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. 2022 Apr 20;16(4):e0010359. doi: 10.1371/journal.pntd.0010359

Fig 6. Proposed mechanism of ADE of ZIKV infection in the term human placenta.

Fig 6

Left panel: In absence of cross-reactive DENV antibodies, ZIKV crosses the placental barrier less efficiently than in presence of cross-reactive flavivirus antibodies through a mechanism that is not fully elucidated yet. Right panel: In presence cross-reactive DENV antibodies, ZIKV immune complexes can be transported across the syncytiotrophoblasts layer through FcRn-mediated transcytosis. In the villus core, some non-neutralized complexes are taken up by the perivascular located HBCs through FcγRII, after which ZIKV can replicate in these cells. To reach the fetal circulation, ZIKV needs to subsequently cross the fetal endothelial barrier, possibly by infecting these cells. IVP; intervillous space, FcRn; neonatal Fc-receptor, STBs; syncytiotrophoblasts, CTBs; cytotrophoblasts, HBC; Hofbauer cell, FcγRII; Fcγ-receptor II. Created with Biorender.com.