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Criticism of the Oxford Coronavirus Vaccine

This piece at Forbes by Bill Haseltine has set off a lot of comment – it’s a look at the Oxford group’s vaccine candidate as compared to the SinoVac candidate, and you may recall (background here) that these are the two teams that have separately reported that their vaccines appear to protect rhesus monkeys from infection after exposure to the coronavirus. Haseltine has some criticisms of the Oxford data, and as you will see from that link to his name, his opinions deserve to be taken seriously. So what’s going on? Update: here’s the take on this at BioCentury.

Looking at the preprint on the Oxford results, Haseltine has a problem with the claim that the monkeys were protected from infection by a dose of ChAdOx1 nCoV-19. The key data are in the preprint’s Figure 3. The Oxford team checked for viral RNA several different ways. One was using bronchoaveolar lavage (BAL fluid), a sampling technique that involves running a bronchoscope down into the lungs and washing out aveolar spaces – a pretty darn invasive assay, which is why you don’t hear about it all that much compared to the still-not-so-nonivasive nose swabs. BAL fluid of the virus-exposed unvaccinated animals showed coronavirus genomic RNA throughout the study, and viral subgenomic RNA (more indicative of active replication) at days 3 and 5 after exposure. Meanwhile, the vaccinated animals showed the genomic RNA in only two monkeys, and no subgenomic RNA at all.

So far, so good. But both vaccinated and unvaccinated monkeys showed the same amount of viral genomic RNA from nose swab samples (Figure 3c). That’s the test that’s used out in the human population, and that means that the vaccinated animals would still be declared as positive for the coronavirus after being exposed to it. And the other thing that Haseltine notes is that the amount (the “titer”, in the lingo) of neutralizing antibodies in the blood of the vaccinated animals does not appear to be that high. You’d like to be able to dilute the blood antibody samples down by hundreds of times or even a thousandfold and still see antiviral activity in an in vitro assay, but in the Oxford case the activity started disappearing at about fortyfold dilution (Figure 2b).

On the positive side, 2/3 of the unvaccinated animals showed clear evidence of viral pneumonia at autopsy, but none of the vaccinated ones did. 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. You’d want to do better than that, if you can. Haseltine’s take is “Time will tell if this is the best approach. I wouldn’t bet on it.

Haseltine compares these results to the SinoVac inactivated virus vaccine, and finds that that one looks better – at its highest dose, no viral RNA was recovered from the tissues of the vaccinated animals, for example. This sort of “sterilizing immunity” is what you’d want to aim for – it gives the virus nowhere to go in the human population if you can vaccinate enough people. But it’s worth noting that the SinoVac results were from three doses of their vaccine (versus one of the Oxford candidate), and the viral exposure challenge was about half as strong (total viral particles) as what the Oxford paper used. The Oxford group also inoculated their monkeys in both the upper and lower respiratory tract, while the SinoVac team used a single inoculation in the trachea. So I agree with that tweet linked from AndyBiotech; I don’t think that a head-to-head comparison is fair. But Haseltine’s point stands, that the results as we have them from the ChAdOx1 nCoV-19 vaccine did not actually protect monkeys from infection.

If you dosed it more than once, perhaps it would. Update: that’s not going to work, of course. After a shot of the adenovirus vector, you’re not only going to have neutralizing antibodies to the desired antigen, but you’re going to have them to the adenovirus as well. It’s probably one shot and done. Update 2: maybe not! See this trial; they’re going to try it and see what happens. But we’re going to have to keep an eye on dosing schedules, of course. We’re looking at a massive effort to vaccinate people all over the world, in the end, and if we have to vaccinate them all twice (at, say, a two-month interval) then the problem becomes just that much harder. Three times, well, that’s something that I think we’re only going to seriously consider if we absolutely have to. If you want to picture an ideal vaccine, it’s one dose, sterilizing immunity, extremely low incidence of side effects. We have no idea at present if we’re going to get that, or even be able to get that, and the only way we’ll find out is human data. Lots and lots of human data. May the best vaccine win, and may the best vaccine be very good indeed. . .

47 comments on “Criticism of the Oxford Coronavirus Vaccine”

  1. PAndriola says:

    But isn’t the upshot that the Oxford vaccine turned the coronavirus into the common cold for the macaques, as opposed to COVID-19?

    1. Charles H. says:

      That may be a bit worrying, as one route that the virus has occasionally used it infection via the neural system…and the results weren’t good. The nasal nerves penetrate the blood/brain barrier, but anti-bodies have a harder time, IIRC needing to get there via intervention by glia cells.

      So this might save people from respiratory infections at the cost of a hugely increased number of paralysis and other neurological problems…whose nature I can speculate on, but can’t really justify guessing.

    2. ChrisW says:

      Isn’t it the case that the upper respiratory tract mucosal immune system is different and doesn’t really get triggered by these type of intramuscularly injected vaccines? That’s one reason I understood that a cold vaccine had never been developed. That would fit with these results. Oxford put the disease into the respiratory tract where it did well, as the vaccine didn’t trigger a response but as soon as it tried to get beyond there into the lungs the immune system responded and the antibodies squashed it. Sinovac put theirs pretty much straight into the lungs as I unserstand it, where it was squashed immediately before it had a chance to spread back into the nose and throat.

      I suspect none of the injected vaccines will stimulate a strong immune response in the nose or throat and so we will end up with something like Oxford’s which turns it into something more like a common cold.

      That would do, as large numbers of people wouldn”t need ventilating in overwhelmed hospitals so we could get on with our lives (while coughing).

    3. Peter Gresswell says:

      Isn’t it better to have a half good vaccine than no vaccine?

      If the reports are correct, large swathes of the population could be given the Oxford vaccine as soon as Christmas. After that other vaccines might come online, and they might work better, but why would you wait for them wholly unprotected for perhaps another 12 months rather than waiting for them partially protected?

      That logic would say let’s not bother giving people Remdesivir now as something better might come along later on.

  2. Adrian Bunk says:

    There are two additional problems that come immediately into my mind:

    1. Most people do not expect COVID-19 vaccines to give lifelong immunity. Which is not a problem if the vaccine protects from infection and is used for getting rid of COVID-19 for good.

    2. COVID-19 did spread so far because up to half of the infected people are asymptomatic, but they are anyhow spreading the infection. Something that turns symptomatic spreaders into asymptomatic spreaders is making it easier for COVID-19 to spread.

  3. Andy II says:

    In the meantime, Moderna reported a positive phase 1 preliminary data: https://investors.modernatx.com/news-releases/news-release-details/moderna-announces-positive-interim-phase-1-data-its-mrna-vaccine

    ” Immunogenicity data are currently available for the 25 µg and 100 µg dose level (ages 18-55) after two doses (day 43) and at the 250 µg level (ages 18-55) after one dose (day 29). Dose dependent increases in immunogenicity were seen across the three dose levels, and between prime and boost within the 25 µg and 100 µg dose levels. All participants ages 18-55 (n=15 per cohort) across all three dose levels seroconverted by day 15 after a single dose. At day 43, two weeks following the second dose, at the 25 µg dose level (n=15), levels of binding antibodies were at the levels seen in convalescent sera (blood samples from people who have recovered from COVID-19) tested in the same assay. At day 43, at the 100 µg dose level (n=10), levels of binding antibodies significantly exceeded the levels seen in convalescent sera. Samples are not yet available for remaining participants.

    At this time, neutralizing antibody data are available only for the first four participants in each of the 25 µg and 100 µg dose level cohorts. Consistent with the binding antibody data, mRNA-1273 vaccination elicited neutralizing antibodies in all eight of these participants, as measured by plaque reduction neutralization (PRNT) assays against live SARS-CoV-2. The levels of neutralizing antibodies at day 43 were at or above levels generally seen in convalescent sera.”

  4. Andrew Molitor says:

    These things don’t sound like they’re being administered by an innocuous shot in the arm. Is it normal to have super-invasive administration at this stage, to be followed by more, I dunno, kid-friendly methods as the vaccine moves through the process?

    1. A Nonny Mouse says:

      Certainly in the arm for the human test subjects

    2. Ian Malone says:

      From the Oxford pre-print, “animals were vaccinated intramuscularly.” I think the confusion might come from Derek’s ” inoculated their monkeys in both the upper and lower respiratory tract”, which is actually about the viral challenge, “Upon challenge with 2.6 x 106 TCID50 SARS-CoV-2 to both the upper and lower respiratory tract […]” Most of us who don’t do this kind of work are probably more used to seeing “innoculated” as a synonym for “vaccinated”, but it can also just mean to introduce a disease.

      Maybe an imperfect vaccine that vastly reduces the severity of the disease may buy us some time. I also wonder if it might bode well even if we can’t get rid of sars-cov-2 altogether that subsequent infections may be less severe too, but macaques aren’t humans.

      1. eub says:

        (Originally they were one and the same: smallpox inoculation as a preventive = deliberate inoculation with the smallpox virus. Jenner’s innovation with cowpox led to “vaccination” (/vacca/ cow) distinguished from the older “variolation”.

        People do *not* appreciate the smallpox vaccine and eradication program enough. If aliens came to Earth to judge our species on one act, as the defense lawyer I’d point to smallpox eradication.)

    3. Kris says:

      From my reading, the vaccine was given intramuscularly like most vaccines. They did the invasive procedure to analyze the BAL fluid to evaluate viral load.

  5. Peter Kenny says:

    Hopefully no hypochlorite in the BAL fluid…

  6. Giannis says:

    The ChAdOx vaccine needs a higher dose or at least two doses. The results from the MERS vaccines were also totally disappointing. I don’t know why they used such a low dosage after what they knew from MERS vaccine, especially regarding neutralization of the virus in vitro.

    https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30160-2/fulltext

  7. DTX says:

    Excellent summary.

    Producing enough vaccine to meet world demand will be a key challenge and 3 doses makes this even more difficult. Pharmaceutical companies often start manufacturing years in advance of anticipated approval because it is so hard to scale up vaccine manufacturing.

    Considering that creating a world supply of a vaccine will be very difficult, that primates are essential for most vaccine testing and that animal rights groups object the most to this kind of testing, it seems they and their families should be the last people on earth to get any vaccine that was tested in animals (alongside the anti-vaccination groups).

    (the one exception to this appears to be the Moderna candidate – which news reports suggest didn’t undergo animal testing. I’m interested if this is correct – or if the situation was that data from studies of other candidates was used to move mRNA-1273 directly into people).

    1. loupgarous says:

      When my wife and I were in college, she toured a primate clinical testing facility in Louisiana (where we went to school).

      Before leaving, each visitor was given a “PETA ID card”, which listed all the medical interventions developed with animal testing which the bearer shouldn’t receive as a matter of priniciple.

    2. johnnyboy says:

      The only situation where you can go into humans without first testing in animals is when you can convincingly demonstrate that your drug candidate would have no pharmacologic activity whatsoever in any animal species, including macaques. This is usually only possible with biologics, such as the Moderna drugs. I’m guessing this was the case with the Moderna vaccine – either that or they already had animal data for an equivalent mRNA product and used that for their first-in-human trial submission. The FDA is also probably more lenient than usual for COVID19 trials.

    3. Peter Gresswell says:

      How about restricting access to a vaccine from people who post stupid comments too?

  8. RA says:

    Thanks for a great post. A few questions/thoughts:

    1. Can the Oxford vaccine be given in a higher dose or multiple doses to get better results?
    2. Any reason to think the 2 approaches might have different side effect profiles/risk of ADE?
    3. A partially protective vaccine that stops the severe lung complications would be a step in the right direction. Can we assume that this vaccine would also reduce the risk of sudden clotting events, the development of the pediatric multisystem inflammatory syndrome, etc? Is the reduction of severe lung disease a good enough proxy for other bad outcomes?
    4. I think a safe 3 dose regimen at 1-week intervals that is more effective would be worth it for health care workers, nursing home residents, etc who are at highest risk and for whom it would be somewhat easier logistically to do 3 doses than the general public.
    5. If a vaccine with partial protection is available to Americans first, does getting it have any impact on the efficacy/side effects of getting another type of vaccine later? Might some people get ultimately get multiple types of vaccines, or will individuals have to choose one single vaccine “lane?”

  9. Dan says:

    Hi Derek,

    I’m a huge fan of the blog! Thank you for your updates on COVID-19!

    The results from this pre-print are certainly less than ideal. With that being said, both Haseltine and yourself have noted that this vaccine does not seem to cause any disease enhancement. This also appears true for the other COVID-19 vaccines. Granted, these are animal models, but this makes me optimistic that we will have a vaccine sooner rather than later.

    I do hope this is not entirely wishful thinking on my part. My own experience has made me appreciate just how different humans are from animal; there simply is no guarantee that results from animal models will translate to humans.

    That leads me to wonder how well disease enhancement is recapitulated animal models. How likely is it that disease enhancement happens in humans but not animals? Given the diversity of vaccine candidates, if there is no evidence of disease enhancement across all (or at-least most) vaccine candidates in animals, then would this suggest it will most likely not be a problem for humans as well?

  10. Ilya says:

    Thank you as always for your post, I am a huge fan of your blog.

    “if we have to vaccinate them all twice (at, say, a two-month interval) than the problem becomes just that much harder”

    Did you mean “then”?

    Derek, would you mind if we will translate some of your posts into Russian to make them available on one of the best popular science sites, biomolecula.ru?

  11. Tom Boyer says:

    The way we use flu shots now isn’t to eradicate the flu, it’s to protect vulnerable populations. If the Oxford vaccine simply moderates the severity of the disease, it could fulfill the same role as flu shots for older and higher-risk people, as well as medical personnel, first responders, nursing home workers, elderly caregivers etc…

    Of course a 100% vaccine is a better choice, but if Oxford’s is read a few months before the others, this debate becomes academic — we’ll take what we can get, no?

  12. MTK says:

    Manufacturing and distribution on scale for any of these vaccines is going to be very problematic. Not only of the vaccine but even supplies like needles and syringes. How do you actually innoculate say a billion or two people worldwide? Three doses of vaccine obviously makes that even more of challenge than two from a supply and distribution perspective and that doesn’t even include getting people to complete the three dose regimen.

    Certainly at least initially the vaccine availability is going to be limited then the question becomes who gets the first supplies, based on what criteria, and who decides. It’s tempting to say the most vulnerable, i.e. elderly, but is there not an argument that we would get more bang out of each vaccination from those populations most likely to be transmitters of the virus?

    These are not easy problems to solve or easy questions to answer.

  13. johnnyboy says:

    Yes ideally you want a convenient one-dose vaccine. But a worldwide pandemic is not an ideal situation. Having to have a booster vaccination after 2 weeks (not 2 months as written) is not the end of the world if it confers long-lasting immunity. The idea here is not to have a perfect commercial product; the idea is to get enough of the population immune quickly enough to avoid a global economic collapse or millions of deaths. The slight inconvenience of having 2 or even 3 vaccine doses shouldn’t even register – it was a bad move for Oxford to test only one dose.

  14. NotADoc says:

    Let’s posit that manufacture of enough doses/disposable needles/injection techs for the entire world is impractical.

    Assuming that, what if 25% of the world is vaccinated in the 6 months of vx rollout? Vx fewer people, but do so effectively, with as many doses as needed.

    Use Northern/Southern hemisphere alteration, assuming (without proof) that this virus is at least somewhat seasonal. Thus it would be administered in the fall in half the world, then the effort and supplies would xfer to the other half 6 months later. Yes, that probably won’t work politically, it’s a thought experiment.
    So now you’d have, ohhh, a third to a half of the population vaccinated. Might that be enough? Target the vx to those most likely to be: i) severely affected ii) community transmitters.
    So, healthcare workers, the old, ppl w immune system abnormalities, waiters, food delivery scooter ppl, etc.

    I’d think this wouldn’t eradicate the virus as is the goal with polio, but as ncov2019 (aka Wuhan Virus) is naturally burning down, targeted vx could speed and enhance that process even without reaching the herd immunity threshold.

    Would that work??

  15. ezra abrams says:

    I have never worked with virus, but I have worked with phage
    maybe I am all wet, but a two fold diff in the number of virus particles (I assume that is infectious particles not physical or RNA count), from diff labs, is not a real difference

  16. Erik Dienemann says:

    Counterpoint from Dr. Krammer (at Mt. Sinai and one of the leading virologists in the field) and others in this Twitter thread, with their focus being on the fact that it was only a single dose, which might have been expected to not confer full immunity (especially with a strong viral challenge).

    https://twitter.com/florian_krammer/status/1262130059583852545

  17. GW says:

    As I understand it, there are many gene therapies using adenovirus vectors, some approved , many in development. Isn’t there a real danger that widespread use of a common vector in a vaccine could render that adenovirus unusable in other therapies through antibody resistance? Just an amateur question.

    1. Derek Lowe says:

      Oh, that’s a solid question, for sure. I think that you may well “burn out” a particular viral vector with one vaccine, and that’s a real consideration. You would need different serotypes of adenovirus, from what I understand – and there are a lot of them being looked at, but still. . .

  18. Finn says:

    Is there a risk of adenoviral vector sequence recombination with covid19 and producing something that is even more dangerous?

    1. Derek Lowe says:

      Very different types of virus, so no – especially since the adenovirus vector isn’t assembling a replicating virus of its own in this case.

  19. eub says:

    Derek, isn’t it possible in principle to redose the vaccine using multiple adenovirus serotypes? I mean you’d rather not have to, but considering shit’s on fire yo. Or does their vaccine for some reason not allow for that?

    Hm, article linked from name (Nature 2000) suggests that the same adenovirus vector may be able to be re-dosed i.m. In mice, that is, so, well.

    1. Derek Lowe says:

      I saw that article – it gets referenced a lot, but I haven’t seen any experimental follow-up. Have I missed that? At any rate, see the second update.

  20. johnnyboy says:

    “After a shot of the adenovirus vector, you’re not only going to have neutralizing antibodies to the desired antigen, but you’re going to have them to the adenovirus as well. It’s probably one shot and done”

    I think the key word here is ‘probably’. It’s science innit – you don’t know until you’ve tested it. Wouldn’t have been that hard to add another dose and evaluate the response. But I guess the main goal of macaque studies was to support going into human trials, so we’ll see how that goes.

  21. MissMoo says:

    Any idea why the Oxford team is not using the prime-boost strategy?

  22. Doug Benbow says:

    I’m in support of Karolinska Institutes Johan Giesecke’s approach in Sweden. They are projected to achieve ‘herd immunity’ in June so little need for a hit or miss vaccine (as historically it usually is a miss).

    1. Derek Lowe says:

      Projected by whom?

  23. Dan S says:

    Oh brother. People have only been developing respiratory virus vaccines for 60 to 70 years and we still haven’t established a consistent protocol for innoculating patients with the virus or established what type of dosage of virus should be used (ideally a few) in evaluating a vaccine. No wonder it takes forever to develop these things

  24. John Altman says:

    Brilliant summary, Derek.

    I have been thinking about the Haseltine critique in terms of how we might measure efficacy if we do human challenge studies for licensure vs a conventional Phase III RCT. In a Phase III RCT we can use severe disease and death as endpoints – and obviously we wouldn’t want to do those for a challenge study. So, what would the endpoints be for a human challenge study?

    Let’s assume that they would include clinical symptom scores. But, would they also include viral load measures? This is where the potential problems lie. If the monkeys predict the results in humans, then it matters a lot whether you do BAL vs. nasal swabs. (Lots of other things also matter).

    Bottom line, if we ever do human challenge studies, I hope the Haseltine critique informs the trial design.

  25. George says:

    If the AstraZeneca/Oxford University is gonna be the more effective vaccine. Then they should have them license the vaccine to countries that can manufacture the vaccine (USA, China, France, England etc.). This way they can vaccinate there own countries. Not one country or bio pharma company can inoculate the whole world. Let’s not think of profits but saving human lives as fast and safely as possible. Without a vaccine the world will not go back to normal. From what I read the Covid19 will mutate into a weaker strain in a few years, just like the 1918 Spanish flu, it’s still around as a seasonal flu but not as deadly. All we need is to get everybody vaccinated and in a few years this virus is gonna become like the common seasonal flu. I hope I’m right, I ‘m no doctor just a concerned citizen.

  26. Luiz says:

    What about the dose? The study says it was half the one used in human trials… will this generate stronger response and better protection? Combined with the challenge that is significantly more aggressive than what we experience in real setting…

  27. Luis says:

    Derek here is the response from the Oxford group. What do you make of it?

    We are writing in response to the article published on Forbes online on 16th May by William Haseltine relating to the BioRxiv preprint publication ‘ChAdOx1 nCoV-19 vaccination prevents SARSCoV-2 pneumonia in rhesus macaques’ by van Doremalen et al (2020).

    The article compares vaccine research carried out in rhesus macaques by Sinovac Biotech in Beijing, China and at NIH, USA for The Jenner Institute at Oxford University, UK. These are small studies designed to look at the safety of the vaccine before starting human clinical trials. Head-to-head comparison of these studies are difficult since they differ in some important areas.    

    There are a number of key aspects of the studies where the conclusions drawn by the author are incorrect and misleading:    

    • Valid comparisons of virus levels post-challenge in nasal secretions cannot be made: these data are currently not available from the Sinovac group, where there was no intranasal challenge. The challenge protocols used differed between the two studies, in particular the dose and route of challenge used. The NIH study exposed the upper and lower respiratory tract to SARS-CoV-2 at a higher combined dose. The Sinovac study exposed the lower respiratory tract only and at a lower dose.    

    • Virus neutralisation assays are notoriously lab-specific so, to compare titres, the samples should be assessed side by side in the same lab. However, the high neutralisation titres measured in the Sinovac study are from after the live virus challenge rather than after immunisation. Both of these studies show clear promise, with high efficacy in each case against lung disease, and research on both vaccines should continue as planned. So, the headline result is that the both vaccines were able to provide clear protection against lower respiratory tract infection in the respective models.    

    Whilst legitimate to try to ask questions about the relative efficacy of the two vaccines, drawing comparative conclusions about the studies is flawed given the differences in study design. To draw definitive conclusions, one would have to compare the two vaccines side by side under the same experimental conditions. In the end it is the impact on clinical disease that matters. Of course with similar safety and efficacy the single dose Oxford vaccine, now partnered with AstraZeneca, would be preferred to a three dose vaccine for cost, manufacturing and operational reasons.    

    As we write the clinical trials of these vaccines continue and we will soon have results giving us a better indication of the safety and potential efficacy of Oxford vaccine. The world needs multiple vaccines and it is our hope that of the many vaccines in development at least some will show promising efficacy and rapidly move to late-stage trials and subsequent approval as soon as possible    

  28. Stanley S. Levinson, Ph.D., DABCC says:

    I am pretty sure that the nasal/BALB RNA in both vaccinated and control disappeared by 7 days after inoculation of what was apparently a very heavy dose of the virus that I believe was given nasally but I could not find exactly how in the paper. I would say that the virus could survive in the lung for several days but not reproduce since ther was no new RNA in the treated animals. . Moreover, identification of RNA does not mean it is live virus. In fact, according to CDC, CDC recommends 12 days isolation after symptoms because, although RNA can some times be isolated, live virus has not. They seem to think, the RNA is either from dead virus or from antibody inactivated virus. They say 9 days for recovery and then 3 days after, during which some people still shed very low levels of RNA that is apparently non-infectious, So, I think the Authors negative comments are very weak.

  29. James Baker says:

    A few comments about the adenovector;

    Oxford went to chimp adenovirus because essentially all humans have neutralizing immunity to human adenoviruses that cleared the viral vector before immunity to the neo-antigen (in this case SARS-CoV-2) occurs. They showed it conclusively before they made the change.

    Subsequent immunization will likely have the chimp adenovirus vector cleared more rapidly, causing less of a booster effect (although potentially inducing significant inflammation from the adenovirus response).

    This vector required co-administration of a modified vaccinia virus vector to show cellular immunity in malaria (https://pubmed.ncbi.nlm.nih.gov/27307573/), but was at least safe.

    Therefore, while this platform has a bit more human data it has never produced a licensed human vaccine much like the mRNA approach.

  30. Surinder singh says:

    The so called failure of the Oxford vaccine is overstated. The viral load was extremely high (equivalent to 2.6 million TCID50 or roughly 26 billion viral particles) and administered to both upper (nasal) and lower respiratory (lungs) system. In an infected person we only typically see between 1-10 TCID50/ml in lung samples). No human will ever be exposed to the levels these animals were exposed to by orders of magnitude. One also needs to differentiate between gRNA and sgRNA. sgRNA is more important as it is indicative of replicating virus and not from remnant challenge viral particles that was administered. The lungs were clean with no pneumonia and near baseline sgRNA levels. The vaccine worked in the monkeys and protected them. The nasal stuff is an artifact of viral challenge. Additionally, this is also a single dose vaccine unlike the Sinovac (3 shots) and Moderna (2 shots) vaccines.

  31. Harry M Pierson says:

    I’m by no means anti-vaccination nor anti-science

    But I am 71 years old, and I can’t help feeling corners are being cut, and adverse effects may not be known within a year to 18 months

    Accordingly, I’m reluctant to get any of these vaccines during the initial rollout, particularly if that occurs in less than 12 months

    1. fajensen says:

      Sure, but, the virus have side effects also. Some of them nasty if one is unlucky, this is not ‘the flu’!

      F.W.I.W., I think I already got a mild version of Covid-19:

      In Mid-February, I had 5 days with fever and pretty much slept all the time. Then the fever cleared and we put it down to ‘flu’.

      Then, after about another 5 days just feeling tired, I had a pain inside of my bones so I could barely walk, I first though I had a blod-clot or something for a while but of course not in ALL of the limbs at once!?!

      This followed by a nasty on and off cough for 6 weeks (popped a blood vessel in one eye with coughing), all this interspersed with the ‘bone pains’, exhaustion, some kind of ischias so I can’t sleep on one side because the pain in my hip / lower back wakes me up, once the cough dies out, there are bouts of 3 days of feelling like one is breathing in a very fine powder, then a few days where one is feeling better, and then ‘the powder’ is back!

      Basically it has been One Damn Thing after another until finally, mid May, I feel kinda normal again, only I get tired easily. It feels like Covid has several ‘finishing moves’ and iterates through them to find something that works.

      I will risk the vaccine!

  32. Mik says:

    Even if you might ” *like* to be able to dilute the blood antibody samples down by hundreds of times or even a thousandfold and still see antiviral activity in an in vitro assay,” why should that be *expected* ? Why shouldn’t it be enough to exhibit antiviral activity at physiological concentrations?

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