-various papers and attempting to dissect them-
Sorry if this is late and sounds possibly disjointed, I typed this up within about half an hour late last night and had to wait until today for my account to get approved.
For one, NCBI is a database of papers, it's good for finding papers, but it isn't ACTUALLY a journal in and of itself, the journal in question with the first link is PLOS One, which is as far as I've heard personally it's okay as a journal? But it's certainly no Nature in terms of reputation and clout. This is just me correcting your statement about it being in the NCBI database, which isn't really indicative of anything in terms of actual quality.
Looking at the abstract of a paper simply isn't good enough, while the results section of the abstract mention histopathologic changes in the lungs, it is still best to look at the part in the actual results section that is being referred to.
We can see mentions in the conclusion that there are other studies contradicting the results of this study with regards to vector vaccines for the S protein, suggesting that this presentation may generate a response in which sensitization and by extension, immunopathology, does not occur. This was achieved using a VEE (Venezuelan equine encephalitis) vector containing the S gene (basically inserting the CoV Spike protein encoding gene into another virus). The paper even shows this as a nice little table at the very end too, this is why gleaming an abstract is a terrible thing to do, there can be evidence contradicting the evidence in other reports. In this case citation 15 is the paper in question.
https://www.ncbi.nlm.nih.gov/pubmed/16476986
Vaccines are also hilariously difficult to make and get approved, you need to find a balance among many different factors, you want an immune response, but not too intense of one, but you also need it to linger long enough that boosters don't have to come often, it's a tough thing and the primary funders are governments and they're stingy as fuck. The vaccine strain of the disease I work on has no less than three mutations in genes critical for infection, as an example.
The second Nature article you linked also defeats your point, look at the second-to-last paragraph. In it, it states that while CoV-2 can infect T lymphocytes (much like MERS-CoV can!), it fails to replicate in them and eventually degrades, the same occurs with PBMCs (peripheral blood mononucleic cells, jargon for lymphocytes and monocytes). If this was not the case and it
was actually capable of infecting T lymphocytes, you
would then see AIDS-like effects in CoV-2 (it is well known that HIV targets Th cells, a group of T lymphocytes), but you don't.
Infecting cells is all well and good, but if it just gets stuck in there and fails to replicate, the damage will come primarily from the immune system as infected cells may flag themselves as infected. Why this happens in some cells and not others is a massive topic as a whole and it's not something I'm well-versed in so I wouldn't want to spout anything off there that may end up being misinformed.
From how I'm personally looking at this, in severe cases patients are primarily harmed by cytokine storms shown through massive elevation in pro-inflammatory cytokines. As mentioned in the second paper there are strategies trialled to dampen this damaging response. The paper also states that this is suggestive, but as this is still very recent research it isn't truly conclusive. It may also be indicative of a severe infection resulting in a massive immune response, they
are in severe stages of infection after all.
This isn't my area of research personally, I do genetics for another disease, and quite frankly this is mostly me bothering to look beyond the abstract and looking at citations of interest (something I learned thoroughly in uni).
I would enjoy going through this big document of yours for the sole purpose of ripping into it, but I'm quite frankly busy at the moment so this post in itself may look rushed, and I won't have the time to make responses past this post especially since I may get called in as a CoV-2 researcher at my lab and I have other work to do in the meantime.
