As expected for the peak of the immune response where SLECs are critical for protective responses, the majority of cells polarized to a SLEC phenotype following ZIKV infection, expressing high levels of killer cell lectin-like receptor G1 (KLRG1) and down-regulating CD127 (IL-7 Receptor α chain); while only approximately 25% of cells maintained an MPEC phenotype (Fig 7D–7F). Here, IL7R is linked to Zika virus infectious disease.