Dysregulation of RNA editing may help explain pathogenicity mechanisms of congenital Zika syndrome and Guillain-Barre syndrome

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1 Department of Biological Sciences, Kent State University, Kent, Ohio, United States
2 School of Biomedical Sciences, Kent State University, Kent, Ohio, United States
3 Department of Biology, University of Florida, Gainesville, Florida, United States
4 Emerging Pathogens Institute, University of Florida, Gainesville, Florida, United States
DOI
10.7287/peerj.preprints.27401v1
Published
Accepted
Subject Areas
Bioinformatics, Neuroscience, Virology, Global Health, Infectious Diseases
Keywords
Zika virus (ZIKV), Congenital Zika syndrome (CZS), Guillain-Barre syndrome (GBS), Innate immunity, RNA editing, Adenosine Deaminases Acting on RNA (ADAR) editing, Pathogenesis, Dysregulation of ADAR editing
Copyright
© 2018 Piontkivska et al.
Licence
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ Preprints) and either DOI or URL of the article must be cited.
Cite this article
Piontkivska H, Plonski N, Miyamoto MM, Wayne ML. 2018. Dysregulation of RNA editing may help explain pathogenicity mechanisms of congenital Zika syndrome and Guillain-Barre syndrome. PeerJ Preprints 6:e27401v1

Abstract

Many Zika virus (ZIKV) pathogenesis-related studies have focused primarily on virus-driven pathology and neurotoxicity, instead of considering the possibility of pathogenesis as an (unintended) consequence of host innate immunity: specifically, as the side-effect of an otherwise well-functioning machine. The hypothesis presented here suggests a new way of thinking about the role of host immune mechanisms in disease pathogenesis, focusing on dysregulation of post-transcriptional RNA editing as a candidate driver of a broad range of observed neurodevelopmental defects and neurodegenerative clinical symptoms in both infants and adults linked with ZIKV infections. We collect and synthesize existing evidence of ZIKV-mediated changes in expression of adenosine deaminases that act on RNA (ADARs), known links between abnormal RNA editing and pathogenesis, as well as ideas for potential translational applications, including genomic profile-based molecular diagnostic tools and/or treatment strategies.

Author Comment

This is a preprint submission to PeerJ Preprints.