01605nas a2200277 4500000000100000008004100001260001200042653001300054653002300067653001200090653002600102653001500128100001800143700001700161700001300178700001400191700001300205700001300218700001500231245009000246856008100336300001100417490000700428520087800435022001401313 2022 d c01/202210aCovid-1910akynurenine pathway10aleprosy10aPeripheral neuropathy10aTryptophan1 ade Oliveira J1 ade Athaide M1 aRahman A1 aBarbosa M1 aJardim M1 aMoraes M1 aPinheiro R00aKynurenines in the Pathogenesis of Peripheral Neuropathy During Leprosy and COVID-19. uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8907883/pdf/fcimb-12-815738.pdf a8157380 v123 a

Inflammatory disorders are associated with the activation of tryptophan (TRYP) catabolism the kynurenine pathway (KP). Several reports have demonstrated the role of KP in the immunopathophysiology of both leprosy and coronavirus disease 19 (COVID-19). The nervous system can be affected in infections caused by both and SARS-CoV-2, but the mechanisms involved in the peripheral neural damage induced by these infectious agents are not fully understood. In recent years KP has received greater attention due the importance of kynurenine metabolites in infectious diseases, immune dysfunction and nervous system disorders. In this review, we discuss how modulation of the KP may aid in controlling the damage to peripheral nerves and the effects of KP activation on neural damage during leprosy or COVID-19 individually and we speculate its role during co-infection.

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