However, I’m still being really cautious because of the not-well-understood long-term effects. SARS was really nasty on that front. What evidence convinced you that’s not a big deal? If you don’t already have evidence for that, then rationality isn’t the reason you changed your behavior.
Not sure this is directed at me or just a question for poetic reasons, but I’m going to answer it anyway:
The “bradykinin hypothesis” is the only one that has a reasonable model of long term damage, basically attributing it to ACE2 expression in tissues where it would be normally close-to-absent and bradykinin overproduction being triggered in part by that an synergizing badly with it.
This is “hopeful” in that it predicts side effects are non-random and instead associated with a poor immune response. That is to say, youth’s protective role against death also protects against side effects.
I found no quantifiable studies of side effects after the infection, the ones that exist are case studies and/or very small n and in older demographics (i.e. the kind that needs to attend the hospital in the first place and is then monitored long term after the infection passed)
Absence of evidence is not evidence of absence and a model of infection is just a useful tool not a predictor of reality, plus my understanding of it is likely simplistic. But that same statement I could make about a lot of coronavrisues and influenza viruses I expose myself to every year.
(I can’t say more because the study is still being done, but recovered covid patients which have relevant medical complaints having to do with the blood clotting regulation cascade might probably want to keep track of soluble fibrin in their plasma. I do promise to make a note here if the study doesn’t find an effect and to add a link to the publication, whenever it is out, regardless of the findings.)
Not sure this is directed at me or just a question for poetic reasons, but I’m going to answer it anyway:
The “bradykinin hypothesis” is the only one that has a reasonable model of long term damage, basically attributing it to ACE2 expression in tissues where it would be normally close-to-absent and bradykinin overproduction being triggered in part by that an synergizing badly with it.
This is “hopeful” in that it predicts side effects are non-random and instead associated with a poor immune response. That is to say, youth’s protective role against death also protects against side effects.
I found no quantifiable studies of side effects after the infection, the ones that exist are case studies and/or very small n and in older demographics (i.e. the kind that needs to attend the hospital in the first place and is then monitored long term after the infection passed)
Absence of evidence is not evidence of absence and a model of infection is just a useful tool not a predictor of reality, plus my understanding of it is likely simplistic. But that same statement I could make about a lot of coronavrisues and influenza viruses I expose myself to every year.
(I can’t say more because the study is still being done, but recovered covid patients which have relevant medical complaints having to do with the blood clotting regulation cascade might probably want to keep track of soluble fibrin in their plasma. I do promise to make a note here if the study doesn’t find an effect and to add a link to the publication, whenever it is out, regardless of the findings.)