"without the virus to disrupt the immune response" - it's probably a stupid question, but what about people who got covid between the vaccine doses. Would the infection right after the first dose of the vaccine disrupt the immune response to the first vaccine dose?
Thanks for your thoughtful response to my inquiries. A couple follow-ups:
1. Is there a plausible mechanism by which COVID vaccines could cause an autoimmune response further down the road, rather than fairly soon after vaccination?
2. If your hypothesis is correct, and long COVID is caused at least in part by a less-than-ideal immune response, would we then expect breakthrough cases to be less likely to develop into long COVID? (I've seen very little on the topic of breakthroughs and long COVID, but here's what Akiko Iwasaki had to say on the topic: https://dearpandemic.org/will-vaccines-prevent-long-covid/).
So, your answer to Sam's question reminded me of one I had. If it's the adenovirus vector that turns out to cause the rare thrombocytopenic thromboses, would that not imply that wild-form adenoviruses might be responsible for normal incidence of that very rare syndrome? Would that perhaps lead to a vaccine search for adenoviral disease prevention?
"without the virus to disrupt the immune response" - it's probably a stupid question, but what about people who got covid between the vaccine doses. Would the infection right after the first dose of the vaccine disrupt the immune response to the first vaccine dose?
Thanks for your thoughtful response to my inquiries. A couple follow-ups:
1. Is there a plausible mechanism by which COVID vaccines could cause an autoimmune response further down the road, rather than fairly soon after vaccination?
2. If your hypothesis is correct, and long COVID is caused at least in part by a less-than-ideal immune response, would we then expect breakthrough cases to be less likely to develop into long COVID? (I've seen very little on the topic of breakthroughs and long COVID, but here's what Akiko Iwasaki had to say on the topic: https://dearpandemic.org/will-vaccines-prevent-long-covid/).
OK, this will get meta.
So, your answer to Sam's question reminded me of one I had. If it's the adenovirus vector that turns out to cause the rare thrombocytopenic thromboses, would that not imply that wild-form adenoviruses might be responsible for normal incidence of that very rare syndrome? Would that perhaps lead to a vaccine search for adenoviral disease prevention?
How about the use of adenovirus vectors for (actual) gene therapies, as Steve Novella wrote about here: https://sciencebasedmedicine.org/viral-vectors-for-gene-therapy/ ?