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. 2022 Dec 20;19:307. doi: 10.1186/s12974-022-02668-8

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 9 — ZIKV-infection of neurons signals for IFNB-dependent microglia activation while inducing Tau phosphorylation. ZIKV-infected mature neurons from immunocompetent mice display a delayed IFNB response unable to stop viral replication leading to the accumulation of viral RNA in association with the induction of pathological phosphorylated Tau protein (P-Tau). ZIKV-infection leads to the activation of the expression of the gene coding for the RNA-dependent kinase PKR in PCNs and mouse brain. A role for PKR in the enhancement of P-Tau is proposed in relation with the capacity of PKR to be activated by viral cytoplasmic RNA and in turn activate GSK3B, one of the main kinases responsible of pTau. Following ZIKV infection of neurons, neuronal IFNs-I directly signal microglia for activation and the establishment of a DAM-like phenotype. The diagram was created using BioRender.com