Proposed answers to questions 1- 4
1. How could persistent PGE2 explain the remarkable breadth of symptoms and abnormalities?
Chronic PGE2 upregulation is reported to play a principal role in promoting:
Viral persistence; cytokine activation; autoimmunity; thrombosis; microbiome disruption; mitochondrial dysfunction; endothelial dysfunction; serotonin dysregulation; autonomic dysfunction; apoptosis of dopaminergic; insulinergic cells; oligodendrocytes; muscle-neurons, resistances to endocrine hormones and numerous other pathological phenomena.
For references see the three links below:
PGE2 functions
PGE2 and LC Mechanisms
PGE2’s antagonizing strategies
2. How could PGE2 remain elevated?
The proposed mechanism
From acute inflammation to chronic disease
Immune dysregulation and autoimmunity
Hormonal multiresistance
3. How can this hypothesis be tested?
4. What are the implications of a validated hypothesis?
Clinical phenotypes and potential biomarkers
Therapeutic implications
Perspectives of a validated hypothesis