Abstract
Newly re-emerging viruses are of great global concern, especially when there are no therapeutic interventions available during the time of an outbreak. There are still no therapeutic interventions for the prevention of Zika virus (ZIKV) infections despite its resurgence more than a decade ago. Newborns infected with ZIKV suffer from microcephaly and delayed neurodevelopment, but the underlying causes are largely unknown. All viruses hijack the host cellular machinery to undergo successful replication. Our tandem mass tag mass spectrometry-based proteomic monitoring of cells infected with ZIKV revealed that among the thousands of host proteins dysregulated over time, many protein candidates were linked to neurodevelopmental processes, including the development of the auditory and visual/retinal system. The role of these dysregulated neurodevelopmental-associated host proteins for ZIKV propagation in eukaryotic cells remains elusive. For the first time, we present temporal neurodevelopmental proteomic responses in cells undergoing ZIKV infection. The future goal is to identify host proteins whose dysregulation results in neurosensory alterations reported in children born to ZIKV-infected mothers.