I am not familiar with the observations around type-O blood, but I have been following the discussions on ACE2 and ACE/ACE2 inhibitors (blood pressure meds) which is interesting. The jury is still out on that one, but the theory for ARB's is forcing a binding that blocks nCoV from attaching to the receptor. [4]
[1] - https://examine.com/supplements/quercetin/
[2] - https://www.ncbi.nlm.nih.gov/pubmed/25050823
[3] - https://www.youtube.com/watch?v=vE4_LsftNKM Chloroquin, Quecertin 6 mins in
[0]: https://www.jqknews.com/news/388543-The_novel_coronavirus_pn...
Also the most recent french study is here: https://drive.google.com/file/d/186Bel9RqfsmEx55FDum4xY_IlWS...
In the malaria parasite, it kills the parasite by hitting up the lysosome (or something intracellular at least - interaction with a protein, can't remember details).
In humans, things get a little bit more fuzzy. It accumulates in lysosomes, and then how it stops Coronaviruses or is effective in lupus treatment isn't very clear. I've seen arguments that it changes pH, or the caspases can't work any more, but that doesn't explain very much.
My bet is that it's screwing with the organisation of the secretory system, which means that virus can't get out properly (maybe budding is broken).
The ABO blood system link is something else altogether, but probably hints towards other functions of blood type in regulating something other than self/other recognition (although virus itself may carry ABO epitope).
[citation appreciated]
Type A: 1.20:1 Type O: 0.67:1