| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T75 |
0-333 |
Sentence |
denotes |
The formation of a strong complex between ACE-2, a self-component, and viral S1 (or S Protein), constitutes the basic context for developing allo-antibodies and generating a delayed autoimmune response, with antibodies first targeted to viral antigens, but which can extend to the associated self-component through epitope spreading. |
| T76 |
334-446 |
Sentence |
denotes |
Then, antibodies to ACE-2 could develop, or eventually to another cell protein close to or complexed with ACE-2. |
| T77 |
447-760 |
Sentence |
denotes |
We then hypothesize that an allo-immune response can follow the initial immune reaction to the viral infection, and that epitope spreading can induce antibodies to ACE-2, or to proteins with which it is complexed, thus targeting the immune system to cells exposing ACE-2 (abundant in lungs and some other organs). |
| T78 |
761-874 |
Sentence |
denotes |
This delayed autoimmune response can contribute to the cytokine storm and generate tissue injury and destruction. |
| T79 |
875-1137 |
Sentence |
denotes |
This can activate hemostasis, beyond acute hypercoagulability, stimulate tissue injury, and totally impair the body’s regulation of hypertension and physiological defense mechanisms such as existing pathways of haemostasis/ thrombosis and inflammatory processes. |
| T80 |
1138-1350 |
Sentence |
denotes |
We do not know, at this stage, if interaction between ACE-2 and S Protein, or its S1 subunit or with another viral or cell protein, can induce structural modifications of ACE-2 and expose cryptic or neo-epitopes. |
| T81 |
1351-1465 |
Sentence |
denotes |
This possibility needs to be considered as it could yet stimulate the immune reaction and generate autoantibodies. |
