A simple dose-response relationship likely has little to do with the results seen for the Astra-Zeneca/Oxford vaccine, though. Much more likely is what Derek Lowe said this morning in his blog on this vaccine, below. The issue of the adenovirus vector (even a chimp adenovirus which humans haven't been exposed to) stimulating the human immune response with the first dose and then having the body's "new" antibodies essentially deactivating the 2nd dose (and will possibly also be an issue for J&J's vaccine which uses a human adenovirus as its vector of delivery) has been talked about since day one. Let's hope the 90% efficacy for the half-dose/full-dose design holds when we see more data on this one.
Also, none of the vaccinated patients who became infected with the virus had serious illnesses (only 1 such case for Pfizer and 0 for Moderna - need final data to be sure this difference is real), which is very good. Also, the AZ vaccine is stable under refrigerated conditions vs. cyro storage for Pfizer's (-70C/-94F) and regular freezer (-20C/-4F, with one month refrigerated ok, for Moderna). There were no major side effects seen for any of the vaccines to date, which is great.
Why might there be such a significant split in efficacy? My own wild guess is that perhaps the two-full-dose protocol raised too many antibodies to the adenovirus vector itself, and made the second dose less effective. This has always been a concern with the viral-vector idea. It is, in fact, why this effort is using a chimpanzee adenovirus – because humans haven’t been exposed to it yet. Earlier work in this field kicked off with more common human-infective adenoviruses (particularly Ad5), but there are significant numbers of people in most global populations who have already had that viral infection and have immune memory for it. Dosing people with an Ad5 vector would then run into patients whose immune systems slap down the vaccine before it has a chance to work. That’s not the case for a chimpanzee-infecting form, naturally (few if any people have ever been exposed to that one!) but the two-dose regime may have run into just that problem. Immunology being what it is, though, there are surely other explanations, but that’s the one that occurs to me. Update: there’s always the outside nasty chance that the smaller N in the 90% group is giving a number that won’t hold up. I would hope this isn’t the case, but without a better look at the statistics, it’s not possible to rule that out.
https://blogs.sciencemag.org/pipeline/archives/2020/11/23/oxford-az-vaccine-efficacy-data