"Once someone is infected with SARS-CoV-2, the immune system is mobilized. As the virus replicates, cell and viral debris or virions may interact with the nAChRs blocking the action of the cholinergic anti-inflammatory pathway. If the initial immune response is not enough to combat the viral invasion at an early stage, the extensive and prolonged replication of the virus will eventually disrupt the cholinergic anti-inflammatory pathway seriously compromising its ability to control and regulate the immune response. The uncontrolled action of pro-inflammatory cytokines will result in the development of cytokine storm, with acute lung injury leading to ARDS, coagulation disturbances and multiorgan failure. Based on this hypothesis, COVID-19 appears to eventually become a disease of the nicotinic cholinergic system."
"Nicotine could maintain or restore the function of the cholinergic anti-inflammatory system and thus control the release and activity of pro-inflammatory cytokines. This could prevent or suppress the cytokine storm. This hypothesis needs to be examined in the laboratory and the clinical setting."
This article is actually spot on, and is a pretty good cheat sheet.
I have a very rare immune mediated neurological disease affecting nicotinic receptors in my peripheral nervous system called autoimmune autonomic gangliopathy.
I am ganglionic nicotinic acetylcholine receptor antibody (nAChR, α3 subunit) positive, at high and abnormal levels, which means this antibody blocks signals at the ion channel level, in my neurons of my autonomic ganglia, which is supposed to control bodily functions—but it malfunctions in my body. Some people with the disease I have, (supposedly ~22% according to this PMC article on PUBMED: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2536520/) have alpha7 subunit nicotinic acetylcholine receptor antibodies (α7 nAChR antibodies), which effectively block signals in general, affecting transmission of signals via the ion channels of neurons in the central nervous system. This type of central nervous system blockade of the autonomic nervous system causes inflammation.
The article that the above poster linked is an ominous warning for people like me, who have the same very rare disease I have, even if one is just alpha3 nAChR antibody positive only—and is not also alpha7 nAChR antibody positive. I am glad I have been taking extreme steps to protect myself.
Also, some people that never recovered from COVID-19 have sympathetic nervous activity have similarities to the condition I have.
As for the people who have a post COVID-19 inflammatory syndrome affecting their sympathetic (as in autonomic nervous system) nervous system, as in sympathetic over activity, they very likely have a form of dysautonomia:
Researchers may want to look into these antibodies/tests, in which there are several peer reviewed articles available to read. However, several of these tests are not commercially available in the US, but can be mailed/performed in Germany. See: https://www.celltrend.de/en/pots-cfs-me-crps.html
There is an immune mediated dysautonomia panel available at the Mayo Clinic (which I was found to have one of the antibodies), but one is far less likely to test positive for something in these screens. See this panel: https://www.mayocliniclabs.com/test-catalog/Overview/92121
A lot of this immune mediated autonomic nervous system stuff is just starting to emerge and come to fruition.
"Nicotine could maintain or restore the function of the cholinergic anti-inflammatory system and thus control the release and activity of pro-inflammatory cytokines. This could prevent or suppress the cytokine storm. This hypothesis needs to be examined in the laboratory and the clinical setting."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7192087/#!po=22...