Besides, CXCL10 and CXCL11 bonded the receptor CXCR3 and exerted a potent chemotactic effect on activated T lymphocytes [28–30]. Additionally, CH25H was induced in response to ZIKV infection, and its enzymatic product 25HC was a critical mediator of host protection against ZIKV, which had also been characterized as a broad-spectrum antiviral drug that inhibited viruses including ZIKV [31–33]. This evidence concerns the gene CXCL10 and Zika virus infectious disease.