In reply to jkarran:
> This is interesting, not that R is rising so much* but buried in there is strong evidence against the argument some make that most of us are somehow naturally immune without exposure: 657 of 1000 abattoir workers were positive with active covid cases. We can safely assume more than that were exposed and recovered (the seeds of that outbreak) and that there will be a few false negatives there too.
I'm starting to think that a plausible model is that a less virulent version of the current virus may have been in widespread circulation before the current pandemic, which would account for some partial immunity being present in some populations.
At some point, this virus acquired one or more mutations to its S-protein, imparting an extra enzymatic cleavage site (for furin, for example, but also other enzymes like TMPR-SS2). Enzymatic cleavage at this site seems to be associated with at least increased viral infectivity for cells in the lung (and for cell to cell transmission) and some reports say it may be required for infection of these cells. When this new, more infectious and more pathogenic, virus took off, it would seem logical that it would hit those with no previous exposure (as well as those with co-morbidities) hard.
All speculation, and possibly bollocks, but something weird does seem to be happening with the pattern of infection and the paradox of the apparently low level of immunity as measured by antibody titre. Maybe this is because the circulating IgG and IgM levels aren't really correlated with protective immunity (because, presumably, that's more strongly related to an effective CD8+ T-cell response).
Equally, other, non-immunological, mechanisms might be involved; levels and pattern of tissue expression of ACE-2 expression, ditto TMPR-SS2 or other cellular protease expression, genetic factors controlling intensity and control of inflammatory response... who knows?