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Steere and Duray (1988) talking about how Lyme looks like post-sepsis syndrome with reactivated EBV:

http://www.actionlyme.org/clinical-pathologic-correlations-of-lyme-disease-by-stage-Steere-Duray.pdf

 

Steere saying you only need band 41 and that IgM bands mean the bug is still alive regardless of treatment:

http://www.actionlyme.org/1986_Steere_band_41_tmt_fails_half.pdf

CDC 1990 case definition showing this was adopted – just look for new IgM bands:
https://www.cdc.gov/mmwr/preview/mmwrhtml/00014526.htm

 

The Hu grant, talking about immunosuppression and tolerance to other kinds of microbes (TLR4 agonists or LPS)
https://projectreporter.nih.gov/project_info_description.cfm?aid=9292262&icde=38560878&ddparam=&ddvalue=&ddsub=&cr=1&csb=default&cs=ASC&pball=

Steere using the “Seronegative Lyme Assay” to assess chronic late neurologic Lyme because it can be “seronegative”:
http://www.actionlyme.org/1990_Steere_Chronic_Seroneg_NeuroLyme.pdf

 

Nicole Baumgarth talking about how Lyme causes you to not react to secondary viral infections:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4489802/

 

Baumgarth talking about how IgM is more important than IgG (most of the IgM bands were thrown out of the 1994 Dearborn case definition, which was not a consensus anyway):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358496/

“Notably, and consistent with earlier studies (2829), the number of IgM antibody secreting cells was higher than the IgG ASC in the wild-type mice, indicating a strong low affinity antibody response early in Bb infection. Like the IgG response, however, CD4 T cells clearly enhanced the IgM response.”

 

This is a disease of immunosuppression, secondary opportunistics, tolerance and cross tolerance , AND NOT the Dearborn case definition of a “chronic inflammatory disease of autoimmune arthritis.”

 

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