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. 2021 Sep 30;15:695106. doi: 10.3389/fncel.2021.695106

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Copyright © 2021 King and Irigoyen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ZIKV causes ciliopathy and forces premature neurogenesis. During asymmetric division of apical NPCs, the daughter cell that reforms the primary cilia remains attached to the ventricular surface whereas the other daughter cell that does not undergo ciliogenesis delaminates from the ventricular surface and differentiates. ZIKV NS5 protein interacts with cellular proteins at the base of the primary cilia in NPCs causing an atypical ciliopathy and premature neuron delamination (adapted from Saade et al., 2020, created with Biorender.com).