These data showed that infection by SFTS virus drives infected THP-1 differentiation toward first an pro-inflammatory M1 phenotype characterized by increase of TNF-α, IL-1β, IL-6, and CD86 mRNA within the first 12–24 h followed by change to the anti-inflammatory M2 phenotype characterized by CD163, CD206, IL-10, and CCL22 mRNA expression. Here, CCL22 is linked to infection.