10th International Virology Summit
Nanjing Agricultural University, China
Title: Persistent TGEV infection enhances ETEC K88 adhesion by promoting epithelialmesenchymal transition in intestinal epithelial cells
Biography: Qian Yang
Transmissible gastroenteritis virus (TGEV) is a coronavirus, characterized by diarrhea, high morbidity, and the mortality is 100% in piglets less than 2 weeks old. Pigs infected with TGEV are often suffer secondary infection with other pathogens, which aggravates the severity of diarrhea, but the mechanisms remain unknown. Here, we hypothesized that persistent TGEV infection stimulates the epithelial–mesenchymal transition (EMT), thereby generating cells that more easily adhere to enterotoxigenic Escherichia coli (ETEC). Intestinal epithelial cells are the primary targets of TGEV and ETEC infection. We found that TGEV can persistently infect porcine intestinal columnar epithelial cells (IPEC-J2), and cause EMT, consistent with multiple changes in key cell characteristics. Infected cells display fibroblast-like shapes, exhibit increases in mesenchymal markers with a corresponding loss of epithelial markers, have enhanced expression of IL-1β, IL-6, IL-8, TGF-β, and TNF-α mRNAs, and demonstrate increases in migratory and invasive behaviors. Additional experiments showed that activation of the PI3K/Akt and ERK signaling pathways via TGF-β are critical for the TGEV-mediated EMT process. Cellular uptake is also modified in cells that have undergone EMT. TGEV-infected cells have higher levels of integrin α5 and fibronectin and exhibit enhanced adhesion of ETEC K88. Reversal of EMT reduces ETEC K88 adhesion and inhibits the expression of integrin α5 and fibronectin. Overall, these results suggest that TGEV infection induces EMT in IPEC-J2 cells, increasing the adhesion of ETEC K88 in the intestine and facilitating dual infection.