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Potential contributors include immune dysregulation, residual tissue injury, autonomic dysfunction, central sensitization, co-infections, reinfection, and possibly bacterial persistence, although the role of persistent infection remains an area of ongoing scientific investigation

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GGT catalyzes the degradation of extracellular GSH, thereby allowing recovery of constituent amino acids, including cysteine, which is often rate-limiting, for subsequent intracellular GSH re-synthesis