FIG 6 .

ZIKV-infected hBMECs release ZIKV basolaterally. (A) Polarized hBMECs, grown for 5 days in Transwell plates, were apically or basolaterally infected with ZIKV (MOI, 5) in triplicate, and TEER was measured 1 to 3 dpi. To demonstrate monolayer barrier function, EDTA was added (10 mM for 10 min) to hBMEC monolayers; this resulted in an ~100-Ω reduction in TEER. (B) hBMECs apically or basolaterally infected with ZIKV were assayed for permeability to FITC-dextran (40 kDa), which was added to apical medium at 3 dpi; fluorescence over time was measured in the lower chambers. (C) hBMECs grown on Transwell inserts for 5 days were evaluated for TEER. Cells were apically or basolaterally infected (MOI, 5) with ZIKV, and titers present in apical and basolateral supernatants were quantitated at 1 dpi. (D) Potential model of the spread of ZIKV systemically and to neuronal compartments from hBMECs.