March 3, 2026Open Access

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

Puntos clave

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.

Resumen

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.

Connected Papers

Building similarity graph...

Analyzing shared references across papers

Discussion

Authors

Xinyi Yu

Yan Dai

Xuewen Ji

Journals

Virus Research

SHILAP Revista de lepidopterología

Actions

Institutions

Nanjing Medical University

Nanjing University of Chinese Medicine

References and Citations

Connected Papers

Building similarity graph...

Analyzing shared references across papers

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

Puntos clave

Resumen

Citation Network

Connected Papers

Discussion

Authors

Journals

Actions

Institutions

References and Citations

Citation Network

Connected Papers

Discussion

Cite this study