Zika virus infection reprograms global transcription of host cells to allow sustained infection

Zika virus (ZIKV) is an emerging virus causally linked to neurological disorders, including congenital microcephaly and Guillain–Barre´ syndrome. There are currently no targeted therapies for ZIKV infection. To identify novel antiviral targets and to elucidate the mechanisms by which ZIKV exploits the host cell machinery to support sustained replication, we analyzed the transcriptomic landscape of human microglia, fibroblast, embryonic kidney, and monocyte-derived macrophage cell lines before and after ZIKV infection. Overall design: To analyze factors contributing to ZIKV pathogenesis, we selected four human cell lines, microglia, BJ (foreskin fibroblast), 293FT (embryonic kidney), and THP-1 derived macrophages (monocyte-derived macrophage), and inoculated them with ZIKV produced in Vero and BHK cells at a multiplicity of infection of 1.