In our analysis, we observed a statistically significant change in the expression of 316 proteins during TGEV infection in vitro. This number includes protein changes that were unique for a specific time point as well as those shared at these different time conditions. For example, the expression level of HSP90a expression was unchanged at 48 hpi, but decreased at 64 hpi, making this change unique for the latter time point. On the other hand, TGF-b1 was observed to increase at both of the time points,Quinidine and was thus labeled a shared protein change. Moreover, the 316 altered proteins also includes proteins that changed from 48 hpi to 64 hpi, rather than one of these time points compared to noninfected cells. For example, mitochondrial aldehyde dehydrogenase 2 and MHC class I antigen were not changed at 48 or 64 hpi compared to the control group, but increased at 64 hpi compared with 48 hpi. We also observed a larger proteomic shift at 64 hpi compared to the 48 hpi time point in the infected ST cells. Further, some proteins previously reported to play a role in virus-induced host cell death, such as caspase-8, caspase-3, caspase-9, and Rifabutin porcine aminopeptidase-N, were also identified using this iTRAQ technique. These caspase proteins are known to be involved in TGEV-induced cell apoptosis processes, while pAPN is the cell receptor for TGEV. Our results indicate that TGEV infection caused significant upregulation of caspase-8 expression at two time points in the virus-infected ST cells, and this change was verified by western blotting analysis. However, the expression of caspase-3, caspase-9, and pAPN was not significantly altered, indicating that the pathways involving these genes are not altered or that other proteins are compensating for their lack of change. In this regard, we identified an additional 15 proteins involved in cell death pathways that had significantly altered expression levels, with the exception of PRDX2 and BCL2L13 were upregulated at one or two time points. Regulation of cell death is known to be important for replication and pathogenesis in various coronaviruses, and we believe that further research on these proteins will lead to a better understanding of cell death regulation during TGEV infection. In order to determine what other processes, in addition to cell death, were affected by TGEV infection, we performed a GO enrichment analysis for the different temporal conditions.