The examination of the subnetwork formed by CD4, CCL2, CCL3, CCL4, and CCR5 leads to the hypothesis that the CCR5 allelic variant CCR5delta32 (rs333) may affect the TBE outcome not only affecting the entry of TBEV into the cell, but also modulating chemokine activity towards neural cells and CD4 glycoprotein functioning. This evidence concerns the gene CCL4 and tick-borne encephalitis.