The mechanism of action behind the broad symptoms we see is actually reasonably straightforward- the ace2 receptor the virus uses to enter cells is everywhere i

The mechanism of action behind the broad symptoms we see is actually reasonably straightforward- the ace2 receptor the virus uses to enter cells is everywhere in your body. In vitro, they replicate in pancreatic cells and intestinal cells, which lends a mechanistic explanation for the link to gastrointestinal distress and diabetes seen in correlative findings. Heart muscle also has high concentrations of the ACE2 receptor. One of the mechanistic hypothesis for clotting [0] proposed is that the complement system and immune cascades trigger clots, since they saw evidence of the virus binding to an element in the complement cascade. This could turn out to be entirely wrong of course, but that's a hint at the other key aspect of this that allows varied results - your immune system can react poorly and is capable of screwing up in fascinating and varied ways. It could be the virus killing pancreatic cells, or an autoimmune response triggered by the virus that causes pancreatic cell death since the virus infects them and marks them for destruction. Are these the driving forces behind increased clots etc? Maybe not. Maybe its contributing equally with people staying at home, or maybe not at all. But the mechanistic reasons for the broad symptoms are there and they're relatively straightforward, driven by the ability of the virus to infect lots of different cells and the variability of the human immune system [0]https://news.weill.cornell.edu/news/2020/07/what-is-known-about-covid-19-and-abnormal-blood-clotting https://news.weill.cornell.edu/news/2020/07/what-is-known-ab...