Version 1
: Received: 30 September 2019 / Approved: 2 October 2019 / Online: 2 October 2019 (08:28:09 CEST)
How to cite:
Turpin, J.; Frumence, E.; Harrabi, W.; Kalamouni, C.E.; Desprès, P.; Krejbich-Trotot, P.; Viranaïcken, W. Crosstalk Between Endoplasmic Reticulum Stress and The Unfolded Protein Response During ZIKA Virus Infection. Preprints2019, 2019100024. https://doi.org/10.20944/preprints201910.0024.v1
Turpin, J.; Frumence, E.; Harrabi, W.; Kalamouni, C.E.; Desprès, P.; Krejbich-Trotot, P.; Viranaïcken, W. Crosstalk Between Endoplasmic Reticulum Stress and The Unfolded Protein Response During ZIKA Virus Infection. Preprints 2019, 2019100024. https://doi.org/10.20944/preprints201910.0024.v1
Turpin, J.; Frumence, E.; Harrabi, W.; Kalamouni, C.E.; Desprès, P.; Krejbich-Trotot, P.; Viranaïcken, W. Crosstalk Between Endoplasmic Reticulum Stress and The Unfolded Protein Response During ZIKA Virus Infection. Preprints2019, 2019100024. https://doi.org/10.20944/preprints201910.0024.v1
APA Style
Turpin, J., Frumence, E., Harrabi, W., Kalamouni, C.E., Desprès, P., Krejbich-Trotot, P., & Viranaïcken, W. (2019). Crosstalk Between Endoplasmic Reticulum Stress and The Unfolded Protein Response During ZIKA Virus Infection. Preprints. https://doi.org/10.20944/preprints201910.0024.v1
Chicago/Turabian Style
Turpin, J., Pascale Krejbich-Trotot and Wildriss Viranaïcken. 2019 "Crosstalk Between Endoplasmic Reticulum Stress and The Unfolded Protein Response During ZIKA Virus Infection" Preprints. https://doi.org/10.20944/preprints201910.0024.v1
Abstract
Flaviviruses replicate in membranous factories associated with the endoplasmic reticulum (ER). The replication rate generates a high polyprotein integration that can contribute to ER stress. Therefore, the host cell can develop an Unfolded Protein Response (UPR) to this protein accumulation which will stimulate appropriate cellular responses in the infectious context (Adaptation, autophagy or cell death). These different stress responses can help to overcome the virus and usually support antiviral strategies initiated by infected cells. In the present study, we investigated the capacity of ZIKA virus (ZIKV) to induce ER stress in epithelial A549 cells with a special focus on the causal factors behind it. We observed that the cells respond to ZIKV infection by implementing an UPR through activation of the IRE1 and PERK pathway but surprisingly without activation of the ATF6 branch. When we examined the effects of modulating the ER stress response we found that UPR inducers significantly inhibit ZIKV replication. Interestingly, our findings provide evidence that ZIKV can altered the UPR in order to escape to the host cell defense system.
Keywords
ZIKA virus; ER stress; Unfolded Protein Response; ATF6
Subject
Biology and Life Sciences, Virology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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