Read this lucid wonderfully readable article by @liammannix
🇬🇧 UK variant (B.1.1.7)
🇺🇸 South African variant (B.1.351)
🇧🇷 Brazilian variant (P.1)
* Difference between: Mutants, Variants, Strains
* Spike Protein mutations
* Vaccines efficacy smh.com.au/national/what-…
🇬🇧 UK variant (B.1.1.7)
🇺🇸 South African variant (B.1.351)
🇧🇷 Brazilian variant (P.1)
* Difference between: Mutants, Variants, Strains
* Spike Protein mutations
* Vaccines efficacy smh.com.au/national/what-…
Best article I’ve seen yet
See those orange dots?
That’s the Kent B1.1.7 variant taking over
Seeing the timetable of events (esp late Nov alarm growing at the prevalence of the spike drop out samples tested and that, on 13th Dec we had 21,991 cases ) promoted another look.
See those orange dots?
That’s the Kent B1.1.7 variant taking over
Seeing the timetable of events (esp late Nov alarm growing at the prevalence of the spike drop out samples tested and that, on 13th Dec we had 21,991 cases ) promoted another look.
Worth bearing in mind now that At the end of the Nov lockdown on 3rd Dec, moving into tiers we had 15,654 cases (by specimen date).
A couple of days at 12/13k & up it went to 21k
33k by 15th December but Johnson doesn’t want to cancel Christmas.
47k by 21st Dec
81k by 28th Dec
A couple of days at 12/13k & up it went to 21k
33k by 15th December but Johnson doesn’t want to cancel Christmas.
47k by 21st Dec
81k by 28th Dec
It also flags what happens when you expose the virus to low levels of antibodies. It is more likely to mutate as it has. That has happened in lab conditions in 3 months
So PREVALENCE drives that condition.
So PREVALENCE drives that condition.
The burning question for us in the UK is whether 1-shot of vaccine with an extended interval will also drive it or whether the antibodies one shot delivers are more powerful than that.
The horns of the dilemma. Such high prevalence that hospitals are overrun & deaths piling up
The horns of the dilemma. Such high prevalence that hospitals are overrun & deaths piling up
Hence driving the one shot decision. Get as much immunity as poss in as many people as poss as quickly as poss to drive down prevalence.
But will it be enough to do that without giving birth to another mutation that escapes the vaccine?
But will it be enough to do that without giving birth to another mutation that escapes the vaccine?
I get the dilemma. Each decision bears risks.
But this is why I am very keen to see interim data as we go, not wait for the 12 week experiment to end and then see whether or not it works.
But this is why I am very keen to see interim data as we go, not wait for the 12 week experiment to end and then see whether or not it works.
BUT I think that we owe it to the world, having introduced B1.1.7 Kent variant into it, to make sure that we aren’t creating condition for more viral escape.
That can be done through prevalence.
That can be done through prevalence.
BUT Let’s make sure that antibody production is high throughout the extended interval period (both vaccines) and sustained enough to not create the second condition driving viral escape and be prepared to reverse ferret mid way through if immunity drops.
There’s approximately 500k December 1 dose Pfizer vaccine patients. How are they comparing to the similar 2 dose Pfizer patients (some getting their second shot early to mid January) ?
I hope we see some data this week.
I hope we see some data this week.
Meanwhile. Just a little reminder that PREVALENCE has already created conditions where the B1.1.7 Kent variant has acquired a new variant of its own.
The disagreeable E484K mutation that is associated with the SA and Brazilians partial resistance to vaccines.
The disagreeable E484K mutation that is associated with the SA and Brazilians partial resistance to vaccines.
A little bit more about that little devil from @GuptaR_lab that has been doing work on the SA variant and the effectiveness of the Pfizer vaccine.
It’s almost as if the bad boys and girls like to hang out together, smoking their illicit fags and planning their next disruption.
It’s almost as if the bad boys and girls like to hang out together, smoking their illicit fags and planning their next disruption.
This @bmj_latest blog details why interim efficacy data is needed particularly for the Pfizer vaccine.
There are no comparable types of vaccine against which to make educated assessments of how they will work with a longer interval or to assess the risks at 4/6/8/10 wk intervals
There are no comparable types of vaccine against which to make educated assessments of how they will work with a longer interval or to assess the risks at 4/6/8/10 wk intervals
I would very much like the longer interval to work well because it would be such a great gift to policy and implementation decisions behind vaccination programmes all around the world.
But jumping from 3 weeks to 12 weeks and in our most vulnerable groups seems like a big risk
But jumping from 3 weeks to 12 weeks and in our most vulnerable groups seems like a big risk
Especially when we seem to be having some of the nastier variants that need more neutralising antibodies to quell their activity.
blogs.bmj.com/bmj/2021/01/05…
blogs.bmj.com/bmj/2021/01/05…
Why am I a lot less troubled about an extended interval for the AZ vaccine, a viral vector vaccine unlike the mRNA Pfizer vaccine.
There’s evidence from other vaccines of similar types that a delayed interval might improve booster effect.
And here’s data from the trials.
There’s evidence from other vaccines of similar types that a delayed interval might improve booster effect.
And here’s data from the trials.
Published yesterday in the Lancet.
“There were no hospitalisations in the ChAdOx1 nCoV-19 group after the initial 21 day exclusion period, and 15 in the control group.”
papers.ssrn.com/sol3/papers.cf…
“There were no hospitalisations in the ChAdOx1 nCoV-19 group after the initial 21 day exclusion period, and 15 in the control group.”
papers.ssrn.com/sol3/papers.cf…
“Vaccine efficacy after a single standard dose of vaccine from day 22 to day 90 post vaccination was 76% (59%, 86%), and modelled analysis indicated that protection did not wane during this initial 3 month period. “
“Similarly, antibody levels were maintained during this period with minimal waning by day 90 day (GMR 0.66, 95% CI 0.59, 0.74).
In the SD/SD group, after the second dose, efficacy was higher with a longer prime-boost interval: VE 82.4% 95%CI 62.7%, 91.7% at 12+ weeks,..”
In the SD/SD group, after the second dose, efficacy was higher with a longer prime-boost interval: VE 82.4% 95%CI 62.7%, 91.7% at 12+ weeks,..”
...compared with VE 54.9%, 95%CI 32.7%, 69.7% at <6 weeks. These observations are supported by immunogenicity data which showed binding antibody responses more than 2-fold higher after an interval of 12 or more weeks compared with and interval of less than 6 weeks GMR 2.19 “
We still need more data. Bigger numbers. Especially in the over 55 age group (not for safety - that was tested in the full x 2 dose shorter interval group) but for effectiveness.
But the Pfizer vaccination suggested the over 80s suggested they needed a bit longer to get going.
But the Pfizer vaccination suggested the over 80s suggested they needed a bit longer to get going.
So there are good reasons to be hopeful.
We also now need data on its efficacy re the U.K.variants but especially the SA and Brazilian variants.
Maybe they were already tested unknowingly in the SA & Brazilian trials? Might explain the slightly lower efficacy.
We also now need data on its efficacy re the U.K.variants but especially the SA and Brazilian variants.
Maybe they were already tested unknowingly in the SA & Brazilian trials? Might explain the slightly lower efficacy.
Just spotted the helpful explanatory thread from one of the Oxford Uni AZ vaccine team
https://twitter.com/ProfKatieEwer/status/1356627765060075521
• • •
Missing some Tweet in this thread? You can try to
force a refresh
