. 2018 Feb 15;9:229. doi: 10.3389/fimmu.2018.00229

Table 1.

Some outstanding questions regarding ME/CFS, which are addressed in this conceptual review.

The hypothesis gives rise to several verifiable general questions
What is the nature of the genetic predisposition? Can the infection history of ME/CFS patients be traced? Does it differ from those of other diseases, e.g., autoimmune ones? Is there a common sequence of infection, postexertional malaise, and comorbidity occurrence during ME/CFS pathogenesis? Can defects in tolerance development be detected in ME/CFS patients? Can the path of B cell clones from germ line to various autoreactivities be traced in ME/CFS patients? Which autoantibodies can be detected in ME/CFS patients and its comorbidities? Can clues to ME/CFS biomarkers be derived from this explanatory model?

The hypothesis gives rise to several verifiable general questions

What is the nature of the genetic predisposition?
Can the infection history of ME/CFS patients be traced?
Does it differ from those of other diseases, e.g., autoimmune ones?
Is there a common sequence of infection, postexertional malaise, and comorbidity occurrence during ME/CFS pathogenesis?
Can defects in tolerance development be detected in ME/CFS patients?
Can the path of B cell clones from germ line to various autoreactivities be traced in ME/CFS patients?
Which autoantibodies can be detected in ME/CFS patients and its comorbidities?
Can clues to ME/CFS biomarkers be derived from this explanatory model?