Zika virus infection in a non-neural cell host promotes differential expression of proteins associated with neurological conditions.

Abstract

The Zika Virus (ZIKV) is a Flavivirus that caused a recent outbreak worldwide resulting in different neurological outcomes that are still poorly characterized and understood. Concerning this issue, in vitro and in vivo models are being applied to improve the molecular understanding of ZIKV infection. In this work, applying shotgun proteomics we revealed the differential ZIKV infection proteome in Vero cells, a non-neural cell model. A dramatic change resulting from infection was found including the differential expression of several proteins previously associated with brain diseases. The molecular alterations caused by this pathogen were further characterized through bioinformatics such as Gene Ontology and protein-protein interaction network of resulting differential proteome. Our findings identified molecular markers that were differentially expressed during ZIKV infection and had been previously linked to neurological conditions and infections caused by ZIKV and/or SARS-CoV-2. The results presented in this article highlight molecular markers associated with neurological dysfunctions, demonstrating that ZIKV infection can dysregulate neural-specific genes, even in non-neural cells.