Objective：To investigate the role of poly（C）- binding protein 2（PCBP2）in the pathogenic process following Dabie Banda virus（DBV）infection and its mechanism of action through the regulation of ferroptosis. Methods：The THP-1 human monocytic cell line was used as a model，the mitochondrial structural changes under viral infection were observed via transmission electron microscopy. Lentivirus - mediated PCBP2 - overexpressing and lentivirus - mediated PCBP2 - knockdown THP - 1 cell lines were constructed. FerroOrange fluorescent probe was used to measure Fe2+ levels，2，7-dichlorofluorescein diacetate（DCFH-DA）assay was employed to determine reactive oxygen species（ROS）levels，and Western blot was performed to assess the expression of solute carrier family 7 member 11（SLC7A11）and glutathione peroxidase 4（GPX4）proteins，thus to evaluate the impact of PCBP2 modulation on ferroptosis. Cells were treated with ferroptosis inducers（RSL3，erastin）and inhibitors（Fer - 1，Lip - 1）. Viral replication levels were examined by qRT - PCR and immunofluorescence to explore whether PCBP2 influences DBV replication by regulating ferroptosis. Results：In DBV -infected cells，both mRNA and protein levels of PCBP2 were significantly downregulated. DBV infection induced typical ferroptosis features，including mitochondrial cristae reduction and swelling. PCBP2 knockdown and overexpression in THP -1 cells were confirmed by qRT-PCR and Western blot. PCBP2 knockdown decreased the expression of ferroptosis-related genes of solute carrier family 7 member 11（SLC7A11）and glutathione peroxidase 4（GPX4），leading to increased ROS and Fe2+ levels. Conversely， PCBP2 overexpression elevated SLC7A11 and GPX4 expression while reducing ROS and Fe2 + accumulation. The 50% tissue culture infective dose and protein level assays further demonstrated that ferroptosis inducers partially counteracted the pro - viral effect of PCBP2 overexpression，while ferroptosis inhibitors partially reversed the antiviral effect caused by PCBP2 knockdown. Conclusion： This study reveals that PCBP2 inhibits ferroptosis by maintaining the SLC7A11/GPX4 system，thereby restricting DBV replication. These findings not only elucidate the regulatory role of PCBP2 in DBV infection but also provide novel insights into the pathogenesis of severe fever with thrombocytopenia syndrome（SFTS）. Moreover，targeting the PCBP2-ferroptosis pathway may represent a potential therapeutic strategy for SFTS，offering new directions for antiviral drug development.