(With thanks to @StridLab for drawing my attention to it.) 2/
First, I want to note that this data is from BNT162b1. This is the same platform as the vaccine that was approved (BNT162b2) but a shorter mRNA. It was equally immunogenic, but was not taken forward because it was slightly less well tolerated. 3/
That said, the response to BNT162b1 in the absence of a boost – which this paper looked at – will probably give us a good idea about what will happen with BNT162b2 (the approved vaccine). And it’s not promising. 4/
Below, I highlight the 30ug dose with a boost at 21d (the approved schedule) in blue and the dose without a boost in red. 5/
Neutralising antibody titres are hardly higher than pre-vaccination... 6/
CD4+ and CD8+ T cell responses are lower by ELISpot for IFNg... 7/
And RBD-specific CD4+ and CD8+ responses (measured by flow cytometry) are also lower... 8/
For the Oxford/AZ vaccine, there is some evidence to suggest that a delayed boost strategy might work, but it’s confounded by all sorts of other variables. Fuller explanation from @dgurdasani1 here... 10/ https://twitter.com/dgurdasani1/status/1344727697524740101?s=20
So I feel marginally better about the delayed boost strategy for that vaccine, but I am still wary. 11/
I get that we’re in a mess (largely of our own making) but I’m not convinced that stretching limited supplies of vaccine in this way is the way out of it. Particularly for the Pfizer/BioNTech vaccine, partial/waning protection seems likely and could even make things worse. 12/12
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