In agreement with previous studies, the dysregulation observed in the fatal group during the late phase of the infection mainly consisted in the upregulation of secreted inflammatory mediators, such as CCL2, CCL3, CCL13, CXCL1, CXCL10, CXCL11, CXCL12, IL6, MIF, SPP1, which are produced by myeloid cells and normally play a role in the defense mechanisms with the regulation of the adaptive immune response, specifically the migration of immune system cells associated with the trafficking of leukocytes in immune surveillance and inflammatory cell recruitment [24,25]. This evidence concerns the gene CCL2 and infection.