New England Journal of Medicine has an excellent review of the placebo & nocebo effects. I believe it’s a freely available article. “Placebo and Nocebo Effects,” Luana Colloca, M.D., Ph.D., and Arthur J. Barsky, M.D.

    2. sPh says:

      The headaches could be a reaction to receiving any kind of injection at all, whether saline or anthrax vaccine. My body has weird reactions to being stuck with any kind of needle even though the rational part of my brain knows that that tiny piece of metal poked 1 cm into my arm can’t possibly hurt me, so I would not be surprised at all if some people experienced headaches afterwords.

      1. Marko says:

        aka : The Inaccupuncture Effect

    3. Bell4 says:

      I’m guessing you folks haven’t paid much attention to clinical trial outcomes til now. Volunteers are generally told to refrain from caffeinated beverages before the study, so cafffeine withdrawal symptoms like headache and fatigue are common in all groups.

      1. Marko says:

        No caffeine allowed? That does it, no vaccine for me.

        If they really wanted to boost vaccine uptake, they’d suspend the vaccine in a solution of “5-hour ENERGY®”.

        1. Marko says:

          Or, even better, make the vaccine with”Brawndo”. It has electrolytes.

      2. Sc says:

        No such request was made in the Pfizer trial, nor anything similar. Can’t speak to Moderna or JnJ or anyone else though.

        1. guneapig says:

          Agreed. No mention of cutting caffeine or anything of the sort in Pfizer trial.

          It’s not surprising to see nocebo effects– people in the trial pay extra attention during the days after the shot, because they know they’ll be asked. What percentage of the population will report headaches, malaise or some fatigue if you asked them to track them for 3 days?

  24. Luis Filipe says:

    It will take a few months to have a good idea how well the vaccines are working in the general population i believe that Israel has a very early study showing that the Pfizer/BioNTech vaccine is helping cutting transmission by around 50% if i am not mistaken,these are very early studies but if that holds then it is really promising…

    1. Adrian says:

      If transmission is reduced by only 50%, then vaccines alone won’t be enough to stop COVID-19.

      The more contagiousness new variants would then spread between vaccinated people about as fast as the original less transmissible variants of COVID-19 did in 2020 without vaccines.

      1. Chris Phillips says:

        Judging from news reports, these are estimates only of the reduction in the likelihood of being infected as a result of vaccination. That is part of “transmission”, but the other part is the likelihood that vaccinated people who become infected will go on to infect others. Of course, if that is also reduced, the total reduction in transmission will be much greater. And for any of these estimates to be consistent with the Phase III trials, the great majority of these post-vaccination infections would have to be very mild or asymptomatic.

        1. Adrian says:

          These numbers are not estimates for anything, this is an average of the raw data of positive test results.

          Asymptomatic infections are less likely to get tested, the current data from Israel might even be consistent with an assumption that vaccines only convert symptomatic infections to asymptomatic infections without any reduction in infections and transmissions.

          The difference between 60% or 33% drop of infections 14 days after the first shot seen by different health providers might then be explained by different testing capacity (7.6% of all tests are positive) or contact tracing catching different shares of asymptomatic infections.

          1. Chris Phillips says:

            I’m not clear whether your comments are based on anything other than the information I posted. Perhaps if you know anything more you can cite your sources. There’s definitely too much speculation going on at the moment.

  25. Iknownothing says:

    83% measured over 5 months if I understand correctly though vs median 3 months for the 90%+ ones

  26. Marko says:

    These reactions seem like the result of delayed hypersensitivity (CD8-mediated cytolysis, etc) against the muscle cells expressing spike Ag :

    No way am I convinced that immune cells are the only target, or even the primary target, of the LNPs in the vaccine.

  27. myst_05 says:

    “To be sure, a 50% or 60% effective vaccine (with a reasonable safety profile) is surely better than no vaccine at all. But it means that you have to vaccinate a lot more people before you start to make a dent in a pandemic like this one, which is a significant real-world limitation.”

    This seems like a vague criticism of the Oxford vaccine which is quite perplexing: if you don’t have enough Pfizer/Moderna for all, making the Oxford available to everyone is a complete non-brainer. Yes, you have to vaccinate more people, but the math still works out so that Oxford should be immediately approved worldwide, no questions asked and without waiting for more data.

    1. sgcox says:

      Ok, I will be a bit provocative here.
      Oxford/AZ will never get approved in US.
      It is distributed for no profit because of Oxford licensing deal and so is very cheap.
      No way it can be “as good as” Pfizer or Moderna, which are proper pharma money spinners.
      Lets’ see how much J&J will charge as its production cost should be identical to AZ vaccine.

      1. Adrian says:

        A dent in the pandemic itself would only happen if a vaccine would reduce transmission.
        So far it is not proven for any vaccine that it actually reduces transmission, the headline numbers of 95% reduction in symptomatic cases do not exclude that the only effect of these vaccines might be turning symptomatic COVID-19 infections into asymptomatic spreaders.

        The Oxford vaccine has the problem of a not properly working booster shot due to the mistake of using the same vector twice. Sputnik V is a bit like the Oxford vaccine done right, this one would be a better comparison with the Pfitzer/Moderna vaccines.

  28. Peter Waldo says:

    Heading into the weekend there was reporting about deaths in Norway following vaccinations and reports that China “experts” are calling for some kind of suspension or halt related to vaccination of elderly groups (may or may not be “official”?). Pfizer’s public announcement about delaying EU vaccine shipments may also be a sign that something is going on. We’ll have to see.

    1. Ex Pharma R&D says:

      BMJ link to Norway report:

      Covid-19: Norway investigates 23 deaths in frail elderly patients after vaccination

      “It may be a coincidence, but we aren’t sure,” Steinar Madsen, medical director of the Norwegian MedicinesAgency (NOMA), told The BMJ. “There is no certain connection between these deaths and the vaccine.”

  29. Chris Phillips says:

    The preprint for the UK study on reinfection has now been published at MedRxiv:

    1. Marko says:

      Thanks, I’ve been waiting for that. Regarding the comparative efficacy of vaccines vs. natural infection, this is the money shot from the Discussion section :

      “The recent SARS-CoV-2 vaccination trials have typically investigated protection from symptomatic infection. The ChAdOx1 trial reported protection against symptomatic infection of between 70.4% and 90%, and the BNT162b2 vaccine phase 3 results report 95% protection over two and three months of follow-up respectively. Our findings, after a longer period of follow-up, of 94% lower odds of symptomatic infection, demonstrate equivalent, or higher protection from natural infection, both for symptomatic and asymptomatic infection. “

      1. Chris Phillips says:

        I’m pleased you found it useful. I can’t make much out of it, and I don’t think I can spare any more time to try. Apparently the reason we were finding it hard to make sense of the figures previously was that the average time assessed for the initially positive cohort was 202 days while that for the negative cohort was only 131 days. Quite why or how that could be, particularly given that the stated length of the study period was 144 days, I’m not sure, but I suppose the answer is buried in there somewhere.

        1. Marko says:

          Here’s a similar UK study that presents their data in a more comprehensible form. They also come up with a 94% protection figure (against symptomatic illness), extending beyond seven months. The only reinfections were picked up in Dec., 7+ months after the bulk of the first wave:

          To me, this fits the pattern of waning immunity that’s seen in the common cold coronaviruses. Hopefully, severe disease and death will be rare among reinfection cases going forward , i.e. much more rare than among primary infections, giving us hope that once everyone is either infected or vaccinated, the pandemic will truly be over, without the need for new vaccines/boosters as for flu.

        2. Marko says:

          This may provide a clue to why the SIREN study is hard to interpret. This is a tweet from the primary author in reply to a question about the “possible” cohort of reinfections:

          “All had positive Pcr tests but many of the possible at very high levels and no symptoms and unable to genome sequenced because of poor quality rna. so it is very difficult to confirm whether it is a current circulating strain or residual rna.”

          By “very high levels”, she can only mean “very high Cts”, meaning low levels of intact virus. You can get the gist of what she’s saying, but not without more effort than should be required.

        3. Marko says:

          Goodness, it’s worse than I thought , she’s totally jumped the shark. Asked to “Please define “at very high levels””, she replied “Ct<25". That makes absolutely no sense. At lower Ct levels, you'd expect a greater likelihood of successful sequencing, not lesser. She's totally backwards on the meaning of Ct levels, and she's the principal author of the paper :

        4. Marko says:

          At least one of her co-authors gets it right :

          “…many of the possible infections will likely be persistent PCR positives, but with high Ct values that mean we will never have sequencing proof”

          1. ghyu says:

            That’s the optimistic view. High Ct values may be due to a lower viral load during illness resulting from reinfection. A pessimist might also say immunity is going to continue to wane and the protection against the new variants is almost certainly going to be worse than the original variant. Vaccinations, especially with the Oxford/AstraZeneca vaccine, will be even less effective against reinfection. Even the Moderna and Pfizer studies used a less stringent case definition than this study, so they’d be less effective if very mild cases were also counted.

            In the future the annual winter flu may be exacerbated by seasonal SARS2 cases. Booster vaccinations may be needed every few years.

          2. Marko says:

            “Vaccinations, especially with the Oxford/AstraZeneca vaccine, will be even less effective against reinfection. ”

            Any data to back that up? Why wouldn’t you expect a vaccine to boost immunity in a previously-infected person even more than one who had never been infected? The antibody titer data in the vaccine trials showed that those previously-infected showed an increased response compared to those who were not. And I can’t imagine why you’d expect a previously-infected person to be at higher risk of reinfection after receiving the Oxford vaccine than one of the others , without some data to support that.

          3. ghyu says:

            Asymptomatic infections or those with unreported symptoms were detected in 69 participants (table 2). Vaccine efficacy in the 24 LD/SD recipients was 58·9% (95% CI 1·0 to 82·9), whereas it was 3·8% (−72·4 to 46·3) in the 45 participants receiving SD/SD (table 2).


            Not a lot of data, but protection from reinfection is not good.

          4. Adrian says:

            If this data gets confirmed, it would mean that protection against infection only comes from the booster – no protection from the first shot.

            And then the misdesign by the University of Oxford to use the same vector twice ruins everything for that vaccine.

          5. Chris Phillips says:


            Please could you clarify what data you are talking about?

            It’s often not clear which comments people are replying to here.

          6. Adrian says:

            “Vaccine efficacy was 3.8% in the 45 participants receiving SD/SD”

          7. Chris Phillips says:


            Thanks for clarifying. You say:
            “Vaccine efficacy was 3.8% in the 45 participants receiving SD/SD”

            The previous poster said:
            “Vaccine efficacy … was 3·8% (−72·4 to 46·3) in the 45 participants receiving SD/SD …”

            I ask you.

            Trying to be polite. I don’t think you should have left out the statistical range. You know what they say about lies, damned lies and so on.

          8. Marko says:

            @ghyru said:

            “Asymptomatic infections or those with unreported symptoms were detected in 69 participants (table 2)……Not a lot of data, but protection from reinfection is not good.”

            “Asymptomatic infections or those with unreported symptoms” are NOT reinfections. They are primary infections that fall outside of the headline efficacy analysis, which is based on symptomatic infection.

            Out of the entire study involving tens of thousands of participants, there were only three reinfections among the 138 who were seropositive at baseline, and two of those reinfections were in the placebo group. You can’t conclude anything from numbers like this.

            Jeez, why do I bother?…….

          9. Marko says:

            Actually, the rate of reinfections was even lower than 3 out of 138, it was 3 out of 373 (138 in the UK plus 235 in Brazil). Here’s the relevant text from the study :

            “A small proportion of participants were seropositive at baseline (138 [1·3%] of 10 673 in the UK and 235 [2·3%] of 10 002 in Brazil). Three participants seropositive at baseline had subsequent NAAT-positive swabs. One participant had an asymptomatic infection 3 weeks after a first dose of ChAdOx1 nCoV-19. Two other participants in the control group had symptomatic infections 8 weeks and 21 weeks after their baseline sample was taken.”

            “Results from sensitivity analyses, including participants who were seropositive at baseline and by intention to treat, were very similar to main results (data not shown).”

          10. Adrian says:

            Chris, please stop abusing me for responding to your requests for clarification.

          11. Chris Phillips says:


            Abusing you?????????

            By a mighty effort of self-control, I just politely pointed out that when purportedly quoting another commenter, you shouldn’t have suppressed the statistical range of uncertainty, which in this case amounted to a factor of about 30 relative to the figure you were “quoting”.

            If I had been trying to abuse you, I assure you I would have been nowhere near so forebearing about such a misleading comment.

  30. Chris Phillips says:

    An interesting insight into the possible time-course of the UK vaccination effort comes from figures for the projected supply of vaccines published by the Scottish government, later removed at the request of the UK government as their publication “would create difficulties for the pharmaceutical companies”. But of course, copies had been saved before their removal:

    These figures suggest the supply would be sufficient for everyone over 50 and others over 16 deemed to be “at risk” to receive a first dose by 22 March and for the whole adult population to receive two doses by 12 July.

    1. Adrian says:

      Around March 22nd is also when the crunch time will start for second doses after 3 months when no reserves are kept for that.

      Looking at the low bars in late March and some weeks in April it becomes obvious why mixing different vaccines is being discussed: The amount of Pfitzer vaccine available in January is a lot higher than the amount in April, so based on these numbers getting a different vaccine for the second shot will happen for a six digit number of (mostly elderly) people.

  31. Uncle Steve says:

    On behalf of an older relative, can I ask if anyone has links to data on vaccine health impact events?

    The best I have found so far is the link below to a presentation from the US. Anaphylaxis aside, Slide 6 indicates around 3% “health impact events”, so 97% okay after first dose.
    (If you don’t want to click on the link, search for: “ACIP COVID-19 Vaccines Work Group – Clark”. It’s dated December 19.)

  32. sPh says:

    I am curious if anyone knows the root source of this inchoate concern about “post-vaccination asymptotic COVID spreaders”, which is generally paired with the question “does this vaccine prevent infection or prevent disease?”. This doesn’t seem to be a concern about any other virus, viral disease, or vaccine – particularly chicken pox which one would think tests the ‘prevent infection or prevent disease’ question to the maximum extent – yet in every discussion about the COVID19 vaccine on science-based discussion sites these memes pop up. Is there some central source for this line of questioning?

    1. Adrian says:

      What you call “memes” is what the data says.

      Both early results from monkey trials and what is being observed in humans shows that while the current 1st generation vaccines is good at preventing serious COVID-19, infection and transmission are not prevented.

      With COVID-19 infection and transmission mainly happens in the initial “mild cold” phase in the upper respiratory tract, and having plenty of antibodies in your blood might only prevent the main COVID-19 disease where the virus spreads to the whole body.

      From a discussion of monkey data for the Oxford vaccine Derek discussed here in the blog 8 months ago:
      “The conclusion is that the vaccinated animals were indeed infected – the vaccine did not protect against that – but that the disease was definitely less severe. But these results mean that the virus might well still be transmissible from people who had been so vaccinated, even if the disease course itself was not as deadly.”

    2. Marko says:

      “This doesn’t seem to be a concern about any other virus, viral disease, or vaccine…”

      Huh? Long-term sterilizing immunity is the exception, rather than the rule, among currently marketed vaccines. You catch repeated colds throughout your life from viruses that have given you a cold in the past.

      Most people expect the Covid vaccines to reduce transmission risk, but the question remains as to the degree and duration of that reduced transmission.

    3. DTX says:

      sPh asked about whether the concern about “post-vaccination asymptomatic” spread was unique to Covid. This also happens with polio. Injected polio will protect patients, but they can still be infected by the virus and transmit it to other people.

      Several years ago, Israel detected polio in sewage, despite that they weren’t seeing cases of polio in their population (due to high vaccination rates). To stop the community spread of asymptomatic polio, Israel also had its population also receive the oral polio vaccine (the inactivated to protect them and the OPV to stop the spread).

      Previously, Egypt and Hispaniola also experienced transmission of post-vaccination of asymptomatic spread of oral polio vaccine strain. It was estimated it circulated in Hispaniola for 2 years and 5 years in Egypt before it mutated back to the wild type (i.e., that causes illness).

  33. Bill says:

    I’ve been tracking US daily vax rate and watching the slope. Currently at 800k/day and increasing about 50k/day. Ironically that means it should hit 1M/day on Inauguration Day.

    Biden’s first success. 🙂

    1. Marko says:

      Everyone is showering praise on Biden for his promise to vaccinate a million people a day over his first 100 days , but as you note , we’re likely to reach that level under Trump. CVS claims to have the capacity to vaccinate a million today within their own system. Surely with Walgreens and others we could get to a rate of ~3 million per day, or around 1% of the population, allowing us to be done with this mess within 3 months or so, limited only by available supply, rather than the by easily solvable issue of vaccine distribution logistics.

      We’ve set a very low bar for Biden’s success, a “soft bigotry of low expectations” , which, given his declining mental capacity, might well be justified. It’s just sad that he’s the best that the Dems could offer.

      1. Adrian says:

        Note that 1M shots/day are only 0.5M vaccinations/day, a proper vaccination is two shots.

        1. Marko says:

          Yes, it’s even worse, by a factor of 2, unless we’re saved by the J&J vaccine.

      2. Chatter says:

        How many flu shots per day are given in a typical season?
        Those, of course, don’t require scrupulous dry-ice level refrigeration and are stockpiled months in advance. Still, the ability of various outlets to get shots into arms seems rather large to me before any government help. Perhaps less so after it.

  34. Adrian says:

    I am still skeptical regarding the J&J vaccine.

    It is quite similar to Sputnik V Light (only the first shot of Sputnik V), for which their creators claim to only 3-4 months protection.

    Good numbers after 57 days for the J&J vaccine are good, but numbers after 120 or 180 days might be much worse.

    1. Adrian says:

      That was regarding the one-shot application of the J&J vaccine.

      For two shots they are having the problem of using the same vector twice that already hurts the Oxford vaccine.

      1. Mariner says:

        It should be that a combination of any two of the AZ, Sputnik and J&J vaccines works out better than two of the same vector.

        Hopefully the combined trials of using the AZ/Sputnik Ad26 (I presume) announced towards the end of 2020 have commenced so we’ll have some data sooner rather than later. I like the idea of international collaboration. Heaven knows we’ve had little enough of it so far during this pandemic, at least not at political levels.

        1. Adrian says:

          Estimated Study Start Date : March 16, 2021

          1. Mariner says:

            Ah, that’s a pity. I thought I’d read it was to commence right at the start of 2021.

  35. Richard of Loxley says:

    Re the UK NHS SIREN study press release: Study hereby renamed RISEN, after Study Director, beavering away in the Imperial College kitchen, overdid the bicarb of soda in the pastry mix for the celebratory pork pie lunch to mark the GOV.UK press release.

    Thank you, Chris Phillips, for posting medRxiv link, although even you have to admit that you, “can’t make much out of it.” Abstract reads like rehash of press release (or vice versa).

    Maybe Study Director can set to and graft away at the full paper for submission to a peer reviewed journal – plenty of preceding Pipeliners on this thread who’d be delighted to act as reviewers. Getting impression might not be too onerous to make up your minds.

    Quick trawl among websites tells immunology goes way back to Thucydides in 430 BC Athens… then forward again via 10th century Chinese and Persian physicians… picked up later by Pasteur, Paul Ehrlich and Metchnikoff, etc, etc… and brought up to date by Medawar, Jerne and Hoffmann, etc, etc… Boils down to… if you’ve survived a plague, you don’t usually catch plague again. Otherwise, humanity hypothetically extinct millenia ago.

    Ah, but maybe not so simple for a virologically pernicious version of the common colds we all catch at the drop of a hat winter in, winter out? Which is why everyone getting in such a tizzy? Thank you, Marko, for highlighting that Journal of Infection pre-print, a far more cogent and coherent account of re-infection studies in South London Hospitals, that does seem to document cases, and, if Richard of Loxley reading right, puts the probability of re-catching at 6%?

    Thank you also, Marko, for drawing attention to the latest bird songs tweeting around the trees in various London hospital and university grounds. Seems the Study Director from Public Health looking for something that might not even be there, based on molecular biology tools and amplification cycles the Study Director doesn’t really understand? As posted elsewhere, Richard of Loxley inclined to think Study Director not alone in the amplification cycle department.


    Scroll down the RISEN press release and you come to the real meaty morsel, RISEN Study Director, PHE Senior Medical Advisor and Imperial College Faculty member, all rolled up into one single Super Nanny, instructing…

    “It is therefore crucial that everyone continues to follow the rules and stays at home, even if they have previously had COVID-19, to prevent spreading the virus to others.”

    Over to you, Thucydides, to send Nanny packing for an afternoon nap to sleep off GOV.UK’s latest immunological non-sequitur. Rehash of the De Pfeffel Corollary to the Cunnin’ Dominaigh Principle of Viral Transmission, which enabled the UK’s Prime Minister to go into hiding for a couple of weeks in the run up to Christmas…

    …To avoid catching again a virus caught and courageously fought off once already, a principle which last spring also broadly rationalised the PM’s former Special Minder’s notorious 500 mile two week round trip to take brass cheek rubbings at St Dominic’s Church, Barnard Castle. Government by non-event press release, non sequitur and utter nonsense.

    Whoah… Usual Sherriff or two or three will be going not for the ball, but for the man’s front lobal anterior cruciates. Yet again. C’mon, got to admit it, Guys – at this rate, sooner or later heading for least popular GOV.UK since the 12th century of Sherwood Forest, Sherriff of Nottingham, King John and All That. Risible RISEN press release latest nail in coffin.

    Richard of Loxley better be on the safe side for sake of the old lobal anteriors – off for a while to lie low in the badlands and the forest, where old chums Prince of Thieves, Little John and Friar Tuck hang out, living off nuts, wild berries and the odd slaughtered sheep. Be dense mist, for Sherriff’s men blunderin’ in t’forest from t’castle. A’ter ‘im, Get ‘im! No chance.

    Might even be the occasional rattler, coyote and other fore’gn varmints hanging out in t’forest too. Leftovers, maybe, from a movie shoot, with running order written in black marker pen, on that whiteboard left in that foresaken derelict cabin, next to that forbidding lake seriously edged with what looks, from the distance, like serious quicksand.

    Bring me my bow and All That, but beware quicksand. Not many alive left who knows how to cross it. Whatever you do, don’t rely on GPS or satnav. Sadly, even an out of date old Ordnance Survey map might not save you. These days, the badlands really are that bad.


    Off into the forest with bow and arrow at the ready, and so on through the glen to meet up with the merry men…

    Now by now, scientifically inclined and literally minded readers, who in Richard of Loxley’s general experience do tend to be one and the same thing, will be wondering what the hell Richard of Loxley’s witterin’ on about. Yet again. His fellow outlaws witterin’ too.

    Only recently realised himself. That BBC Radio 4 series “In Our Time,” part heard pretty much by chance couple of months ago. Erudite academics discussing “Piers Plowman”, a 14th century dream vision committed to words, thought to be by William Langland, that begins with a prologue…

    Apparently, agreed the erudites, Piers Plowman all allegory, a 14th century fashion nowadays long out of fashion. Allegory it must be, thinks Richard of Loxley, idea of medieval tale standing, maybe, for a different longer standing tale.

    Now here’s an odd thing. When out and about for essential shopping, from time to time Richard comes across acquaintances past and present. Masked Tesco raiders out a foragin’. Bit of an etiquette minefield with all the other masked raiders around too. Fleeting eye contact. Is it or isn’t it?

    One of them takes the plunge. It is! Within verbal transmission limitations of snout masks, news and views exchanged. Sooner or later Richard of Loxley atop soapbox, tree stump, or whichever metaphor suits. Limited dataset, but one thing emergent. More letters acquaintance has after name, less comfortable the eye contact and demeanour. Shutters at best only part way up. No real meeting of minds.

    Whereas with lesser or no letters after name… Eye contact, spontanaiety and engagement. Minds duly met. Now maybe it’s sentimental old Richard of Loxley’s turn to be be looking for something not really there. Who can tell for sure? Sense of accord with something sensed decades ago, at time of going to university. Last words with Piers Plowman, in an 1887 edition:

    I seigh somme that seiden
    Thei hadde y-sought seintes;
    To ech a tale that thei tolde
    Hire tonge was tempred to lye,

    If any Pipeline reader cares to ask, Richard of Loxley can supply a more readable undated translation from 14th century English, lifted from website “The Geoffrey Chaucer page”. Suspect wording would flush out usual type of scientifically inclined and literally minded player who generally goes for man not ball. Just thought I’d better mention that in advance.

    Usual disclaimer: Richard of Loxley not denying patients in hospitals up and down the land are dying of viral infections.

  36. Marko says:

    New study suggests the relative growth rate of the UK variant, at ~6% per day, is considerably lower than previously reported:

    Fauci and other talking heads have been warning that the UK variant would be the dominant strain in the US in another 5 or 6 wks., based on a doubling rate of prevalence of ~1 wk, i.e., if it’s at a 1% relative prevalence today, it would be the dominant strain at ~64% prevalence in 6 wks. If the above paper is correct, the prevalence doubling rate would instead be ~12 days, giving us a little over 10 wks. to reach the same point. That could provide a significant extra buffer for the vaccines to help mitigate the impact of the new variant, if we can just get the vaccines into people’s arms.

    1. Chris Phillips says:

      Thanks. I think 6% faster a day would be pretty similar to the recent estimate that the R number was 35% greater from Public Health England.

      It’s interesting that they find the difference between the two growth rates decreased (significantly, I think) from 9% to 4% in the most recent “epoch” used in their analysis. 6% is an average of the two rates. That is a bit difficult to interpret, because the epochs depend on the shapes of the curves and are different for each region. Presumably it means the difference in transmissibility is smaller for the transmission modes that are relatively commoner when tighter restrictions are in place (such as household transmission, I suppose). But the analysis doesn’t extend as far as the current national lockdown in England, so the present difference may be different again (even smaller?).

      1. Marko says:

        I think the “epochs” and “addition rather than replacement” mumbo-jumbo are just constructs to try to support the ongoing transition from BJ’s intial “70% greater transmission” warning to later estimates of 50-60%, then 50%, now 35% and soon to be 25% , if not lower. Everyone got out over their skis at the outset and now they’re trying to arrange it so their inevitable pile-up occurs into a soft, fluffy snow bank rather than into hardpack.

        I’m not buying their story. It smells iffy.

        1. Ex Pharma R&D says:

          Looking very iffy from UK side of the pond too.

          Last November’s UK lockdo*n V2 generally accepted as predicated on out of date case and death projections.

          New Year lockdo*n V3 predicated on mutant transmissibility and hospital admissions/deaths.

          Now looking like transmissibility not all it was cranked up to be.

          Wondering what lockdo*n V4 will be predicated on, assuming GOV.UK BJ V1 lasts that long…

          1. Marko says:

            “New Year lockdo*n V3 predicated on mutant transmissibility and hospital admissions/deaths.
            Now looking like transmissibility not all it was cranked up to be.”

            And hospitalizations and deaths looking like more than they were cranked up to be. 1100 deaths per day in the UK is equivalent to >5300 deaths per day in the US. At that rate, you can believe we’d be locking down hard too, increased-transmissibility mutants or no.

            Go back to your “pandemic all but over in the UK” denialist gurus if you’re looking for support for your crackpot ramblings.

          2. The ref says:

            @ M**** says: 18 January, 2021 at 12:38 pm
            @ C**** P******** says: 18 January, 2021 at 12:55 pm

            Temper, temper. Yet more afters*. Ball not man, please. FYI, bloggeromically metrically data analytically determined league table for current thread’s total 153 comments:

            M**** 34 comments (22%)
            A**** 18 (12%)
            C**** P******* 17 (11%)
            Score 69 (45%)

            Ex PR&D 3 (2%)
            The ref 1 (0.7%)
            Score 4 (2.7%)

            Final score: 69 – 4

            Now okay, Ex PR&D crackpot got time to stand and stare for first time in 50 pretty much non-stop years, but do you madly sane guys actually have a day job?

            And what a hoot! Even afters* between the same side….

            17 January, 2021 at 4:24 pm

            ‘Cos now am on sidelines, all I wanna do allegorically** is watch a decent game o’ football (fat chance, this and last forsaken seasons). As one and only sixties LFC manager once said, “Somebody said that football’s a matter of life and death to you, I said ‘listen, it’s more important than that’.”


            *What happens in the English Premier League when Harry squares up to Tyrone, just before the ref reaches for the red card.

            **allegory n. a narrative in which abstract ideas are personified; a description to convey a different meaning from that which is expressed; a continued metaphor. [Gk. allos, other; agoreuein, to speak]. Source: The New National Dictionary, Collins London and Glasgow, first published 1959, reprinted 1961.


            Cosmic scriptwriter on good form yesterday morn. Out of driveway for essential shopping, to Chariots of Fire, then comes news of stunning Ind win in Aus. By over 90 runs, highest ever 4th inns at the Gabbatoir, where Aus last lost in 1988 – to Fire in Babylon, no disgrace in that.

            Aus pretty much full strength, Ind missing Kohli and all frontline injured bowlers – 10 career test wickets between stand in Ind attack vs 1000 career wickets for Aus attack, yet Aus bowled out twice. Bad luck, Aus. Ind take Series 2-1. Sensational.

            Next up Eng in Ind. Tough task – Eng lost 4-0 last time. No home crowd might help, but, as ever, heat won’t. With a Super Hero, a Super Veteran, Super Cerebral and Super Speccy Four Eyes all in the side, anything’s possible. All that’s missing is a deity, but on average only two of ‘em per cricket century (n = 1, C the 20th).

            Back from essential shopping to news of day before’s viral death stats. Over 1100 in total. Some UK hospitals again near-overwhelmed and short staffed. But where’s the compelling evidence proving that 9 million kids, backed up by 12 million parents, all showing solidarity with the NHS through online learning in lockdo*n for months on end, make any difference to the death stats?

            Even a minus six leftie (as per two paragraphs on) thinks solidarity a dodgy concept and school closures rarely even been done before, except in war zones. Callous old ba*tard, aren’t I, to even put it like that? But someone’s got to say it.

            Back inside house, to be greeted by…

            “Request for expedited federal investigation into scientific fraud in COVID‑19 public health policies, 10 January 2021”

            …Back off, away team. Home team man not ball brigade won’t like it. Will say you’re denialists, alt rightists, Chump supporters (good riddance – This Be The Day). Signatories include backwoodsie politico, Monaco resident, USAF brass hat retired at suspiciously young age. Backwoodsie sounds interesting. Started out as electrician – not a working physical reality to be trifled with by theoreticians.

            All in all, not usual company kept by aged ex-teenage crackpot, who in last half hour took political compass and scored minus 6, minus 6, leftie libertarian. Arguably not much changed from 50 years ago, but with much variation suspected in between. Bernie Sanders territory, the Political Compass says. And here crackpot is, thinking become a bit of a rightie. That’s politics for you, says a retired scientist. Hardly an exact science.

            But you can only read what’s put in front of you and what’s put in front on pages 11-16 of the FBI Expedited Investigation Request is a dissection of PCR mass testing, along with the rest of the pages dissecting loads of other things gone by over the last year.

            Now what’s a limey to know, but maybe fair chance that Expedited Investigation Request will get buried after today’s Inauguration Ceremony. Chucking it down here in Limeyland this morning. If same in Wash DC, better look after Gentleman Joe. Don’t want the Old Fella catching a bad cold on first day in office.

            Over and out. Please refer to…


            …Posted 17 January, 2021 at 9.40 am, but only displayed overnight 18/19 January. For those prone to the apoplectic, best taken with a bacardi and coke, better still laced with 2 or 3 slugs of malted vinegar.

            Time to catch up with Dr Derek’s next post and the commenters. OMG, new kid on the block…

        2. Chris Phillips says:

          Looking at the original presentation of that 70% figure in a Zoom symposium, in scientific terms it clearly didn’t justify the emphasis it was given in the media. I don’t know why that happened. Perhaps someone thought the fear of God needed to be out into the public (or the politicians).

          On hospitals, I shudder to think what would have happened if we hadn’t gone into lockdown and the rate of infection had continued to rise.

          1. Mariner says:

            I tend to lean to the journalistic incompetence side of things rather than any plan to influence folk to stay at home. The initial reports certainly clearly noted increased transmissions ‘up to 50 to 70%’, but it was quickly bumped up to stating the 70% figure as fact. The government soon mentioned 70% as fact on every occasion in following days but that was just a variant on their usual boosterish bullcrap which exaggerates everything and anything in an attempt to claim success of policies or shift the blame.

        3. JS says:

          Latest info from the Danish SSI is here:

          In particular they have tried to estimate the increase in in R here:

          Estimate is a factor of 1.36 (95% CI [1.19; 1.53]), but as they point out the statistics are poor and there are many assumptions.

          Note that the UK and Denmark sequences a much larger fraction of positive tests than any other countries with significant case numbers. The number of (PCR) tests in Denmark corresponds 10-15% of the population per week over the last few weeks, so the coverage is good. Thus Denmark is probably the only other place where the increase in R can currently be estimated.

          Plan is to sequence 100% shortly. Capacity is getting close. Remarkably also, the latest estimate of the overall Rt is about 0.6.

  37. Marko says:

    New variant in California, called L452R, has 3 spike mutations and is increasing in prevalence :

    It sounds like it’s been associated with some superspreading events, so it’s probably too early to say it’s more transmissible.

  38. Not-an-epidemiologist says:

    Derek, would have been nice to have a link to the medRxiv preprint for the SIREN study ( rather than a link to a press release!

    Also, re. that study — although there are many reasons why you can’t compare rates between the SIREN study and vaccination trials (not-age-or-sex-matched, HCWs in the SIREN study likely to receive higher viral loads, etc) … if you want to compare apples to oranges, at least note that the 83% stat represented the symptomatic + asymptomatic reinfection rate, something that vaccine trials have not looked at. The symptomatic-only reinfection rate was:

    “Restricting reinfections to those who were symptomatic we estimated participants in the positive cohort had 95% lower odds of reinfection, aOR 0.08 (95% CI 0.05-0.13).”

    i.e 93% efficacy. Which means that being vaccinated with an mRNA vaccine is statistically indistinguishable (at this stage, and with all the caveats mentioned above) to having had covid. At least at the 5 month mark.

  39. Marko says:

    “Further data on immune responses following the Pfizer mRNA vaccine against pseudo virus bearing Spike protein with mutations in the B.1.1.7 variant (del69/70, del 144/145, N501Y, A570D, P681H, T716I, S982A, D1118H). There is a modest reduction in efficacy of vaccine sera.”

    This is a big improvement in methodology over previous studies of mutation effects, which looked only at individual mutations in isolation. Why it took so long to see this kind of work is beyond me, because it’s obvious that the mutation cluster can have greater effects ( i.e. more than additive, due to epistasis, etc. ) than what might be suspected by looking only at the single mutations.

    This also makes me believe that there might be an immune escape component of the increased transmissibilty seen in the UK variant, even though studies to date haven’t seen it. I suggest they look again.

    1. Marko says:

      This is what Pfizer had said previously about the UK variant mutations:

      You can understand why Pfizer would want to do the study this way – the results are more likely to make their product look good. Public health scientists shouldn’t operate that way.

    2. Marko says:

      Speaking of the immune-escape devil , this just now :

      “When convalescent sera from 44 people infected in first wave in South Africa was confronted with 501Y.V2, antibodies from 21 out of 44 did not recognize the variant. ”

      1. Marko says:

        YouTube “Scientific panel discussion on the new variant, 501Y.V2” :

    3. Chris says:

      I suppose that if that were the case it should show up in a correlation between the regional variations in the ONS antibody survey and the regional variations in the difference between the two growth rates in the paper you linked to. I put some numbers in, and there doesn’t seem to be any clear evidence of that. For the most recent “epoch” the trend is in the right direction but non-significant (p=0.14), but for the previous one it’s marginally in the opposite direction. The data are very scattered.

      1. Marko says:

        The correlation could be significantly masked if a large proportion of reinfections are not detected by testing, due to mild or asymptomatic disease, i.e. a larger proportion than is normal in primary infections. Those reinfections could still contribute to the increased growth rate as “silent” spreaders.

        To really sort it out, you’d probably need a SIREN-style cohort study with periodic PCR testing. In fact, since that study is still ongoing, that may be how we eventually get an answer.

  40. Nate says:

    “95% effective”????
    Come on man!
    Effective at what?
    What was the endpoint of either of those studies? Covid of any severity?
    Everything they reported was relative not absolute.
    Some people are asserting that the studies may have been unblinded as well.
    Not saying any of these 3 are better but to say the mRNA vaccs without even a season of data are 95% “effective” given the news coming out on both this past week is a head scratcher to me.

  41. John Wayne says:

    A general issue with the data as presented is the labels need to be much more detailed to convey what is being measured and the time points involved. For example, I think the correct label for some vaccines is “95% effective at preventing reportable symptoms out to 3 months”

    If you are using iterative PCR on your patient cohort, that is another thing that can’t be directly compared to lack of symptoms (and a higher bar). I can imagine that some companies/organizations/countries will report efficacy with an even lower bar so keep your eyes open.

  42. An Old Chemist says:

    COVID-19 Vaccine Runner-Up Update: Who Will Reach the Finish Line Next? (BioSpace, Jan 22):

  43. Chris Phillips says:

    Anthony Fauci has indicated Johnson and Johnson is expected to submit data to the FDA in either the coming week or the following week:

    I think I’m right in saying that the interim results for the major Phase 3 trials so far have all been announced on Mondays before the opening of the European stock exchanges.

    1. Marko says:

      I hope tomorrow is the day we get the trial results.

      The AMA created the CPT billing codes for the Moderna and Pfizer vaccines before they had been approved. Medscape recently reported that they’ve now done the same for the J&J vaccine, so maybe that’s a good sign.

      The J&J vaccine will give a major boost to the rollout effort if approved, assuming efficacy is reasonable and it gains equivalent public acceptance. J&J has pledged to have 100 million US doses by April, and I assume they’ve made similar commitments to other countries.

      1. Chris Phillips says:

        I believe the UK has ordered 30 million doses and the EU 200 million, though I don’t know about the timescale for those.

    2. debinski says:

      I read somewhere last week that their database cutoff was Jan 20 (last weds). I guess Monday might be possible if they had everything ready to roll.

  44. Jens says:

    Merck just announced that their vector-based corona vaccine failed and any further development will be stopped

    1. Chris Phillips says:

      In fact both its vaccines. More information here, including a link to brief details of the Phase 1 results:

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