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A schematic representation of the proposed model for the mechanism by which miR-218 assists PRRSV in evading the host innate immune response. PRRSV infection results in a decrease of miR-218 that negatively regulates SOCS3 expression. The upregulated SOCS3 can block the interferon signaling pathway. This establishes a model by which PRRSV-induced miR-218 downregulation augments virus replication via SOCS3-mediated suppression of ISGs expression.
