ZIKV infection modulates expression of immune responses and neuronal markers in HEK293 cells and neural precursor cells

Zika virus (ZIKV) is a neurotropic virus that results in microcephaly in newborns when it infectspregnant mothers. Previous studies have yet to clarify the effects of ZIKV infection in causingmicrocephaly. Here, we aimed to investigate the effects of ZIKV infection in cells with neuronalcharacteristics or neuronal cell fate, the former being human embryonic kidney (HEK) cells andthe latter being neural precursor cells (NPCs). RNA-seq was performed to comparetranscriptome distributions between these cells under ZIKV infection. Additionally, the effects oflaminin on HEK cells were analyzed, due to its reported ability to guide cells toward neuronaldifferentiation. NPCs express a tremendous number of markers of neuronal differentiation, whilelaminin induced several neuronal characteristic markers in HEK cells. We found that HEK cellsirrespective of laminin treatment, but not NPCs, induced immunity-related transcripts, includingcytokines and proinflammatory molecules under ZIKV infection. Additionally, ZIKV infectioninduced neuronal transcripts in HEK cells, laminin-treated HEK cells and NPCs. Significantinductions of neuronal pathways were confirmed by PANTHER analysis in HEK cells,irrespective of laminin treatment. On the other hand, ZIKV infection downregulated variablegenes in all these cells. Altogether, our results suggest that ZIKV infection differently impactstranscriptome distributions, based on the level of neuronal differentiation.