Skip to main content

Clinical Trials

New Data on the Oxford/AZ Vaccine

The hype began building late last week around the Oxford vaccine results released today, and I will confess to wondering just what was going on. The British press has a history of going berserk over drug research – I wouldn’t care to count how many times Alzheimer’s “breakthroughs” have hit the headlines over there, and I figured this might be part of the problem. But now we have the numbers. So how are they?

Recall this this one is an adenovirus vector vaccine – a chimpanzee adenovirus (used because humans don’t have exposure and thus pre-existing immunity to it) has had its own genetic material stripped out and the genetic sequence for the coronavirus Spike protein added instead. There are four groups in this study: Group 1 had 88 participants who received either the ChAdOx vaccine or a commercial meningitis vaccine as a control and who were followed up on at Days 3, 7, 14, 28, and 56. These were the true “Phase I” part of the current work. Group 2 had 412 (also split 50/50) who were vaccinated and assessed for both antibody and T-cell counts. Group 3 (10 patients) all had the ChAdOx vaccine, and then a booster at Day 28. And Group 4 (567 patients, split 50/50) were only evaluated for antibodies. These latter groups are the Phase II trial, who are being evaluated for how many in each group actually contracted the coronavirus (data not available yet!) Everyone got the same dose: 5×10 to the tenth viral particles.

The adverse events are (as in the other vaccines that have reported so far) just what one would figure: pain and tenderness at the injection site, along with fatigue, muscle and joint pain, fever in some cases, etc. There were no severe events. Some participants got prophylactic paracetamol (acetaminophen), and this did indeed lower the side effects, as it should. I found it interesting that the second dose (in those ten patients who got one) did not seem to bring on a more robust reaction than the first (the paper’s Figure 2).

OK, antibodies: overall antibody titers hit their peak at Day 28 and had declined a bit at Day 56 (albeit with a rather wide spread in response in both sets of data – see the paper’s Figure 3 and note the log scale on the y axis). The ten patients who got the booster shot definitely saw raised antibody titers. As for neutralizing antibodies (the paper’s Figure 4), the booster-shot people did have a higher response than the single-dose cohort, an effect that’s most noticeable as you move to more stringent assays (in some of the others, they look nearly the same). But from what I can make of the actual neutralizing antibody titers, they all seem comparable (if not perhaps a bit lower) than those seen in the convalescent plasma control group. The activity for that comparison group does not seem to be reported in those other assays; it would be good to have that comparison. It’s also worth noting in those figures that there were a couple of patients who started out with high antibody titers to the coronavirus – as the paper notes, there was not time to check everyone as the trial was enrolling, so they picked up some people who are already had the infection.

As for T cells, the text of the paper says that induced T cell levels peaked at Day 14 and were maintained out to at least Day 56, with no real effect of a booster in that case. There are no actual data presented, and there’s nothing on CD4+ cells versus CD8+ ones.

These results, overall, are fine – but I think that they would have been more impressive had they come out before the Moderna and Pfizer mRNA ones. As it is, I have trouble reconciling the big buildup from the British media (and, I have to add, from the editorial staff at The Lancet) with what’s actually presented here. I’m very glad that I don’t have to pick which vaccine to get based on the limited data we have (there are no efficacy numbers to compare, to pick the biggest gap in our knowledge!) But if I were forced to make such a choice, right now I’d take the Pfizer/BioNTech candidate. But let’s see how everyone performs where it counts.


64 comments on “New Data on the Oxford/AZ Vaccine”

  1. daksya says:

    In terms of expected completion of trials, is Oxford still the frontrunner?

    Meanwhile, India has started a trial of BCG vaccine in older adults (60+) in order to check if disease severity is reduced upon infection.

    1. Toni says:

      There is also an important vaccination trial with the recombinant BCG strain (rBCGΔureC::hly), which harbors genes for listeriolysin and urease.

  2. M says:

    The potential for us to have more than just one vaccine choice (which should be a positive on many levels) is becoming more plausible daily. But we still have a long way to go, and a lot fo research/clinical trials to carry out. As always, good work here, Derek!

  3. silverlake bodhisattva says:

    Since I see lots of “game-changer” hype for interferon beta from Synairgen this am, will that be next up for your coverage?

    1. Marissa says:

      You can usually safely discard anything labeled as a “game changer” .

      1. Ross Presser says:

        I’d say that if any phrase, like “game changer”, becomes widely used by President Trump, we should form an immunity to that phrase and start disregarding it.

        (Admin, go ahead and reject or delete my comment if this is too political in nature. I was just trying to make a joke though.)

        1. Walter Sobchak says:

          Don’t quit your day job.

    2. Luke says:

      If you look at the results of that the confidence intervals are huge on their results.

      Also not even a peer reviewed piece of work. Not really comparable to the Oxford Vaccine

      1. Erik Dienemann says:

        Derek – you’re on fire today – great stuff, thanks!!

        Agree 110%, Luke. This may be too long for a comment not on the blog topic (so feel free to delete, Derek), but wasn’t sure where to put it. Certainly looks promising on the surface, as it was a randomized, controlled clinical trial, but no paper yet, so the data can’t actually be reviewed by anyone, and the statistical significance of the clinical benefit is there, but just barely, likely because it was such a small trial (100 patients). Below is a nice write-up in Biospace on exactly what that means.

        “It’s worth noting that the p-value of the 79% figure was 0.046, which only provides a narrow margin for being statistically significant. P-value, or probability value, is a determination of statistical value. The smaller the p-value, the stronger the evidence is that the null hypothesis should be rejected. The null hypothesis is that there is no significant difference between specified populations, and any difference observed is related to sampling or experimental error. A p-value less than 0.05 is statistically significant; greater than 0.05, not statistically significant. Still, it is statistically significant, although barely.”

        Taking this a step further, the press release shares the following data, which I haven’t seen in most of the articles for some reason, but is important. It’s on the “odds ratio” confidence interval for the data. What it shows is that the 79% reduction in the odds of developing severe disease is, statistically a range of 3% to 96% reduction, meaning, yes major reduction is possible, but so is very minor reduction. Similar analysis for the odds ratio of being 2.19 times as likely to recover (HR = 2.19) – the 95% confidence interval for this is 1.03X to 4.69X as likely to recover, so it could be a major score or a very minor improvement.

        This is the problem with very small trials. Personally, I wouldn’t bet the farm on this drug until I saw results from larger trials, which are in the works, but the data are probably still good enough to warrant emergency use and fast-tracking of larger trials. I’d also be saying similar things if the p-value was just slightly above 0.05, i.e., despite that not being statistically significant, the results would’ve been considered very encouraging and would mean certainly a larger trial would be warranted to definitively determine efficacy and would mean consideration for emergency use. And as many know, the p-value of <0.05 was developed by Dr. Fisher in the 1920s (it coincides with the point where 2 standard deviations from a normal mean lies) and is not the 11th commandment, i.e., it's not an absolute cut-off.

        "The odds of developing severe disease (e.g. requiring ventilation or resulting in death) during the treatment period (day 1 to day 16) were significantly reduced by 79% for patients receiving SNG001 compared to patients who received placebo (OR 0.21 [95% CI 0.04-0.97]; p=0.046).

        Patients who received SNG001 were more than twice as likely to recover (defined as ‘no limitation of activities’ or ‘no clinical or virological evidence of infection’) over the course of the treatment period compared to those receiving placebo (HR 2.19 [95% CI 1.03-4.69]; p=0.043)."…SNG001-in-hospitalised-COVID-19-patients.html

        1. Silverlake Bodhisattva says:

          Thanks for the extended discussion; sort of what I suspected, but I’m just a lawyer, not a doctor (“Dammit, Jim!“) and if I read a pharma press release before I’ve had enough coffee, my hype filter isn’t fully activated….

        2. loupgarous says:

          One minor caveat, Erik: your last article came to us via Globe News Wire. Any source ending in “News Wire” is a press release and entirely unreviewed by anyone but the company whose PR staff wrote it. So any claims for effectiveness and/or safety have to be confirmed by outside authorities.

    3. Marko says:

      It may be hype but it could also be real. Need to see the data and even then , no doubt , subsequent larger trials. Still , the mechanism makes some sense , as this recent paper supports:

      “…Our data establish that one of the major immune evasion factors of SARS-CoV-2, Nsp1, efficiently interferes with the cellular translation machinery resulting in a shut-down of host protein production. Thus, major parts of the innate immune system, that depend on translation of antiviral defense factors such as IFN-β or RIG-I (45) are disarmed. Although SARS-CoV-2 encodes additional potential inhibitors of the innate immune defenses, a loss of Nsp1 function may render the virus vulnerable toward immune clearance….”

  4. a says:

    How easy is it to scale up production for the adenovirus vaccine verses these mRNA vaccine attempts. If both approaches seem to work well, then whichever is cheaper and easier to make will probably win out globally.

    1. Mammalian scale-up person says:

      “It depends” (wasn’t helpful, I know)

      -There are some folks set up for handling BSL-2s. Scale is similar to the mRNA type: it’s a lot like doing mammalian cell culture up to about 2kL scale (i.e. can all be done in single use things that people might happen to have laying around a pilot lab) with the exception of the infection by adenovirus in the mammalian production reactor: let your cells grow up to density, add your thawed virus via a side port, let ferment another week or so. Different folks have different tricks for shortening up the takt to increase production rate, but we can make a good amount of doses in a few pilot-scale facilities that already exist.

      -At 5E10 particles/dose, that’s about 2mL of cell culture = 1 dose for the usual host cell lines. We can knock that out in four single use 2kLs in a year (40-50% yield losses in purification which is typically orthogonal IEX), but let’s assume we need it a bit faster than that: Samsung, WuXi, etc all currently have capacity for bulk production *right now* to supply the world within six months of thaw. We don’t even need to buy anything long lead time, we just need to figure out what to prioritize – I think everyone can spare some capacity though. Companies that have previous experience working with adenovirus platforms will be better positioned to validate faster, since they’re able to leverage standard protocols. There are a few of these.

      -Bottlenecks will be fill-finish materials (vials, caps as Derek has said before), single use plastics. Most of the modern purification methods use charged membrane separation rather than IEX resin, as it’s faster (less than half the time demand of traditional chrom) and enables a much shorter takt – but these will be in short supply if we need a lot of them. They’re typically one use. Single use bioreactors are also going to be in short supply, but it’s not nearly as big an issue, especially if your host cell is a garden variety HEK293 and you can harvest-refeed a cell line indefinitely as opposed to doing new thaws per batch.

      -A BIG PLUS is that operationally, we know how to do mammalian cell culture. We know how to make weird additions. We know how to do the titers, and we know how to work with BSL-2s. We know how to run orthogonal IEX and HIC if needed. We’re not trying to do anything super new in terms of weird processes to be developed from scratch – unlike the RNA vaccines. You tell me to go make a batch of adenovirus, I can use all my pre-existing batch record and automation templates with very few tweaks and it will run a lot smoother with very few engineering / development batches crapping out. You tell me to go make some RNA in kg amounts, and I will have some questions and a LOT of automation work to do, and the first few batches will not even be fit for a BALBc mouse.

      1. Simon Auclair the Great and Terrible says:

        Whats a takt?

        1. Marko says:

          Per Wikipedia : Takt time is the average time between the start of production of one unit and the start of production of the next unit, when these production starts are set to match the rate of customer demand. For example, if a customer wants 10 units per week, then, given a 40-hour work week and steady flow through the production line, the average time between production starts should be 4 hours (actually less than that in order to account for things like machine downtime and scheduled paid employee breaks), yielding 10 units produced per week. In fact, takt time simply reflects the rate of production needed to match the demand.

          1. Simon Auclair the Great and Terrible says:


        2. Mammalian scale-up person says:

          Demand frequency: if you need to produce 100 batches in a year, the takt time = (365 – preventative maintenance downtime – changeover time)/100 for a takt time of about 3 days. If your fermentation process requires a 12 day fermentation + infection period, you need four bioreactors to achieve the demand. So named by the German word for an orchestra conductor tapping his baton for everyone to follow. If your downstream purification system requires several long slow chromatography steps, it won’t be able to keep up with the fermentation production – so you need to purchase parallel equipment.

          1. Some idiot says:

            Quick comment from someone who sings in a choir in Denmark… Music is written in bars with a particular length, and these are the main units of movement in the music (think 4 beats for most music, 3 for waltz, etc, and other wierd stuff When the composer wants it). So yes, this is what the conductor beats after. The German (and Danish) word for “bar” is “takt”… In addition, whereas in English one usually says something like “keep in time”, in Danish (and I think German) one says “hold takt”.
            So yes, makes sense!!! 🙂

  5. Bickle says:

    Can you tell us why you would take Pfizer/BioNTech over the others?

  6. Barry says:

    Interesting that no boost was seen upon the second dose. It may be that–along with antibodies to the Spike protein–this approach also elicited immunity to the adenovirus vehicle, and that the second dose was neutralized w/o doing anything.

  7. Andrew Robinson says:

    Oxford uses “a chimpanzee adenovirus (used because humans don’t have exposure and thus pre-existing immunity to it)”. Does one develop immunity to the vector chimpanzee adenovirus? What happens when you need a booster at year 2?

    1. Mathijs van den Bergh says:

      “Oxford uses “a chimpanzee adenovirus (used because humans don’t have exposure and thus pre-existing immunity to it)”. Does one develop immunity to the vector chimpanzee adenovirus? What happens when you need a booster at year 2?”

      You do develop some immune response to Chimp ads, previous work has found about 8% seropositivity in parts of West Africa due to wild-type exposure.

    2. A Nonny Mouse says:

      There was something about this in the other 113 pages, but I only skimmed. I think that they did a test for it, though.

  8. Marko says:

    “….I have trouble reconciling the big buildup from the British media (and, I have to add, from the editorial staff at The Lancet) ”

    What ? You mean that some of these people may have an agenda ? That reported science may not be free of the effects of outside influence and corruption ? Oh , the horrors !

    Who could have imagined ??…….

    1. matt says:

      It’s not necessarily about the favoring, it’s about the tone. I can understand being favorably disposed toward the Beatles’ music, it’s the three hours of shrieking interspersed with overexcited fainting that gets to you. Especially when it turns out not to be the Beatles, but a co-worker’s teenage kid and his not-really-musically-talented friends tunelessly trying to bang out “Free Bird.”

      If you are writing an article about an entrepreneur and his startup business, it’s pretty understandable they think it could be bigger than Amazon. But normally you expect a journalist to be a little more grounded and to have heard such hype before, and to recognize for example if the entrepreneur hasn’t even gotten past the “drawing on a paper napkin” stage. In medical coverage, the UK press seems to be repeatedly of the “reporter was born yesterday” variety.

  9. Rhenium says:

    I’m not a immunologist (just a regular chemist) but I am a human and I do not think this specific vaccine is going to make it.

    Remember the uproar about adjuvants (specifically thiomersal) in vaccines amongst certain portion of the populations. Anything that includes the phrase “chimp virus” is not going to pass the “sniff test” in the media despite any good science, and the science here is a bit of a mixed bag as noted above. The more fringe parts of the internet will have a field day.

    It is frustrating that the above is the case, but it is the present timeline we are living in.

    1. Mantis Toboggan says:

      Anti-vaxxers will reject any vaccine for any reason.
      I don’t see reasonable people having a problem with “chimp virus.”

      1. Dr. Manhattan says:

        Have to agree on that. The antivaxers will “shop around” until they can find some reason, any reason, not to take it, no matter how irrational.

        I have seen some fall back on a misunderstanding of herd immunity. Herd immunity acts to slow down or break the transmission chain. It does nothing to protect an unimmunized individual from the disease if exposed. However it does decrease the likelihood of exposure, through the good graces of others who are immunized.

        1. Rhenium says:

          I fully agree that “shopping around” is exactly what will occur. However the sale-ability/meme-ability of the phrasing is what matters. Mercury is a much bigger bugaboo than Thiomersal, and “chimp virus” will be an easier sell to scare a sceptical public than “mRNA”.

          Ultimately it doesn’t matter whether the anti-vaxxers take the vaccine or not (may the devil take the hindmost) but whether they dissuade others and thereby reduce the efficacy of the herd immunity.

          1. Charles H. says:

            You are assuming that “herd immunity” is possible. But if the antibodies die back as quickly as reported it may not be. It could just be that the TCells will just ensure that repeated exposures will be cases mild enough to ignore. (This has been worrying me ever since some early reports on testing the Oxford antivirus on apes…and that was the response they got.)

            If that happens then we can expect COVID to become a chronic episodic disease, continually spreading to those in the population who haven’t had it recently, but almost always as something about as serious as a cold. However if you’re immune compromised, elderly, etc. there’s a reasonable chance that it might be fatal, or at least impart irremediable harm (strokes, kidney failure, etc.).

            It would be much better if a really immunizing vaccine is developed. But it’s not clear this is possible. I hope there’s evidence that this is wrong.

    2. Anon says:

      >Remember the uproar about adjuvants (specifically thiomersal) in vaccines amongst certain portion of the populations. Anything that includes the phrase “chimp virus” is not going to pass the “sniff test” in the media despite any good science, and the science here is a bit of a mixed bag as noted above. The more fringe parts of the internet will have a field day.

      Thimerosal was used as a preservative in some vaccines- it is not an adjuvant.

      I’m also surprised there is not more low quality noise (yet?) about the “chimp virus” given that HIV-1 derived from chimp SIV- “The most likely route of transmission of HIV-1 to humans involves contact with the blood of chimps that are often hunted for bushmeat in Africa.”

    3. Barry says:

      Thimerasol’s not an adjuvant per se; it’s a preservative. Not necessary in any vaccine in a single-dose vial.
      The mRNA vaccines may have an advantage here. Because our Innate Immune response recognizes some RNA sequences, they may act as their own adjuvant. That may allay some fears of some critics

    4. Barry says:

      There is a vaccine variant that I don’t expect we’ll ever see in 21st c. U.S. An attenuated virus that remains infectious but lacks virulence (can’t block interferon expression…) could spread through the community w/o needles, w/o vials, w/o sterile manufacture (but also w/o profit and w/o consent). The oral polio vaccine actually did this in a small way, although it rarely spread beyond a household.
      Any other vaccine will face compliance resistance in some quarters, of course..

  10. Paul W says:

    Typo in paragraph 4: “some people who are already had” should be “some people who had already had”. Great job as always, Derek!

  11. Mantis Toboggan says:

    If one were in a clinical trial for a vaccine that turned out to be less efficacious than anther vaccine, could they after the trial receive the more efficacious vaccine?

    Would any immunity (even if not sufficient for complete neutralization) to Spike from the first vaccine prevent immunity raised by the second vaccine or would administration of the second vaccine lead to higher titers (as second doses of mRNA vaccines do)?

    I imagine this question is mostly relevant for a small population of people, but am curious.

    1. Bob Marlee says:

      It depends on the composition of the vaccines, are they targeting the same sequence or different sequences? Based on previous posts here, it looks like we don’t have just dozens of efforts testing different means of delivering the same payload, but also different antigens.

      1. Mantis Toboggan says:

        Sorry if I wasn’t clear in the first post, yes I mean to the same antigen. I’m sure that it also depends on the delivery vector too.

    2. Also A Chemist says:

      Derek, I was also interested in the efficacy of receiving more than one vaccine. I was interested in participating in the Phase III trial for the Moderna vaccine, but if the Oxford or Pfizer vaccines turn out to be the one(s) that are widely distributed, will my participation in the Moderna trial compromise the effectiveness of the vaccine that I ultimately receive?

  12. debinski says:

    Mantis, I am wondering about this also. I have signed up for the Pfizer vaccine trial and wonder if I will regret it if it turns out not to be efficacious.

  13. David E. Young, MD says:

    You said “everyone got the same dose 5×10 to the 10th viral particles. Is that what you meant to say?

    1. Marko says:

      Yes. That’s what was claimed in the paper. In perhaps a more conventional form : “5 × 10^10 viral particles”.

  14. Chris says:

    Are we aware of how the Oxford vaccine’s (or any other vaccine) t-cell response compares to people who have been infected? And if not, is there any correlation between t-cell and antibody response – ie if neutralising antibody response is similar to recovered people, will the t-cell response also be similar in comparison.

  15. Grasshopper says:

    I am in the UK, so this is interesting. The media have definitely been going crazy about the Oxford vaccine trials, but I assumed that the media in *every* country would be doing the same about ‘their’ equivalent (because we’re all so fed up of the pandemic, of course). Are the American media not going nuts about the moderna trial then?

  16. Anon says:

    I am surprised that they did this: “As it was not possible to screen for negative SARS-CoV-2 serology in all participants, some enrolled participants had high-level anti-spike antibodies at baseline and their data are included in all analyses.”

    These participants should have been excluded from the analyses. Both their Ab and T-cell data contaminate the results, definitely a positive bias. Analyzing them separately might be interesting to look at re: boosting after a natural virus infection.

  17. G. T. Tenet says:

    Is the Oxford T-cell response directed to the Covid Corona virus (eg, viral antigen and in in vitro assays), Or a generalized measure of T-cell ? Could this T-cell response be to just the Chimp Adeno ChAdOx shell component of the vaccine?

    1. Bean says:

      good question. I would like to know the answer to that too. How are they assayed, anyone?

  18. A Nonny Mouse says:

    The lead of the trial was on the radio yesterday evening and said that there were now 11,000 that had had the vaccine, so it seems to be progressing well.

    My daughter has just been accepted for the Imperial second phase (after almost a month!), so it will be interesting to see how that goes. No adenovirus there.

  19. Druid says:

    The UK press hype around the Oxford/AstraZeneca vaccine is because the UK government has substantially funded the development in return for 100 million doses asap, so if it works, the UK has a guaranteed supply of effective vaccine. Ultimately, the world needs to be vaccinated, but initially every country will want to be first. The UK government has also just made a deal with BioNTech/Pfizer for 30 million doses but over 2 years (which could be a major problem), and another deal for 60 million doses from Valneva. In the middle of the next winter, we may all be desperate for doses of any effective vaccine. Of course, the UK press is mostly keen to support the conservative party in any way, and these contracts are one of the few things they have got right about covid-19. AZ says there are deals in place for 2 billion doses. That could take several years to supply. I foresee a lot of angry words from world leaders when the first vaccine is approved and delivery begins.

    1. Riah says:

      UK press hype or not, I think we are very lucky to have the ultra bright and capable Kate Bingham doing a fantastic job as Chair of the UK Vaccine Taskforce. She recognises that a single vaccine won’t work for everybody and the UK has also contracted for monoclonal antibodies from Astra Z for those who cannot have vaccines.
      A British/Scottish company is also looking at a T-cell solution:

      1. Adrian says:

        One fascinating aspect of this pandemic is how nationalistic press reporting is – in nearly every country “our researchers/companies” are at the forefront of the fight against COVID-19.

        British press reports on British research and trials and companies.
        Indian press reports on Indian research and trials and companies.
        German press reports on German research and trials and companies.

        Sometimes people are making a fool out of themselves when boasting with the superiority of their country by citing their local nationalistic press reporting in international forums.

        1. Riah says:

          that is exactly why I think Kate is absolutely right to play down the British effort and hedge her bets, excercise plenty of caution and contract for alternative options at the same time

          1. Adrian says:

            I think I am very lucky not living in the UK, the country with most COVID-19 deaths in Europe where even the Prime Minister had to be treated in an ICU.

  20. Adrian says:

    Is the expectation from the monkey trial results that the Oxford vaccine might not be providing sterilizing immunity still true, or does anything in the available data indicate otherwise?

    1. A Nonny Mouse says:

      This was addressed yesterday on the radio by the lead investigator; the doses of virus that they used in that study were pretty huge. No pneumonia, but there was some virus found in the upper respiratory tract. Expectation would be that people would get a mild form and not need hospital treatment.

    2. Riah says:

      “I think I am very lucky not living in the UK, the country with most COVID-19 deaths in Europe where even the Prime Minister had to be treated in an ICU.”

      yes you certainly are – not to mention everything else that’s going wrong here too- but we can only try and make the best of a bad job….

      1. Adrian says:

        My point was not to bash your country, just point out how ridiculous your “we are very lucky to have the ultra bright and capable” sounds to people outside your national filter bubble.

        Most of us are living in a national COVID-19 filter bubble without even noticing.
        And lack the humbleness to even realize how much better some pretty poor contries have handled COVID-19.

        Thailand has 70 million people, single digit daily new infections, and the last of the 58 deaths was on June (sic) 1st.

        Vietnam has 96 million people, a border with China and no local COVID-19 transmissions for over 3 months.
        Vietnam has 0 deaths so far, and the Scotsman who was for 2 months on ECMO in Ho Chi Minh City might not have survived in many other places in the world.

        All the praise you are heaping at some person who has some role in your countries COVID-19 response is pretty lame compared to these incredible success stories I am really in awe of.

        I am worried that here in the Western countries all eggs are in the vaccine basket, and investing in 3 different vaccines still gives you an 80% chance than none of these 3 will ever get approved.

        1. Riah says:

          Well maybe you should bash my country. The fact is that things have been pretty badly managed here so forgive me for being delighted that finally we get someone in charge of something that is actually capable. FYI I actually come from a country similar to those you mention and I’m sorry for the way it came across.

  21. Matthew Gruner says:

    Does anyone know of a meta-analysis on the age demographics of all the current vaccine trial cohorts? Specifically, is there an emphasis being put on people >60 years old? Based on what we know about immune correlates between >60 and <60 year olds I think there is a good rationale for separating the too groups when evaluating the different vaccines. This begs the question, will I have any say in which vaccine I get? I can think of the scenario in which many vaccines produce an appropriate interferon response in people 60 years old.

    1. Derek Lowe says:

      Haven’t seen enough data to answer that question. Everyone has been testing almost entirely in younger cohorts so far – understandably – with plans to broaden out in Phase II/III. But how broad, that doesn’t seem to have been released yet. . .

      1. Barry says:

        would they need a new Phase I in older subjects before Phase II/III if the first Phase I excluded them?

    2. A Nonny Mouse says:

      Imperial had an age cut off of 70 in the second phase of their trial which has just started; it will be interesting to see if they actually used anyone around that age. Given the rigorous medical and medical history that has to be examined to get selected, then they would have to be pretty fit to start with (at least there are no problems regards pregnancy or illicit drugs).

      1. eub says:

        Eh, 70-year-olds today were 19 in the summer of ’69.

  22. Barry says:

    This report leaps to assume that measuring IgG in circulation is representative of the whole protective immune response

    “The primary endpoints for immunogenicity were the geometric mean titres (GMTs) of specific ELISA antibody responses to the receptor binding domain (RBD) and neutralising antibody responses at day 28”

Leave a Reply

Your email address will not be published. Required fields are marked *

Time limit is exhausted. Please reload CAPTCHA.

This site uses Akismet to reduce spam. Learn how your comment data is processed.