March 3, 2026Open Access

PCBP2 inhibits antiviral innate immune responses via the MAVS-mediated signaling pathway in severe fever with thrombocytopenia syndrome

Key Points

PCBP2 promotes viral replication by degrading MAVS, impairing antiviral signaling.
During DBV infection, PCBP2 functions as a critical negative regulator of immune responses, influencing outcomes.
The study reveals insights into immune evasion mechanisms relating to DBV, focusing on the MAVS pathway.
Targeting PCBP2 may provide a host-directed therapeutic strategy to enhance antiviral immunity against SFTS.

Abstract

These findings identify PCBP2 as a critical negative regulator of RLR-mediated antiviral signaling during DBV infection. By facilitating MAVS degradation and suppressing innate immune responses, PCBP2 promotes viral replication, providing new insights into DBV immune evasion mechanisms and highlighting PCBP2 as a potential host-directed therapeutic target for SFTS.

PCBP2 inhibits antiviral innate immune responses via the MAVS-mediated signaling pathway in severe fever with thrombocytopenia syndrome

Key Points

Abstract

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