Dynamic bidirectional regulation between Stk38 and rabies virus M protein coordinates apoptosis progression during neurotropic infection.

Rabies virus (RABV) causes fatal encephalitis in untreated humans, representing a critical global zoonotic threat. Although the viral matrix protein (M) is established as a mediator of mitochondrial apoptosis and enhancer of viral replication, its regulatory mechanisms remain incompletely characterized. This study reveals a reciprocal regulatory axis between RABV M protein and the host kinase Stk38.