I know all about the ACE2 receptor phenomena with this virus. It's actually much worse than you think.https://www.preprints.org/manuscript/202002.0407/v3/download
When the virus binds to ACE2 receptors, it mimics the normal function of Ang II, which ACE2 receptors are supposed to down-regulate. This leaves excess circulating Ang II in the tissues, which creates a whole lot of fucking inflammation, enough to basically destroy a lung. The autoimmune reactions are huge. Your own inflammatory response does more to attack the tissues than the virus does.
With ADE, normally, like in Dengue, you have to get two different strains for the second one to fuck you, because the incomplete antibody response due to the faulty memory B cell antigen experience means that the virions are carted off to the Fc receptors where they start to infect your immune system, and then the Dengue fucks you to death. If SARS-CoV-2 can do this with the same strain and the same infection, that's really, really, incredibly fucked, because it means immunity is difficult or even impossible to develop. I've heard that they've cured some people with serum antibodies, so it's possible that at least some people have good antibody responses. I've also heard of people relapsing with the disease, which is not encouraging at all.
I've been trying to tell people for fucking weeks, this thing can have serious neurological consequences. SARS-CoV-2 can attack the medulla of the brain stem and the blood vessels of the brain. It can cause viral encephalitis and make people to collapse to the ground with abnormal posturing like drowning victims.https://i.4cdn.org/pol/1585628928272.webm
When they tested SARS-CoV on hACE2 transgenic mice with human ACE2 receptors in their cells, they found it could enter the olfactory bulb and pass through the cribriform plate, just like naegleria fowleri amoeba, and from there, it could enter the brain and brain stem. Lights out.