Together, these four factors suggest a feed-forward loop in ZIKV infection whereby ECM remodeling (THBS1) and enhanced leukocyte trafficking (ITGAL), coupled with pro-inflammatory chemokine (CXCL8) and cytokine (IL-1A) release, synergize to both recruit additional susceptible cells and compromise barrier integrity, amplifying viral spread and immunopathology. This evidence concerns the gene ITGAL and Zika virus infectious disease.