Hepatitis C virus subverts liver-specific miR-122 to protect the viral genome from exoribonuclease Xrn2.

摘要: Summary The abundant, liver-specific microRNA miR-122 forms extensive base-pairing interactions with the 5′ noncoding region of hepatitis C virus (HCV) RNA genome, protecting viral from degradation. We discovered that 5′-3′ exoribonuclease Xrn2, which plays a crucial role in transcription termination polymerase II, modulates HCV abundance cytoplasm, but is counteracted by miR-122-mediated protection. Specifically, Xrn2 depletion results increased accumulation of viral RNA, while overexpression diminishes abundance. Depletion did not alter translation or replication rates affected stability. Importantly, during sequestration miR-122, restored abundance, arguing eliminates requirement for Thus, has cytoplasmic, antiviral function against HCV's subversion to form protective oligomeric complex at end genome.