CCL5 and infection: As demonstrated in dizygotic twins, which present different outcomes after infection with a Brazilian isolate of ZIKV, trophoblasts from the ZIKV-nonaffected twin secreted increased levels of inflammatory chemokines (RANTES/CCL5 and IP10) because the nonaffected twin more efficiently activated genes (induced by IFN-g) involved in placental ZIKV immune protection, thus preventing ZIKV dissemination into developing foetus tissues.32