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. 2020 Dec 10;10:21604. doi: 10.1038/s41598-020-78735-y

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© The Author(s) 2020

Open Access This 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/.

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Schematic illustration of some cellular targets of ZIKV in neural cells. Our data reinforce the strong neurotropism of ZIKV, which was able to readily increase the expression and/or release of pro-inflammatory mediators, such as cytokines and iNOS. Inflammatory response is mainly coordinated by NFκB. In contrast, Nrf2 and its transcriptional products, such as HO1, are important regulators of adaptive responses to cellular stresses. HO1 is able to counteract inflammatory response and NFκB transcription activity. However, both Nrf2 and HO1 were downregulated by ZIKV exposure. More specific neuronal and astroglial ZIKV-induced effects could also be observed. A decrease in BDNF release, an increase in NSE and in A2a receptor gene expression can be mainly attributed to neurons (although A2a can be also expressed by astrocytes and microglia). Moreover, a decrease in S100B release, as well as an increase in mRNA levels of AQP4 and in GSH content can indicate an acute ZIKV-induced glial commitment in the hippocampus of adult rats.