Yet Another Cycling Forum
General Category => The Knowledge => Health & Fitness => Topic started by: Whitedown Man on 03 January, 2021, 02:52:29 pm
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News reports (whether old or new media channels) typically tend to state that the Oxford vaccine is “70% effective” without ever explaining their terms. Does “70% effective” mean that 70% of recipients are rendered 100% immune (and presumably the other 30% of recipients are therefore not rendered immune)? Or that 100% of recipients are rendered 70% immune (compared presumably to some prior / base level of immunity)? Or something else entirely?
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LMGTFY
Vaccine efficacy is the percentage reduction of disease in a vaccinated group of people compared to an unvaccinated group, using the most favorable conditions.[1] Vaccine efficacy was designed and calculated by Greenwood and Yule in 1915 for the cholera and typhoid vaccines. It is best measured using double-blind, randomized, clinical controlled trials, such that it is studied under “best case scenarios.”[2] Vaccine effectiveness differs from vaccine efficacy in that vaccine effectiveness shows how well a vaccine works when they are always used and in a bigger population whereas vaccine efficacy shows how well a vaccine works in certain, often controlled, conditions.[1] Vaccine efficacy studies are used to measure several possible outcomes such as disease attack rates, hospitalizations, medical visits, and costs.
https://en.m.wikipedia.org/wiki/Vaccine_efficacy
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On "How to Vaccinate the World" it was explained like this:
If a vaccine is described as 90% effective in a trial, that means that for every 9 people on the placebo that got the disease, 1 person who had the vaccine also got the disease.
That does not make sense to me. Using that definition, if 10 people get the disease and 5 are in each group it would be described as 50% efficacy, whereas in normal terms the vaccine has no effect so should be describes as 0% effective.
Perhaps they meant to say "for every 10 people".
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It means 70% fewer test subjects got ill compared to the control group.
Whether that's because it only works partially on everybody or it doesn't work at all on some people is a whole other question.
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It means 70% fewer test subjects got ill compared to the control group.
Whether that's because it only works partially on everybody or it doesn't work at all on some people is a whole other question.
Does this mean I'm wrong in my understanding that if we vaccinate 100 people, 70 people actually get protection, and 30 nothing happens ?
Then comes the question how many people need to get the vaccine at a specific efficacy rate, for it to make a difference to the population as a whole...
J
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It means 70% fewer test subjects got ill compared to the control group.
Whether that's because it only works partially on everybody or it doesn't work at all on some people is a whole other question.
Does this mean I'm wrong in my understanding that if we vaccinate 100 people, 70 people actually get protection, and 30 nothing happens ?
It doesn't work like that, it's a random process which is why you need population data. No-one is 100% protected (they can't bathe in virus soup and expect to be safe), and neither is anyone 0% protected (so that a single virus will definitely give them the disease).
Then comes the question how many people need to get the vaccine at a specific efficacy rate, for it to make a difference to the population as a whole...
J
That depends what you mean by "make a difference". For the million or so people already vaccinated, a number of people in that group would have died over the next year or so without it, so it's already made a difference. For herd immunity it depends on the infection rate for an unvaccinated population as well as the efficacy of the vaccine. Eg, measles is very contagious and needs 90-95% vaccination rate for herd immunity. Or perhaps to eradicate it? Probably more than are willing to have the vaccine, unfortunately.
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One expert today on BBC news explained that those who had the vaccine but still caught the virus, did not have as serious symptoms compared to those who hadn't had the vaccine, so it's not a simple binary result.
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Indeed, I believe not a single hospital admission for anyone that had the Oxford vaccine in the trial.
Unfortunately with the increased R for the new variant the % reqd for herd immunity is that bit higher and must be close to 75%. I don’t think that is likely any time soon.
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As the folks have explained, its a measure of effectiveness in a large group compared to those not given a placebo instead.
The other very misleading term that gets used is 'immune'. A vaccine doesn't make anyone immune. It primes your body to recognise the particular virus more quickly and to take the appropriate response. So if you have been vaccinated, the chances that the virus is killed off before it can start replicating or replicating at any significant level are greatly reduced. But your natural response is still in a contest, being vaccinated means its much quicker of the line. That contest can still be compromised by other health conditions, age and plain simple chance.
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The other very misleading term that gets used is 'immune'.
Working in health journalism, one of my pet hates is when writers refer to “immunity” when they mean “the immune system”. It’s lazy shorthand, and very misleading.
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Indeed, I believe not a single hospital admission for anyone that had the Oxford vaccine in the trial.
Unfortunately with the increased R for the new variant the % reqd for herd immunity is that bit higher and must be close to 75%. I don’t think that is likely any time soon.
If the vaccine is 70% effective, and the R number is 3, you need approx 95% vaccination to give an effective R of 1 with no other measures in place.
(You need 66% of the population to be immune, which is achieved with 94.2% vaccinated at 70% effectiveness).
Given that none of the vaccines are approved for children, 95% is not achievable. Even if it was, you'll be lucky to vaccinate more than 70%.
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70% is good.
But not as good as Dettol, which kills 99%
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Indeed, I believe not a single hospital admission for anyone that had the Oxford vaccine in the trial.
Unfortunately with the increased R for the new variant the % reqd for herd immunity is that bit higher and must be close to 75%. I don’t think that is likely any time soon.
Quite possibly higher than 75%
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Indeed, I believe not a single hospital admission for anyone that had the Oxford vaccine in the trial.
Unfortunately with the increased R for the new variant the % reqd for herd immunity is that bit higher and must be close to 75%. I don’t think that is likely any time soon.
Quite possibly higher than 75%
75% the corresponds to a basic R number of 4.
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Indeed, I believe not a single hospital admission for anyone that had the Oxford vaccine in the trial.
Unfortunately with the increased R for the new variant the % reqd for herd immunity is that bit higher and must be close to 75%. I don’t think that is likely any time soon.
If the vaccine is 70% effective, and the R number is 3, you need approx 95% vaccination to give an effective R of 1 with no other measures in place.
(You need 66% of the population to be immune, which is achieved with 94.2% vaccinated at 70% effectiveness).
Given that none of the vaccines are approved for children, 95% is not achievable. Even if it was, you'll be lucky to vaccinate more than 70%.
Your figure is based on 0% of the population being excluded from infection by other means for example previous infection. I was just saying that if the basic R is for the new variant is 4 rather than 3 then 75% rather than 66% would need to be not susceptible whether through vaccination or other means. This is all very simplistic and no statistics on the effect of the vaccines on transmissibility is yet available. On a separate point the level of detail in epidemic modelling now is incredible. The imperial college model (and others I am sure) use census and other data to model down to individual household level.
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70% is good.
But not as good as Dettol, which kills 99%
Lifebuoy soap is being advertised on the radio as killing "everything including Covid" . . . but it tastes awful ;D ;D ;D
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In answer to the original question about 70% ....
There were 23,848 people involved in the trial with half getting a placebo.
131 got covid with symptoms
These 131 were split 101 unvaccinated control versus 30 vaccinated, so 70% less people got covid with symptoms than would be expected if it did nothing.
However there was effectively two trials because some got the wrong dose.
So overall it was 101 vs 30 - 70%
But wrong dose it was 30 vs 3 - 90%
Correct dose it was 71 vs 27 - 62%
The numbers of people taking part in the trial 23,848 is large and so the vaccine is very safe. The numbers getting infected were very small. They are large enough to see it does something very positive but I would not read too much into the efficacy rates. Just looking at the 30 vs 3, that could so easily been vs 2 or 4, based on how much someone coughed.
Edit: the other aspect is that within the control group there were the expected number of hospitalisations and fatalites. Within the vaccinated group nobody was severe enough to require hospital.
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Interesting, that the number of viral particles in the vaccine full doses was approx twice the number of white blood cells we all have.
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Indeed, I believe not a single hospital admission for anyone that had the Oxford vaccine in the trial.
Unfortunately with the increased R for the new variant the % reqd for herd immunity is that bit higher and must be close to 75%. I don’t think that is likely any time soon.
Quite possibly higher than 75%
75% the corresponds to a basic R number of 4.
I’m afraid so.
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Indeed, I believe not a single hospital admission for anyone that had the Oxford vaccine in the trial.
Unfortunately with the increased R for the new variant the % reqd for herd immunity is that bit higher and must be close to 75%. I don’t think that is likely any time soon.
Quite possibly higher than 75%
75% the corresponds to a basic R number of 4.
I’m afraid so.
I had thought they were saying basic R had gone up by 0.4 - 0.7. It was the effective R had gone up by that amount, so it is much worse than I thought. Even more reason to get vaccinated.
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Indeed, I believe not a single hospital admission for anyone that had the Oxford vaccine in the trial.
Unfortunately with the increased R for the new variant the % reqd for herd immunity is that bit higher and must be close to 75%. I don’t think that is likely any time soon.
Quite possibly higher than 75%
75% the corresponds to a basic R number of 4.
I’m afraid so.
I had thought they were saying basic R had gone up by 0.4 - 0.7. It was the effective R had gone up by that amount, so it is much worse than I thought. Even more reason to get vaccinated.
When a figure of 3 is bandied about, that’s the R0 number not the R number. R0 is what you get with this virus in a population with little or no immunity. But you only get that if you remove all the restrictions. No intervention to social norms and way of doing things. So if life was continuing on as it had before the pandemic hit, you’d see R settle around 3. There are some estimates R0 is as high as 6. Maybe it is for the new variant? So if you want to remove all restrictions you need that level of vaccination / immunity to keep it under control / but not fully eliminated.
For comparison the R0 number of measles is somewhere between 12-18.
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I had thought they were saying basic R had gone up by 0.4 - 0.7. It was the effective R had gone up by that amount, so it is much worse than I thought. Even more reason to get vaccinated.
I don't really know how to interpret an increase in R specified as an absolute value. There's a big difference between, e.g., going from 1.0 to 1.4 compared to going from 3.0 to 3.4. Surely it should be a percentage?
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Indeed, I believe not a single hospital admission for anyone that had the Oxford vaccine in the trial.
Unfortunately with the increased R for the new variant the % reqd for herd immunity is that bit higher and must be close to 75%. I don’t think that is likely any time soon.
Quite possibly higher than 75%
75% the corresponds to a basic R number of 4.
I’m afraid so.
I had thought they were saying basic R had gone up by 0.4 - 0.7. It was the effective R had gone up by that amount, so it is much worse than I thought. Even more reason to get vaccinated.
When a figure of 3 is bandied about, that’s the R0 number not the R number. R0 is what you get with this virus in a population with little or no immunity. But you only get that if you remove all the restrictions. No intervention to social norms and way of doing things. So if life was continuing on as it had before the pandemic hit, you’d see R settle around 3. There are some estimates R0 is as high as 6. Maybe it is for the new variant? So if you want to remove all restrictions you need that level of vaccination / immunity to keep it under control / but not fully eliminated.
For comparison the R0 number of measles is somewhere between 12-18.
The basic R number, R0 for the new variant in an environment as it was before covid would be expected to be somewhere between 4.4 and 5.8 based on the effective R increasing somewhere between 0.4-0.7 which is a factor of 140-180%. I had misread and thought the 0.4-0.7 was the change in basic reproduction number.
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The transmissibility of the virus has gone up by around 50%, according to contact tracing data. Around 10% of contacts became infected with the old strain, and around 15% became infected if it's the new strain.
That would scale R0=2 to R0=3. Or R0 = 2.6 (a figure from the BMJ earlier in the pandemic) to R0 = 3.9.
If the Re was around 1 then at 50% would be consistent with a quoted 0.4 to 0.7 increase in Re, given a 50% increase in transmissibility.
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Sorry I was not saying an increase from 0.4 to 0.7. I was saying an increase in the range [0.4-0.7] Or if you prefer 0.55 give or take absolute increase to the current effective R
This was an increase of between 40% and 80%
If the basic R0 went up from 3.0 by a similar % it would be in range [4.2-5.4]
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It is of course dangerous to make such assumptions. For example you could have a virus that originally infects 3 people per original infection. You bring in hand washing and it drops from 3 to 1. Then there is a mutation and it doubles from 1 to 2. If this was because the mutation made the virus more resistant to hand washing then removing the hand washing regime would not cause the original number to jump from 3 to 6.
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I'll repeat Box's original adage: all models are wrong, but some models are useful. That includes epidemiological models. He was expressing the point that models are just that, they're potentially useful approximations of reality based on the selected parameters. There's no innate correctness or truth in them. Change the parameters and the model changes. So all models like this should be interpreted with caution and not as absolutes. Evidence for new more transmissible variant came from models, not (as far as I know) experiment. You can't properly separate transmissibility of the virus itself from people's behaviour in creating events that make transmission possible.
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Sorry I was not saying an increase from 0.4 to 0.7. I was saying an increase in the range [0.4-0.7] Or if you prefer 0.55 give or take absolute increase to the current effective R
This was an increase of between 40% and 80%
If the basic R0 went up from 3.0 by a similar % it would be in range [4.2-5.4]
0.4 to 0.7 i.e. the increase is somewhere between 0.4 and 0.7. So for instance if Re is 1.0 and you increase by 0.4 to 0.7 then Re is now 1.4-1.7.
1.4-1.7 from 1.0 is consistent with 50% (i.e. 1.5).
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It is of course dangerous to make such assumptions. For example you could have a virus that originally infects 3 people per original infection. You bring in hand washing and it drops from 3 to 1. Then there is a mutation and it doubles from 1 to 2. If this was because the mutation made the virus more resistant to hand washing then removing the hand washing regime would not cause the original number to jump from 3 to 6.
Given that the new variant appears to have a higher viral load, the most likely explanation for easier transmissibility is simply greater shedding of virus. This would imply all measures need to be strengthened in order to have the same effect.
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K can check, well I’ll have to later for work, but iirc the Imperial paper suggested a geometric increase in R with best estimate at 1.74 (yes not really that accurate!)
Given we don’t know what R0 is really, but new variant seems to give much higher viral loads in nasal passages and throat - likely at least on driver of increased transmissibility - unconstrained R’0 may well be above 4. Fauvism has been pushing his penetration numbers up recently - now at 85% and still admitting that he’s capping himself to not crush public hope/opinion
To be clear, I’m not a virologist or immunologist:)
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Where is the evidence of increased viral loads coming from?
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Where is the evidence of increased viral loads coming from?
https://www.medrxiv.org/content/10.1101/2020.12.24.20248834v1.full-text
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Where is the evidence of increased viral loads coming from?
From the pcr testing. One of the 3 markers tested, one is missing in the variant so you can identify track and trace tests that have 2 out of 3 targets matched and look at levels.
Oddly increased viral load seems geographical - for the variant it does not appear in tests in Greater London but does in Kent and other areas outside London.
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Thanks, my preprint-fu wasn't working and I couldn't find anything published.
It's somewhat speculative though (it's an interesting coincidence) that we only really detect this variant because it fails one of the PCR tests so we can chart its progress, we obviously don't do whole genome sequencing at levels to make this possible, there will be lots of other variants that we generally don't know much about unless they get sequenced).
A couple of caveats, there are potential limitations on the methodology they discuss. It's worth pointing out that the presence of viral RNA is not necessarily correlative of viral load. If the variant does result in more virus, then there's a counter to transmissibility – it's more likely to be detected in samples and so will appear more prevalent.
I'm mildly sceptical on whether there's a variant with significantly increased transmissibility (now usually reported uncritically) given that the main current evidence is epidemiological modelling. There are several equally compelling explanations (methodology as discussed, human behaviour, and viral population genetics).
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I agree that behaviour, which I have only anecdotal information on, is probably a driver for current rising infection, hospitalisation and mortality rates. At this stage I’m reasonably comfortable that there is reason to consider that the new variant is more transmissible, but perhaps more importantly that we should act to control the worsening situation quickly and not ‘in due course’ when it’s got even worse.
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U.K. does fully sequence quite a lot of positive tests - about 5% I believe.
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I agree that behaviour, which I have only anecdotal information on, is probably a driver for current rising infection, hospitalisation and mortality rates. At this stage I’m reasonably comfortable that there is reason to consider that the new variant is more transmissible, but perhaps more importantly that we should act to control the worsening situation quickly and not ‘in due course’ when it’s got even worse.
Well, I do worry a little that we're blaming the virus for the fact that it's spreading. Regardless of transmissibility, it is providing an interesting way of exploring the epidemiological spread (think of it in ecological terms, if you tag a small proportion of your favourite animal, we effectively have a clearly tagged viral variant). Debate aside, we're clearly providing ample transmission paths despite any claims of lockdown, and that is behaviour.
Davef mentioned it earlier, but our behaviour itself generates a selection pressure and helps not only spread a variant but determine the phenotypic qualities of that variant.
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I agree that behaviour, which I have only anecdotal information on, is probably a driver for current rising infection, hospitalisation and mortality rates. At this stage I’m reasonably comfortable that there is reason to consider that the new variant is more transmissible, but perhaps more importantly that we should act to control the worsening situation quickly and not ‘in due course’ when it’s got even worse.
Well, I do worry a little that we're blaming the virus for the fact that it's spreading. Regardless of transmissibility, it is providing an interesting way of exploring the epidemiological spread (think of it in ecological terms, if you tag a small proportion of your favourite animal, we effectively have a clearly tagged viral variant). Debate aside, we're clearly providing ample transmission paths despite any claims of lockdown, and that is behaviour.
Davef mentioned it earlier, but our behaviour itself generates a selection pressure and helps not only spread a variant but determine the phenotypic qualities of that variant.
Reaches for the like button... yep, we’re still providing transmission paths.
An anecdotal example being the individual (nurse in elderly care setting) who joined parents for lunch on 25/12 after being tested late 23/12. Positive result returned early on 26/12. I’m still trying to make sense of this one really.
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An anecdotal example being the individual (nurse in elderly care setting) who joined parents for lunch on 25/12 after being tested late 23/12. Positive result returned early on 26/12. I’m still trying to make sense of this one really.
Lunacy! We have 85 yr old patients with chronic lung conditions turning down vaccination!!!
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70% is good.
But not as good as Dettol, which kills 99%
Lifebuoy soap is being advertised on the radio as killing "everything including Covid" . . . but it tastes awful ;D ;D ;D
Is that the one that the Orange-utan was proposing we ingest?
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70% is good.
But not as good as Dettol, which kills 99%
Does that mean that only 1 person in 100 survives drinking Dettol?
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I agree that behaviour, which I have only anecdotal information on, is probably a driver for current rising infection, hospitalisation and mortality rates. At this stage I’m reasonably comfortable that there is reason to consider that the new variant is more transmissible, but perhaps more importantly that we should act to control the worsening situation quickly and not ‘in due course’ when it’s got even worse.
Agree, you keep your distance, the new variant can’t spread. Anecdotal but I note that when people are meeting friends outdoors they are not socially distancing. Lucky if they are a foot apart let alone a minimum of 2m. Someone coming the other way, people continue on their straight path. Back in first lockdown you’d do the wide berth passing dance. No longer, if a larger group forms, people aren’t making immediate steps to distance themselves. Dog walkers are some of the worst, being in each other’s faces as they pet each other’s dog.
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An anecdotal example being the individual (nurse in elderly care setting) who joined parents for lunch on 25/12 after being tested late 23/12. Positive result returned early on 26/12. I’m still trying to make sense of this one really.
Lunacy! We have 85 yr old patients with chronic lung conditions turning down vaccination!!!
Is that because they want to wait for the Great British vaccine, as I have seen reported elsewhere?
Useful run-down on current thinking from the BMJ on the extending of dose intervals. My current understanding is that for the Oxford / AZ, there is good evidence to support extending, less so for the Pfizer.
https://www.bmj.com/content/372/bmj.n18?=&utm_source=adestra&utm_medium=email&utm_campaign=usage&utm_content=daily&utm_term=text&s=03
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An anecdotal example being the individual (nurse in elderly care setting) who joined parents for lunch on 25/12 after being tested late 23/12. Positive result returned early on 26/12. I’m still trying to make sense of this one really.
Lunacy! We have 85 yr old patients with chronic lung conditions turning down vaccination!!!
Is that because they want to wait for the Great British vaccine, as I have seen reported elsewhere?
Useful run-down on current thinking from the BMJ on the extending of dose intervals. My current understanding is that for the Oxford / AZ, there is good evidence to support extending, less so for the Pfizer.
https://www.bmj.com/content/372/bmj.n18?=&utm_source=adestra&utm_medium=email&utm_campaign=usage&utm_content=daily&utm_term=text&s=03
I think it’s fair to say that there’s some direct evidence supporting a longer gap for the AZ vaccine and no Direct evidence for or against in the Pf case. However, there is a lot of wider evidence from other vaccines that supports the approach. Further, I would assume that outcomes will be monitored - the issue here is one of how quickly immunity fades and whether the booster dose is still effective in ensuring long term immunity.
Some of the social media rhetoric is shocking - as usual.
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Immunologically, I don't think there's any case where delaying a booster has negative effects other than, of course, you spend a longer period without its protective effects of the second dose. Most people have sloppy adherence to vaccination programmes, get jabbed whenever, and yes, batches and types get routinely mixed up with evident ill-effect.
It's a valid point that we don't know, of course, but given the logistical challenge, as pointed out in that article, sometimes we have to take educated guesses. No vaccination means no protection at all.
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An anecdotal example being the individual (nurse in elderly care setting) who joined parents for lunch on 25/12 after being tested late 23/12. Positive result returned early on 26/12. I’m still trying to make sense of this one really.
Lunacy! We have 85 yr old patients with chronic lung conditions turning down vaccination!!!
Is that because they want to wait for the Great British vaccine, as I have seen reported elsewhere?
Useful run-down on current thinking from the BMJ on the extending of dose intervals. My current understanding is that for the Oxford / AZ, there is good evidence to support extending, less so for the Pfizer.
https://www.bmj.com/content/372/bmj.n18?=&utm_source=adestra&utm_medium=email&utm_campaign=usage&utm_content=daily&utm_term=text&s=03
I think it’s fair to say that there’s some direct evidence supporting a longer gap for the AZ vaccine
There is, the longer dosing regimes were used in part of the trials and it was the longer gap that saw a better immune response. It’s all in the paperwork submitted, which you can see online. I don’t have a link right now, I was looking at it on Wednesday.
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Most people have sloppy adherence to vaccination programmes, get jabbed whenever, and yes, batches and types get routinely mixed up with evident ill-effect.
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ian, did you mean to write that, or is there a missing no?
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Yes, I did miss the no. My brain is up there, my fingers far, far away and now mostly autonomous republics.
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I added the ‘no’ subliminally! Shows how conditioned we can be.
Yes, I’m aware of the AZ dosing regimes, but they were the result (in part at least) of mid ups. Hence, there is some evidence, but it doesn’t cover every age group for example. However, we are in agreement - using evidence from wider experience and sensible judgement is the appropriate approach.
I think there is, on balance, more sense and intelligence displayed in here than on Twitter, say. I accept that’s not a high bar.
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I miss words all the time. But it's true, my fingers are close to declaring independence from my brain. They were encouraged by the successful succession of my mouth.
But yes, I read a lot of arguments for perfection. Of course, we should follow the regimen from the trials. But reality sometimes requires imperfection and making the best decisions we can with the information we have. We don't have unlimited supplies of any vaccine, we know they will take time to arrive (and we are so, so lucky to have this – it's been amazing work on both the current vaccine platforms, bringing mRNA vaccines to fruition after decades of research, and an ample demonstration of a viral-vector platform – the latter was designed to make vaccines quick to develop and manufacture at low cost because it's not just about us in the first-world with funded healthcare systems).
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Did mean ‘secession’? ;)
Agree with all that, but it has occurred to me, amidst the storm of Internet protest, that Pfizer only tested one dosing regime and it’s quite possible, even likely, that it isn’t optimal. It’s even possible that the actual regime used is better than that tested and approved.
I’m being a bit mischievous, but people lock into stuff as though it’s sacrosanct.
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I did some work on projected mortality for Q1 and 2021 on Monday and Tuesday. Nothing particularly sophisticated, but pragmatic enough for our purposes. We agreed an answer that was below my view, but I’m already beginning to think I should have held out a bit harder.