Is autoimmune triggered paralysis caused by enteroviruses, Natural killer cells, and GM gangliosides?

Autoimmune cross-targeting hypothesis: two infections on one target tissue with one inside and one outside triggers autoimmunity.  Typically the outer larger infection is the one stopped and the attack on the internal viral infection is continued.

But what if when enteroviruses infect the ER involving the Natural Killer cells  the entroviruses are stopped first?

Here are my suspects (unproven)

Nodding disease: T. Brucei and polio live vaccine
Epilepsy: T gondii/t.cruzi/malaria and enterovirus
Absent seizure: mycoplasma polio or enterovirus
Guillain Barre: Campylobacter jejune and coxsackie
AFM/Hopkins: Staph and D68
peripheral neuropathy: e.coli and coxsackie

AFM and staph not just virus
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4536609/

Do autoimmune diseases involving enteroviruses involve the stopping of Natural killer cells? Instead stopping the attack on the large infection the immune system stops this pathway?

il-15 calls natural killer cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2191697/

Lower NK cells after seizures
https://www.ncbi.nlm.nih.gov/pubmed/18387608

https://www.sciencedirect.com/science/article/pii/S0014488608000356

https://www.researchgate.net/publication/20211933_Reduced_Natural_Killer_Cell_Activity_and_Okt4Okt8_Ratio_in_Epileptic_Patients

https://onlinelibrary.wiley.com/doi/abs/10.1002/hup.470080608

Lower NK in Guillain Barre
https://www.ncbi.nlm.nih.gov/pubmed/9619642

Peripheral neuropathy and low NK   aka "NK leukemia"
https://www.ncbi.nlm.nih.gov/pubmed/9710063
https://www.ncbi.nlm.nih.gov/pubmed/8414048
https://www.researchgate.net/publication/15601292_Natural_killer_cell_lymphoproliferative_disease_associated_with_neuropathy

How does the immune system stop NK cells?

Ganglioside antibodies are found in Guillain Barre and peripheral neuropathy so are they involved with stopping the NK cells?

guillain barre anti-ganglioside antibodies
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422685/

peripheral neuropathy and anti-gangliosides
https://jnnp.bmj.com/content/75/12/1765

Gangliosides inhibit NK cells
https://www.ncbi.nlm.nih.gov/pubmed/2598999

ganglioside GM2 as a target for NK cells
https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcla.1860010211

https://www.semanticscholar.org/paper/Ganglioside-GM2-on-the-K562-cell-line-is-recognized-Ando-Hoon/1437bc6c70867f826ce64591ffe2370aaf65b008

GM3 and NK
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.502.322&rep=rep1&type=pdf

Gangliosides are highly concentrated in the nervous system

diagram of glycolipids
http://www.brainkart.com/article/What-are-glycolipids-_27515/

diagram of Guillain Barre with anti-gangliosides
http://www.immunopaedia.org.za/wp-content/uploads/2014/12/axonal-or-End-Plate-Terminal-Damage.jpg

so the reason for the formation of anti-ganglioside antibodies according to the Cross-targeting hypothesis is that the immune system can only deal with one infection at a time.  Enteroviruses which  infect the ER and trigger NK cells are shut down so that the immune system can focus on the bacterial infection. The problem is that the anti-ganglioside does more than block NK from seeing GM2. Thus the paralysis.

AFM (acute flaccid myelitis) and anti-ganglioside
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5976313/
https://www.ncbi.nlm.nih.gov/pubmed/29028962

seizures induced by GM1
https://www.ncbi.nlm.nih.gov/pubmed/7472306
https://www.ncbi.nlm.nih.gov/pubmed/8822688
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3177549/

Patients listed on bottom...most include asthma which could be linked to staph
https://www.cdc.gov/mmwr/volumes/66/wr/mm6628a4.htm