diseases that may be due to remnants of the viral infection. Damage to tissue, endothelial damage, heart damage that already occurred, vascular damage that already occurred and we're starting to see that in follow up to those. And finally, then we have the Long COVID the ones that are people with brain fog, for example, that I'm thinking about. That are brain fog for several months that doesn't really fit into the one of the other two categories, so I think, at least for me, this is how I approach Long COVID. I'm thinking about it from one of these three perspectives. Hopefully in time, we'll have better classifications of Long COVID. But I think we're still trying to unravel that picture. Understanding what the different diseases are and how we can classify them is really going to be key in order to start to develop a clinical plan to really deal with these. Mr. Fritsma: Fritsma: Thank you. It is really interesting to me—I met a young man. He was probably 31 or 32 who had developed diabetes after COVID, and that had surprised me at the time. I hadn't heard of that, so your data is interesting related to diabetes. Do the various Long COVID symptoms share one common mechanism and is it an extension of the COVID-19 pathophysiology? Dr. Henry: Henry: No, this is a very interesting question, and we're still just sort of scratching the surface at understanding what drives Long COVID. As I mentioned earlier, as we all know, Long COVID is very heterogeneous collection of symptoms and probably in my opinion represents a number of distinct pathophysiologic processes and different diseases. Let's jump to a couple of short slides and I'll show you what I think we know so far. So, I showed you this classification earlier and I liked it. As I mentioned, because it connects to the path of physiology, at least how I break it down. And here we can see some of the proposed mechanisms of Long COVID. So, the first one we can think about, the prolonged, symptomatic COVID-19. People may have persistent or chronic infection. So, they may be long haulers like those with a sub-acute type infection. They may have some type of persistent inflammation. And that sort of fits into the picture. Those are some of the potential paths of these alleged processes. They may drive this prolonged symptomatic COVID-19. You might think about people here in years past. The post-acute sequela SARS-CoV-2 infection, where it gets a little more complicated. I think certainly we're thinking about direct or indirect viral mediated tissue injury. Ongoing inflammation due to post infection, immune system dysregulation, vascular injury leading to a persistent prothrombotic state or dysregulated renin-angiotensin system. Then we think about the true Long COVID. We're certainly thinking about an autoimmune-type condition or again dysregulated angiotensin-aldosterone system, maybe due to anti-idiotype antibodies. But this is not a comprehensive list. These things likely overlap, and we're just starting to really try to understand what this is and it's going to be a great scientific challenge. A few really interesting things that I think are really worth pointing out, but this was a really great study that was done and published in Cardiovascular Diabetology, and it looked at persistent clotting protein pathology in Long COVID. They found micro clots. Now you're probably going to start hearing a lot about these particular micro clots. They found it to be associated with increased levels of antiplasmin. What they thought, was that we hear a lot about recurring fatigue or muscle weakness or sleep difficulties. They suspected that blood clots might be blocking micro capillaries and thereby inhibiting oxygen exchange. They investigated if lingering symptoms of Long COVID might manifest due to the presence of persistent circulating plasma micro clots that are resistant to fibrinolysis. They found that many patients with Long COVID still had these large amyloid deposits with these