Well yes, if these results are to be believed then that is what it would imply. But of course there is a catch. Not all interferons raise ACE2 levels. Even in this study interferon a2 was much more potent than interferon gamma. So its not all lost. Moreover, the virus has a protein similar to protein found in SARS1. The orf9b of virus is a potential interferon antagonist. It remains to be seen if other than inhibiting antiviral response it also can act to limit severity in some cases. It may be a dynamical system, and eventual result may depend on multiple variables interacting. It needs to studied further.
And yes it seems that people with preexisting pathology have higher risk of contracting the disease and becoming severely ill. The higher ACE2 might be a good plausible explanation.
I think the best treatment approach would be to find small molecules that inhibit ACE2 and Spike binding. This is direction we are taking for now. Nonetheless, there can be other targets esp where protein of virus interacts with host proteins. I can do a post on that later.
Thanks for the clarifications (and raising the fine prints ;) )/
Cheers!