Newly re-emerging viruses are major sources of concern around the world, especially when no treatment options are available during an outbreak. ZIKV is a neurotropic virus that causes congenital abnormalities in babies when they are infected in utero. Some studies have reported that these congenital abnormalities result from ZIKV attacking neural progenitor cells within the brain that differentiate into neurons, oligodendrocytes, and astrocytes. Each of these glial cells plays an important role in fetal brain development. Newborns infected with ZIKV suffer from microcephaly and delayed neurodevelopment, but the underlying causes at the proteomic level are largely unknown. In addition to congenital defects caused by ZIKV, infected patients have been documented to suffer gastrointestinal problems such as diarrhea, nausea, vomiting, and abdominal discomfort, among other things. My PhD thesis for the first time identified host proteins, which we predicted to be linked in the development of; 1) neurosensory alterations that have been reported to occur in babies born to ZIKV infected pregnant mothers and 2) gastrointestinal complications reported in ZIKV infected patients. Invitro proteomic analysis of ZIKV-induced changes was performed in Vero and Caco-2 cells, which are known to be permissive to ZIKV infection. Tandem mass tag mass spectrometry- based proteomic and the SOMAScan were used in monitoring these cells infected with ZIKV. Thousands of host proteins were identified to be dysregulated across selected multiple time point post ZIKV infection. Many protein candidates were linked to neurodevelopmental processes, including the development of the auditory and visual/retinal system as well as gastrointestinal complications as predicted after bioinformatics analysis by IPA. The role of these dysregulated neurodevelopmental associated, as well as gastrointestinal related host proteins for ZIKV propagation, needs to be validated to gain more understanding of ZIKV biology as well as determine the potential of these proteomic candidates for future ZIKV therapeutic modality development. In conclusion, my PhD project was the first to identify temporal neurodevelopmental and gastrointestinal proteomic responses in ZIKV-infected cells.