Are th2 Shifts the reason These chronic infections can establish?

On paper that all sounds good, and you do have things like LDN/mushrooms which shift from th2 to th1.

However there are people who get benefit from ivig which is th2 inducing/th1 reduction.

Even further in my confusion with this is CIRS. Which is described essentially as innate immune system activation (th1) as the adaptive immune system never gets a hold, giving way to mass inflammation. These are the same chronic illness patients said to be th2 dominant…

The CIRS point is also an explanation for why chronic illness patients can have the phenomenon of lack of acute illness - innate immune system is over active.

i think different infections dysregulate the immune systems in different ways

i recall reading that Lyme is unusual in that once chronic the Th1 side of the patients immune system is also typically upregulated and overactive ( rather than Th2 - or as well as Th2)
Buhner writes about this in his books and its the main reason why Astragalus - a herb known to increase Th1 activity is not recommended for people with chronic lyme ( although some seem to get on ok with it)

chronic infections are a bit of an anomaly - our immune systems seem to be mainly designed for fighting off the acute phase of infections -
and are actually supposed to go through first a very inflammatory phase where lots of cytokines are made that recruit and stimulate the innate and adaptive immunity to do their thing - opening up tissues - killing off infected cells etc - and then there is supposed to be a pronounced anti inflammatory phase where damage is repaired an everything cleaned up before recovering back to baseline in readiness for the next challenge

chronic infections only occur when this strategy has failed and the cycle is interrupted or prolonged some how.
of course over the millennia - in this microscopic arms race - microbes have found clever ways to dysregulate the system and prevent the host from clearing them effectively - and hence prevent them from being wiped out as a species.

the ones that needed to do this the most were the ones that were transmitted by relatively infrequent events. like the bite of an infected arthropod
(air born viruses for instance just rely on rapid easy transmission to prevent them from being wiped out).

But the things that have to hang around long enough for a bug to bite the host - then drop of to wait in the undergrowth for some other suitable host to wander along and then bite that - hopefully successfully transmitting the microbe to the new host - these have to survive in a single host much longer and therefore out of necessity have much more complex strategies to enable long term (i.e. Chronic) infection - without killing the host - or being wiped out themselves. its a kind of middle ground - perpetually sick state - exactly as we find ourselves in.

as far as i recall - the Th1 / Th2 classifications refer broadly to groups or classes of cytokines - but i think this is just one way of classifying bits of what is a very complex and still not fully understood larger system

i think there are 30 or 40 or more cytokines and chemokines - and a dozen or more different cell types - and many more signalling molecules all orchestrating a very complex immune response.

i am not sure studies have successfully shown persistent patterns of these in populations with Lyme or other chronic infections - or rather the studies i do recall seeing seemed to have conflicting results
whereas - if there was a clear pattern of simple TH1 suppression - i would think they should be able to measure it easily enough at least in terms of some key cytokine levels

we do know that there are other mechanisms by which lyme and other chronic bacterial infections hamper the hosts normal response
eg
-they seem to be able to disrupt normal antibody responses - eg they damage the germinal centres where B cells lean what antibodies to make

-they also make biofilms - and biofilms have been shown to suppress immune function

-apicomplexans like babesia - are single celled animals- they are much more complex than bacteria and have been shown to have sophisticated machinery for influencing the host immune system through signalling chemicals

so perhaps dysregulated cytokines are just one aspect of a much larger picture