CD14 and viral infectious disease: To assess this objective, naïve human monocytes were stimulated by the presence of ZIKV (MOI 1), mock C6/36 EVs, or ZIKV C6/36 EVs (small and large isolates as the same for the RNase A + UV), which were evaluated for monocyte activation or differentiation (to adherent phenotype cells) by means of the monocytes’ phenotypic shift from a classical (CD14++ CD16−) to an intermediate (CD14++ CD16+) or non-classical (CD14+ CD16++) phenotype, which seems to be the main producer of inflammatory mediators in response to viral infection [49].