Yeah, the fact that this doesn't even need a freezer is great news.
The fact that we have three highly effective vaccines in such a short period is amazing and between them we might stand a chance of making and distributing them at the scale necessary to get things under some kind of control by August.
Another huge differentiator is price. At $3 to $4, many countries will jump on board ASAP and stay away from the expensive vaccines from Pfizer and Moderna.
The key differentiator is the mechanism of action, not the storage system.
The other two current candidates are mRNA vaccines, an approach which hasn't been used in humans before -- looks like the harbinger of a revolution but we have no past experience.
This O/AZ uses the actual spike protein embedded in a simian virus (that does not affect humans and has its own DNA removed). It's possible to generate antibodies to the vehicle (virus) which is why a simian virus is used (humans won't already have encountered it) but also means your own immune system could target the vaccine itself. Loewe speculates that this is why the higher dose was less effective.
I'd argue that it is more accessible to everyone including developed nations. It only requires a standard technology freezer - like that you have in a residential home. COVID-19 has already cost the UK hundreds of billions, so being able to roll out a vaccine with minimum hassle and without needing specialist storage and training on its handling, is an absolutely enormous benefit.
Honestly I feel like this vaccine is going to leave the mRNA-based vaccines trailing in its wake in terms of global government adoption.
Moderna vaccine also seems to have similar storage requirements with a high price tag. BioNTech otoh has impractical storage requirements for the third world. AstraZenca's price and storage combiation may open possibilities for distributing this globally.
An important fact that I haven't seen mentioned in this thread is that 3m doses have been manufactured already and are available in the UK supply chain today. "All" that's required is the approval from the regulator - but I guess that is still a little way off. 3m would do a lot of good though - frontline staff, the most vulnerable, hotspots....
It's interesting to layman's eyes that the dosing regime using 1.5 doses is more effective than the one using 2 doses as I would expect the inverse; are there any plausible explanations for this?
These stats are based on 130 people getting covid out of an experiment of 25,000 people. They dont give a breakdown of the stats (e.g. who was on placebo, who was on which dosing regimen
) but those are small nubmers.
I think its possible that this is just noise. The difference between '60%' and '90%' might just be a handful of cases.
They show that it works though, thats the main thing.
edit: e.g. of those 130 cases lets assume half were in each regimen experiment. So 65 cases in the 'two full doses experiment' if they got 60% efficiacy then that means about 26 people with the vaccine got covid vs 39 with placebo. In the 'half dose then full dose' experiment if they got 90% efficacy then that means about 7 people with the vaccine got covid vs 58 with placebo. So the difference between 60% and 90% is 19 people. They show that the vaccine works but there is lots of uncertainty between the two dosing regimens.
It's because of the way the AZ vaccine works. It uses a different virus to infect cells which then create the antigen to stimulate the immune response. These are a bit unstable, since the vaccine itself, being a virus, is an immune system trigger. The immune system might snuff out the vaccine itself after a huge first dose, then the second dose is wiped out.
This is I think why the mRNA vaccines are doing better. They don't use a virus as a vector, they use a less convoluted vector of a more basic mRNA instruction set. They're also in a way more "scalable" in that a future disease or a mutation of Covid with a new spike protein could have a new vaccine made quickly by tweaking the mRNA sequence.
One theory is that it's due to the vector. This utilizes an adenovirus (which has been used more commonly in vaccines previously, and is different from the novel mRNA viruses developed by Biontech/Pfizer/Moderna). The thought process is that with a larger initial dose of the vaccine, more immune resistance is built up by the body initially, which then neutralizes some of the booster when its given later.
We (Britain) may have totally screwed up our general response to COVID. But at least we’re still pretty good at science. Thanks Oxford for saving the day.
Tyler Cowen made this point a few months ago (https://marginalrevolution.com/marginalrevolution/2020/07/wh...): the public health response has been "generally poor" but the UK was first on the mark with dexamethasone and has been among the first with the vaccines. He went as far as saying the UK has had the best response to COVID despite the public health response.
Also worth noting that we did this by having a board research base that was not tied to immediate returns. A year ago Sarah Gilbert was struggling to get funding for work on the MERS vaccine, which was seen as largely irrelevant.
Not to downplay Oxford or Britain's work, but I think it's safe to argue that the poor general response to COVID is also an indicator of your skill at science. And I say this as American, who's response was just as bad or worse.
People are going to look back at this pandemic with amazement at the work the world scientists did to create a vaccine in record time, but with shame and embarrassment at the loss of life in countries that are considered world powers due to politics, ignorance, and stubbornness.
This statement seems a big deal:
"There were no hospitalised or severe cases in anyone who received the vaccine"
Is that also true of the Pfizer and Moderna trials?
Are the various trials measuring 'effectiveness' in the same way?
Is there a standard for 'effectiveness' in these Covid-19 trials?
It will take some digging and real effort to compare the risks and benefits of the various vaccines coming to market.
This is the information we have on the BioNTech/Pfizer vaccine regarding severe cases: “There were 10 severe cases of COVID-19 observed in the trial, with nine of the cases occurring in the placebo group and one in the BNT162b2 vaccinated group.”
Just as a reminder, that vaccine had more than 40k people in each group, with 170 cases of COVID-19 being observed, 162 in the placebo group, 8 in the vaccine group.
As you can see, the sample sizes get quite small, so I’m not sure how much, if anything, this tells you regarding severe cases. There could have been just as well no severe case in the treatment group, just by luck. What would that tell us?
I didn’t find any info regarding severe cases and the Moderna vaccine but I maybe I missed it. Those press releases are hard to read.
Seems like the sample size is probably too small to draw any conclusions there. 131 got covid in the trial, if 70% effective than 39 should be from the group that got the vaccine (i think. Did i do that right given they're combining the two dosing regime)?
Maybe its chance that none of those 39 got really sick. I'm not sure what the age breakdown of trial participants was- were the people in the oxford trial younger? Did the distribution match the distribution from the mRNA trials? I have no idea.
> Is that also true of the Pfizer and Moderna trials? Are the various trials measuring 'effectiveness' in the same way? Is there a standard for 'effectiveness' in these Covid-19 trials?
Yes, its true that there were no "severe" cases in the other vaccine trials as well.
> This statement seems a big deal: "There were no hospitalised or severe cases in anyone who received the vaccine"
It may be. When considering disease severity, we are no longer looking at a pool of people who have been given the vaccine (which is in the tens of thousands for all of these), we are looking at a pool of people who got sick. That means the sample size is reduced to approximately 90-100 for placebo wing of each vaccine, and 30 for ChadOx vaccine arm, and about 5 for Moderna/Pfizer vaccine arms each. That's fairly small.
Seems like the estimated rate of severe cases is around 10-20%. Assuming its 10% (which would mean its harder to identify an actual reduction in disease severity rate from the placebo group), then in the case of Pfizer/Moderna, there would be a greater than 50% chance of seeing no severe cases in a group of 5 infected, vaccinated patients, even if there was no effect on the severity of the disease. The greatest benefit to the vaccine is that they seem to prevent infections substantially, but that also means it will take months before enough infections occur to get some kind of statistical significance on if severity is also affected.
But with this vaccine, 30 cases with no infections is definitely in the realm of statistical significance. I don't have the exact numbers from the trial, but if it indeed is 0/30 vs around 10/100 between the vaccine/placebo wings, it definitely meets the typical thresholds of statistical significance.
It's important to note that, at least according to my understanding, the Pfizer/Moderna trials are measuring symptomatic cases, not doing actual tests on their trial participants. This means that it could well mean that the reason the vaccines appear to be so effective is because they truly are reducing the severity of the disease to the point of being asymptomatic. We just aren't able to see it yet due to the way the data is being collected.
So, the Oxford vaccine stated "... no hospitalised or severe cases ..."
The Pfizer press release states:
"There were 10 severe cases of COVID-19 observed in the trial, with nine of the cases occurring in the placebo group and one in the BNT162b2 vaccinated group."
So, zero severe cases for Oxford, and one for Pfizer.
Interesting.
Should also point out the Pfizer trial may have had 43,000 participants, and the Oxford one 24,000, so they are different size trials.
Also, it's super easy to miss important details when comparing outcomes like
this, to do this properly really requires a project or in-depth investigation,
not my 15-minutes research effort. :)
There were no hospitalisations or severe incidents for either the Pfizer and Moderna trials were was related to the vaccine.
And it's pretty easy to compare the vaccines. It will mostly come down to price, ease of manufacture and ease of distribution i.e. temperature. Given that for the 3 viruses all have no risks associated with their use.
Here [1] it says the vaccine was designed mostly over the weekend of 11th Jan 2020. Here we are 10 months later and we know it works. If our knowledge of vaccine design is so good experts can design a vaccine that works over a weekend, what new breakthroughs are required to reduce the time between then and now substantially? A lot of benefit could have been had if we'd been able to get along this path more quickly.
Correct me if I am wrong,
Oxford uses traditional Vaccine design technique (using a weaker virus and adding spikes or something similar) while Biontech(Pfizer) and ModeRNA use MRNA which is completely new technique (messenger RNA).
This is awesome for more than just vaccinations. Traditionally the groups allocating govt funding to science and industries are very risk averse and this could be one more example where taking risks can payoff.
> One dosing regimen (n=2,741) showed vaccine efficacy of 90% when AZD1222 was given as a half dose, followed by a full dose at least one month apart, and another dosing regimen (n=8,895) showed 62% efficacy when given as two full doses at least one month apart. The combined analysis from both dosing regimens (n=11,636) resulted in an average efficacy of 70%. All results were statistically significant (p<=0.0001).
Also:
> and no hospitalisations or severe cases of the disease were reported in participants receiving the vaccine.
That headline is not quite correct. From the article:
> Phase 3 interim analysis including 131 Covid-19 cases indicates that the vaccine is [on average] 70.4% effective when combining data from two dosing regimens ... In the two different dose regimens vaccine efficacy was 90% in one and 62% in the other
And to be clear, it's not just one dose vs two:
> tests on two different dose regimens showing that the vaccine was 90% effective if administered at a half dose and then at a full dose, or 62% effective if administered in two full doses.
So "Oxford vaccine is up to 90% effective", perhaps?
Is there any research or early guestimates about risks (or benefits) of getting multiple different vaccines for Covid? E.g. What if one gets this, and then later moderna vaccine? Will they fight each other, or work together or is it unknown whats going to happen?
I'm not a microbiologist, but this is not how vaccines work. The vaccines are going to put "something strange" in your body that "resembles" the virus, but it's not the virus (it's either a deactivated version of it, or some proteins which identify it...) and then is YOUR immune system the one which "attacks" this pseudo-virus. In this way, your immune system is learning how to defend to "this kind" of strange agents.
In a future if your immune system sees the virus, will defend you.
If you get the two kinds at the same time, maybe the two doses are too much for your immune system to handle it properly and the side effects may affect you (e.g. you can get fever because your immune system is under too heavy load).
There are definitely benefits to vaccine diversity. The Oxford ChAdOx1 virus involves putting a modified chimp adenovirus into people. People don't have immunity to chimp adenovirus, so it infects them and delivers the spike protein, which elicits immunity. But that might also elicit immunity to the chimp adenovirus! If that happens, then a later does of the vaccine - say, for a new strain of SARS-CoV-2 in a year or two - might not be as effective, because immunity to the chimp adenovirus will stop the vaccine delivering the spike. In that case, having a different way to deliver a vaccine will be a life-saver.
In case anybody was wondering what this actually is: “The ChAdOx1 vaccine is a chimpanzee adenovirus vaccine vector.” They put a corona spike sequence into it.
By comparison, the Moderna is making a RNA vaccine, and BioNTech an epitope vaccine (the actual protein).
The ‘invasive’ effect is decreasing in that order. Oxford’s ChAdOx1 infects your cells to create RNA, then protein, then T-cell recognition/apoptosis, then epitopes trigger B-cell antibody production. Moderna RNA skips the infection part. BioNTech epitopes go right to B-cells.
But, they also have deceasing stability and manufacturing scalability in that order.
The press release is interesting. Not the best way to present their data. Immediate conclusion of many newspapers is "oxford vaccine is less effective then...".
Incoming possible Silly, Stupid and Lazy Questions,
1. Are there any vaccine ( of any Disease ) that are 100% effective? Or do we operate ( as I would assume ) something like 5 Nines effective rate and call it 100%?
2. Across all type of Vaccine, what are the average or median effective rate? i.e Should we expect Vaccine to be 90%+ effective in the first place? Or is that a wrong expectation to make?
3. What happens in the case of 10% ineffective, do they take a third dose?
"These preliminary data indicate that the vaccine is 70.4% effective, with tests on two different dose regimens showing that the vaccine was 90% effective if administered at a half dose and then at a full dose, or 62% effective if administered in two full doses."
So important:
"A key element of Oxford’s partnership with AstraZeneca is the joint commitment to provide the vaccine on a not-for-profit basis for the duration of the pandemic across the world, and in perpetuity to low- and middle-income countries."
I doubt it would help much, for similar reasons why you don't give a flu vaccine to someone already sick.
A vaccine is meant to stimulate adaptive immunity which culminates in formation of memory cells - highly selected T and B lymphocytes which are very specific to the infectious agent.
This process typically takes a couple days [1] and is rather involved. Once you have the memory cells, however, the next time you get in contact with the virus your memory cells will jump-start the immune response much more quickly, before the virus gets a chance to replicate.
In a regular infection the same mechanisms of adaptive immunity are activated, but on top of that you already have the complications from the virus itself (cell death in lung epithelium, accumulation of excess fluid, hypoxia, cytokine storm etc). A vaccine dose won't necessarily speed it up, there are plenty of virus particles already stimulating the immune system - it's just picking up the slack a bit too late.
There are other factors to consider but that's the general idea.
On one hand, all of these vaccine trials excluded people who already had COVID, so we don't fully know what the effect would be in large numbers. However at least one person with COVID immunity accidentally got into the Oxford Phase 1/2 trial (according to earlier published results), so we at least know it didn't hurt them.
On the other hand, it is generally thought that vaccines can trigger immune reactions that are often much stronger and longer lasting than just being infected, so you would expect there to be a benefit to getting vaccinated even if you already had it. But only time will tell for sure. No one really knows how long immunity of either type will last - we just have to wait and find out!
[+] [-] mcdowall|5 years ago|reply
That’s much more accessible to developing / low GDP countries as opposed the cumbersome and expensive storage requirements of the other two.
[+] [-] noneeeed|5 years ago|reply
The fact that we have three highly effective vaccines in such a short period is amazing and between them we might stand a chance of making and distributing them at the scale necessary to get things under some kind of control by August.
[+] [-] throwawayiionqz|5 years ago|reply
[+] [-] wereHamster|5 years ago|reply
[+] [-] gumby|5 years ago|reply
The other two current candidates are mRNA vaccines, an approach which hasn't been used in humans before -- looks like the harbinger of a revolution but we have no past experience.
This O/AZ uses the actual spike protein embedded in a simian virus (that does not affect humans and has its own DNA removed). It's possible to generate antibodies to the vehicle (virus) which is why a simian virus is used (humans won't already have encountered it) but also means your own immune system could target the vaccine itself. Loewe speculates that this is why the higher dose was less effective.
[+] [-] nbevans|5 years ago|reply
Honestly I feel like this vaccine is going to leave the mRNA-based vaccines trailing in its wake in terms of global government adoption.
[+] [-] Demiurge|5 years ago|reply
[+] [-] kul_|5 years ago|reply
[+] [-] sgt101|5 years ago|reply
[+] [-] ggm|5 years ago|reply
[+] [-] thomond|5 years ago|reply
[+] [-] summerlight|5 years ago|reply
[+] [-] codeulike|5 years ago|reply
I think its possible that this is just noise. The difference between '60%' and '90%' might just be a handful of cases.
They show that it works though, thats the main thing.
edit: e.g. of those 130 cases lets assume half were in each regimen experiment. So 65 cases in the 'two full doses experiment' if they got 60% efficiacy then that means about 26 people with the vaccine got covid vs 39 with placebo. In the 'half dose then full dose' experiment if they got 90% efficacy then that means about 7 people with the vaccine got covid vs 58 with placebo. So the difference between 60% and 90% is 19 people. They show that the vaccine works but there is lots of uncertainty between the two dosing regimens.
Edit: why the downvotes?
[+] [-] thehappypm|5 years ago|reply
This is I think why the mRNA vaccines are doing better. They don't use a virus as a vector, they use a less convoluted vector of a more basic mRNA instruction set. They're also in a way more "scalable" in that a future disease or a mutation of Covid with a new spike protein could have a new vaccine made quickly by tweaking the mRNA sequence.
[+] [-] sanxiyn|5 years ago|reply
Pfizer and Moderna vaccines are not vectored.
[+] [-] cuchoi|5 years ago|reply
[+] [-] NeutralCrane|5 years ago|reply
[+] [-] jonplackett|5 years ago|reply
[+] [-] Smaug123|5 years ago|reply
[+] [-] twoslide|5 years ago|reply
[+] [-] ssully|5 years ago|reply
People are going to look back at this pandemic with amazement at the work the world scientists did to create a vaccine in record time, but with shame and embarrassment at the loss of life in countries that are considered world powers due to politics, ignorance, and stubbornness.
[+] [-] camkego|5 years ago|reply
Is that also true of the Pfizer and Moderna trials? Are the various trials measuring 'effectiveness' in the same way? Is there a standard for 'effectiveness' in these Covid-19 trials?
It will take some digging and real effort to compare the risks and benefits of the various vaccines coming to market.
[+] [-] arrrg|5 years ago|reply
Just as a reminder, that vaccine had more than 40k people in each group, with 170 cases of COVID-19 being observed, 162 in the placebo group, 8 in the vaccine group.
As you can see, the sample sizes get quite small, so I’m not sure how much, if anything, this tells you regarding severe cases. There could have been just as well no severe case in the treatment group, just by luck. What would that tell us?
I didn’t find any info regarding severe cases and the Moderna vaccine but I maybe I missed it. Those press releases are hard to read.
My source is Pfizer’s press release: https://www.pfizer.com/news/press-release/press-release-deta...
[+] [-] bawolff|5 years ago|reply
Maybe its chance that none of those 39 got really sick. I'm not sure what the age breakdown of trial participants was- were the people in the oxford trial younger? Did the distribution match the distribution from the mRNA trials? I have no idea.
[+] [-] NeutralCrane|5 years ago|reply
Yes, its true that there were no "severe" cases in the other vaccine trials as well.
> This statement seems a big deal: "There were no hospitalised or severe cases in anyone who received the vaccine"
It may be. When considering disease severity, we are no longer looking at a pool of people who have been given the vaccine (which is in the tens of thousands for all of these), we are looking at a pool of people who got sick. That means the sample size is reduced to approximately 90-100 for placebo wing of each vaccine, and 30 for ChadOx vaccine arm, and about 5 for Moderna/Pfizer vaccine arms each. That's fairly small.
Seems like the estimated rate of severe cases is around 10-20%. Assuming its 10% (which would mean its harder to identify an actual reduction in disease severity rate from the placebo group), then in the case of Pfizer/Moderna, there would be a greater than 50% chance of seeing no severe cases in a group of 5 infected, vaccinated patients, even if there was no effect on the severity of the disease. The greatest benefit to the vaccine is that they seem to prevent infections substantially, but that also means it will take months before enough infections occur to get some kind of statistical significance on if severity is also affected.
But with this vaccine, 30 cases with no infections is definitely in the realm of statistical significance. I don't have the exact numbers from the trial, but if it indeed is 0/30 vs around 10/100 between the vaccine/placebo wings, it definitely meets the typical thresholds of statistical significance.
It's important to note that, at least according to my understanding, the Pfizer/Moderna trials are measuring symptomatic cases, not doing actual tests on their trial participants. This means that it could well mean that the reason the vaccines appear to be so effective is because they truly are reducing the severity of the disease to the point of being asymptomatic. We just aren't able to see it yet due to the way the data is being collected.
[+] [-] unknown|5 years ago|reply
[deleted]
[+] [-] camkego|5 years ago|reply
The Pfizer press release states: "There were 10 severe cases of COVID-19 observed in the trial, with nine of the cases occurring in the placebo group and one in the BNT162b2 vaccinated group."
So, zero severe cases for Oxford, and one for Pfizer. Interesting.
Should also point out the Pfizer trial may have had 43,000 participants, and the Oxford one 24,000, so they are different size trials. Also, it's super easy to miss important details when comparing outcomes like this, to do this properly really requires a project or in-depth investigation, not my 15-minutes research effort. :)
Pfizer release: https://www.pfizer.com/news/press-release/press-release-deta...
[+] [-] newsbinator|5 years ago|reply
[+] [-] threeseed|5 years ago|reply
And it's pretty easy to compare the vaccines. It will mostly come down to price, ease of manufacture and ease of distribution i.e. temperature. Given that for the 3 viruses all have no risks associated with their use.
[+] [-] arichard123|5 years ago|reply
[1]: https://www.theguardian.com/world/2020/nov/23/coronavirus-sc...
[+] [-] rusticpenn|5 years ago|reply
This is awesome for more than just vaccinations. Traditionally the groups allocating govt funding to science and industries are very risk averse and this could be one more example where taking risks can payoff.
[+] [-] jpxw|5 years ago|reply
> One dosing regimen (n=2,741) showed vaccine efficacy of 90% when AZD1222 was given as a half dose, followed by a full dose at least one month apart, and another dosing regimen (n=8,895) showed 62% efficacy when given as two full doses at least one month apart. The combined analysis from both dosing regimens (n=11,636) resulted in an average efficacy of 70%. All results were statistically significant (p<=0.0001).
Also:
> and no hospitalisations or severe cases of the disease were reported in participants receiving the vaccine.
https://www.astrazeneca.com/media-centre/press-releases/2020...
[+] [-] agd|5 years ago|reply
Moderna: £45, Pfizer: £20, Oxford: £3,
The Oxford one is also easier to store and transport.
[+] [-] threeseed|5 years ago|reply
Many countries e.g. Australia are licensing the formula so this is an important aspect.
[+] [-] londons_explore|5 years ago|reply
[+] [-] pja|5 years ago|reply
[+] [-] howlgarnish|5 years ago|reply
> Phase 3 interim analysis including 131 Covid-19 cases indicates that the vaccine is [on average] 70.4% effective when combining data from two dosing regimens ... In the two different dose regimens vaccine efficacy was 90% in one and 62% in the other
And to be clear, it's not just one dose vs two:
> tests on two different dose regimens showing that the vaccine was 90% effective if administered at a half dose and then at a full dose, or 62% effective if administered in two full doses.
So "Oxford vaccine is up to 90% effective", perhaps?
[+] [-] rixrax|5 years ago|reply
[+] [-] kuu|5 years ago|reply
I'm not a microbiologist, but this is not how vaccines work. The vaccines are going to put "something strange" in your body that "resembles" the virus, but it's not the virus (it's either a deactivated version of it, or some proteins which identify it...) and then is YOUR immune system the one which "attacks" this pseudo-virus. In this way, your immune system is learning how to defend to "this kind" of strange agents.
In a future if your immune system sees the virus, will defend you.
If you get the two kinds at the same time, maybe the two doses are too much for your immune system to handle it properly and the side effects may affect you (e.g. you can get fever because your immune system is under too heavy load).
[+] [-] twic|5 years ago|reply
There are definitely benefits to vaccine diversity. The Oxford ChAdOx1 virus involves putting a modified chimp adenovirus into people. People don't have immunity to chimp adenovirus, so it infects them and delivers the spike protein, which elicits immunity. But that might also elicit immunity to the chimp adenovirus! If that happens, then a later does of the vaccine - say, for a new strain of SARS-CoV-2 in a year or two - might not be as effective, because immunity to the chimp adenovirus will stop the vaccine delivering the spike. In that case, having a different way to deliver a vaccine will be a life-saver.
[+] [-] jl2718|5 years ago|reply
By comparison, the Moderna is making a RNA vaccine, and BioNTech an epitope vaccine (the actual protein).
The ‘invasive’ effect is decreasing in that order. Oxford’s ChAdOx1 infects your cells to create RNA, then protein, then T-cell recognition/apoptosis, then epitopes trigger B-cell antibody production. Moderna RNA skips the infection part. BioNTech epitopes go right to B-cells.
But, they also have deceasing stability and manufacturing scalability in that order.
[+] [-] toshk|5 years ago|reply
[+] [-] ksec|5 years ago|reply
1. Are there any vaccine ( of any Disease ) that are 100% effective? Or do we operate ( as I would assume ) something like 5 Nines effective rate and call it 100%?
2. Across all type of Vaccine, what are the average or median effective rate? i.e Should we expect Vaccine to be 90%+ effective in the first place? Or is that a wrong expectation to make?
3. What happens in the case of 10% ineffective, do they take a third dose?
[+] [-] bigpumpkin|5 years ago|reply
[+] [-] datameta|5 years ago|reply
[+] [-] jakozaur|5 years ago|reply
Good:
+ likely 90% effective if we use optimal dosing
+ no significant side effective. Looks better than Pfizer or Moderna.
+ already pre-produced at huge scale, 3 Bln doses in 2021
+ easy to store and administer, just regular fridge required
+ several times cheaper than mRNA
+ more traditional vaccine than novel mRNA, less tail risk in production and scaling up the process
Not good:
- two doses, efficient one month after first injection
- likely public will be confused about efficiency due to dosing regime
[+] [-] Beggers1960|5 years ago|reply
Every positive announcement raises my spirits slightly.
[+] [-] __warlord__|5 years ago|reply
[+] [-] puzzlingcaptcha|5 years ago|reply
A vaccine is meant to stimulate adaptive immunity which culminates in formation of memory cells - highly selected T and B lymphocytes which are very specific to the infectious agent. This process typically takes a couple days [1] and is rather involved. Once you have the memory cells, however, the next time you get in contact with the virus your memory cells will jump-start the immune response much more quickly, before the virus gets a chance to replicate.
In a regular infection the same mechanisms of adaptive immunity are activated, but on top of that you already have the complications from the virus itself (cell death in lung epithelium, accumulation of excess fluid, hypoxia, cytokine storm etc). A vaccine dose won't necessarily speed it up, there are plenty of virus particles already stimulating the immune system - it's just picking up the slack a bit too late.
There are other factors to consider but that's the general idea.
[1] https://www.researchgate.net/figure/Kinetics-of-CD8-T-cell-d...
[+] [-] ageitgey|5 years ago|reply
On the other hand, it is generally thought that vaccines can trigger immune reactions that are often much stronger and longer lasting than just being infected, so you would expect there to be a benefit to getting vaccinated even if you already had it. But only time will tell for sure. No one really knows how long immunity of either type will last - we just have to wait and find out!