Comment by permo-w
2 years ago
> more likely a chickenpox infection, and related acquired immune responses, will do jack-all with respect to any other infectious agent
why is this?
2 years ago
> more likely a chickenpox infection, and related acquired immune responses, will do jack-all with respect to any other infectious agent
why is this?
Because most viruses differ enough that they don't have similar recognition motifs (antigens). Sometimes a lucky person will get a "universal" response to an entire viral clade, but at some point the clades just diverge enough that they can't offer protection against each other.
If you have to get infected with a pox virus, cowpox or chickenpox are good ones to get infected with. But it's better not to get any, if you have the option.
do you have a source for this?
Just my general training in biology. I work mostly in non-animal organisms, but recall enough of my education and what I read during the COVID pandemic. This is a complex topic, and I was simplifying above.
https://en.wikipedia.org/wiki/Cross-reactivity#In_immunology
This seems to be a good article on the benefits and limits of cross-reactivity: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3352416/
And here seems to be a decent review looking at Antibody-Dependent Enhancement, a key limitation of antibody cross-reactivity for viruses: https://www.sciencedirect.com/science/article/pii/S016158902...
Basically getting infected by some things can help provide protection against some other things, can make infection by some other things worse, or can have no effect on protection against other things. All in all it's generally better to not get infected by a particular thing, but if you're going to be exposed to worse things that infection by the particular thing provides protection against this is an exception.
A book chapter on infections causing, or curing autoimmune diseases: https://www.ncbi.nlm.nih.gov/books/NBK459437/
And a review article on the same: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6723519/
> Available data indicate that viral-induced autoimmunity can be activated through multiple mechanisms including molecular mimicry, epitope spreading, bystander activation, and immortalization of infected B cells. Contrarily, the protective effects can be achieved via regulatory immune responses which lead to the suppression of autoimmune phenomena.