I think you’re largely right about the concept of modality of infection and how one defends. In contrast to antibody interfering with receptors and preventing ensnare of the virus floating by.
But in an over-riding way, it seems unwise to lean on and have confidence in a natural immunity process facing an unnatural, artificial virus. Odds pretty high there was no animal crossover source.
An unnatural virus that is capable of being harbored in animal reservoir, and provable zoonotic transfer to humans at any time/place?-— well, don’t count on those odds, and wouldn’t want to give a %-age on the likelihood of increased infectivity.
The notional endpoint for a “new” variant strain which is defined as a new S-Protein sequence that is “more infective” is for the recipient having considerably more immunity from the entire virus sequence (acquired through the ACE2 receptor/S-Protein matchup) gained from having survived the full genetic sequence effects once it go into an individual.
The conundrum is— what seems to be “said” cannot be supported, unless they are saying the full virion DNA sequence has also mutated to such an extent that prior immunity developed to any and all segments of it are likely negated. On a person to person basis (with all the variability of immune response that is so varied) it seems highly unlikely. If the PCR is the basis for this it is a real stretch for continuing the Wu-wooh honking.