While it does seem there was a certain amount of shotgun aproach following a few different lines of reasoning, that critism is difficult to square with actually reading the paper. It looks like the peptide selection was largely empirical and cited. The decisions about how to actually package that info into a vacine is largely educated guesswork (as you say theory, supported by computer modeling).
“Mapping of linear B-cell epitopes by binding antibodies in convalescent sera to a library of peptides representing viral antigens. A strong signal in a linear epitope mapping study does not guarantee that the epitope peptide in the context of a vaccine will trigger the production of an antibody that binds to this epitope within the context of the virus. However, it is a good indicator that this is at least possible.”
Or as I understood from elsewhere: present antibodies from recovered people to every possible short peptide sequence and see which ones they actually attacked. Make the inference that people with less severe infection had better antibodies than those with more severe symptoms in the event antibodies differed. Package a selection of promising looking pepties into a vacine; choose enough that there’s likely multiple effective peptides even if 2/3rds of the choices are duds.
While it does seem there was a certain amount of shotgun aproach following a few different lines of reasoning, that critism is difficult to square with actually reading the paper. It looks like the peptide selection was largely empirical and cited. The decisions about how to actually package that info into a vacine is largely educated guesswork (as you say theory, supported by computer modeling).
“Mapping of linear B-cell epitopes by binding antibodies in convalescent
sera to a library of peptides representing viral antigens. A strong signal in a
linear epitope mapping study does not guarantee that the epitope peptide
in the context of a vaccine will trigger the production of an antibody that
binds to this epitope within the context of the virus. However, it is a good
indicator that this is at least possible.”
Or as I understood from elsewhere: present antibodies from recovered people to every possible short peptide sequence and see which ones they actually attacked. Make the inference that people with less severe infection had better antibodies than those with more severe symptoms in the event antibodies differed. Package a selection of promising looking pepties into a vacine; choose enough that there’s likely multiple effective peptides even if 2/3rds of the choices are duds.