Elucidation of the mechanism(s) modifying the co-operative apoptosis caused by Land L* proteins, which regulate the persistence of picornaviruses.

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Theiler's murine encephalomyelitis virus (TMEV)-induced demyelination is the representative of virus-induced demyelination and serves as an excellent animal model for multiple sclerosis because of the resembling pathological features. Twonon-structural viral proteins, leader (L) and L*, are thought to play an important role in TMEV biological activities.In this study, it was demonstrated that L increases the number of apoptotic cells while it suppresses the IFN response of host cells. Furthermore, it was demonstrated that L* inhibits the apoptotic cell death induced by L. In addition, L* was demonstrated to be localized to mitochondria. These results suggest that L* may inhibit the intrinsic apoptosis induced by L through the localization to mitochondria.The present studies suggest that the L and L* regulate the apoptosis during viral infection and contribute to TMEV subgroup-specific biological activities.