【摘 要】
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Enterovirus A71(EV-A71)is one of the etiological pathogens leading to hand,foot,and mouth disease(HFMD),which can cause severe neurological complications.The neuropathogenesis of EV-A71 infection is not well understood.The mislocalization and aggregation
【机 构】
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Department of Cell Biology,Harbin Medical University,Harbin 150081,China;Department of Microbiology,
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Enterovirus A71(EV-A71)is one of the etiological pathogens leading to hand,foot,and mouth disease(HFMD),which can cause severe neurological complications.The neuropathogenesis of EV-A71 infection is not well understood.The mislocalization and aggregation of TAR DNA-binding protein 43(TDP-43)is the pathological hallmark of amyotrophic lateral sclerosis(ALS).However,whether TDP-43 was impacted by EV-A71 infection is unknown.This study demon-strated that TDP-43 was cleaved during EV-A71 infection.The cleavage of TDP-43 requires EV-A71 replication rather than the activated caspases due to viral infection.TDP-43 is cleaved by viral protease 3C between the residues 331Q and 332S,while mutated TDP-43(Q331A)was not cleaved.In addition,mutated 3C which lacks the protease activity failed to induce TDP-43 cleavage.We also found that TDP-43 was translocated from the nucleus to the cytoplasm,and the mislocalization of TDP-43 was induced by viral protease 2A rather than 3C.Taken together,we demonstrated that TDP-43 was cleaved by viral protease and translocated to the cytoplasm during EV-A71 infection,implicating the possible involvement of TDP-43 in the pathogenesis of EV-A71infection.
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