| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3428394 | Virus Research | 2014 | 12 Pages |
•We examine infection of PEDV and TGEV in intestinal model cells (IPEC-J2 cells).•Two viruses impair of IPEC-J2 cells in their early stages of infection.•PEDV and TGEV infection affect the microfilaments remodelling of IPEC-J2 cells.•Drug-interfered microfilaments of IPEC-J2 cells inhibit two viral life cycles.•MAPKs affected two viruses infection, the AJ and microfilaments of IPEC-J2 cells.
Viral infection converts the normal constitution of a cell to optimise viral entry, replication, and virion production. These conversions contain alterations or disruptions of the tight and adherens junctions between cells as part of their pathogenesis, and reorganise cellular microfilaments that initiate, sustain and spread the viral infections and so on. Using porcine epidemic diarrhoea virus (PEDV), transmissible gastroenteritis virus (TGEV) and a model of normal intestinal epithelial cells (IPEC-J2), we researched the interaction between tight and adherens junctions and microfilaments of IPEC-J2 cells with these viruses. In our work, the results showed that IPEC-J2 cells were susceptible to TGEV and PEDV infection. And TGEV could impair the barrier integrity of IPEC-J2 cells at early stages of infection through down-regulating some proteins of tight and adherens junctions, while PEDV cloud cause a slight of damage in the integrity of epithelial barrier. In addition, they also could affect the microfilaments remodelling of IPEC-J2 cells, and the drug-interfered microfilaments could inhibit viral replication and release. Furthermore, PEDV + TGEV co-infection was more aggravating to damage of tight junctions and remodelling of microfilaments than their single infection. Finally, the PEDV and TGEV infection affected the MAPK pathway, and inhibition of MAPK pathway regulated the changes of tight junctions and microfilaments of cells. These studies provide a new insight from the perspective of the epithelial barrier and microfilaments into the pathogenesis of PEDV and TGEV.
