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The most frequent scientific hypotheses to explain chronic persistent symptomatology in those suffering from CLD/PTLDS involve multiple mechanisms, including not only co-infections [37,38], but also immune evasion [39,40] with complement evasion and resistance [41], a persistent excessive, dysregulated pro-inflammatory immune response during the post-infectious period [42] persistent antigenic debris including peptidoglycans [43], altered neural networks with central sensitization [15], continuing infection with Borrelia [44,45,46,47,48] and/or a combination of the above [49]

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