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In HCV‐infected cells, the viral TA protein NS5B is partially mislocalized to mitochondria and induces mitochondrial fragmentation, thereby facilitating HCV infection. However, ATAD1, a mitochondrial membrane protein, extracts NS5B and mediates its proteasomal degradation, thus maintaining mitochondrial morphology. In addition to its action on NS5B, ATAD1 also augmented the antiviral function of MAVS.
