Do we know, in cases of molecular mimicry, [if] it is [a] coincidence that the pathogen is similar in structure to [the] host protein, or has the pathogen evolved to mimic proteins in an attempt to limit or prevent an immune response from the host?

That’s a great question, and here, Tiffany is talking about molecular mimicry in the context of autoimmune disease and when our immune system is mounting a response to a microorganism like ​Klebsiella,​ that then cross-reacts with some of our own tissues, therefore causing an autoimmune disease, so certain microbes like ​Klebsiella​ and ​Prevotella​ those are going to have an antigen on them that if we make antibodies to that, they’re then going to cross-react to their own tissues triggering an autoimmune, we’ll say, an autoimmune disease, essentially. And it’s a great question. I don’t know whether or not how that evolution occurred and if it was the microbes found that they were able to evade our immune system a little bit better. It’s a great question, and it’s just not something that I have looked into, but [it’s a] good question.