White spot syndrome virus IE1 protein blocks the integrin-FAK signaling to enhance viral infection in shrimp.

DNA viruses commonly utilize immediate-early proteins to manipulate cellular signaling pathways in order to facilitate their infection. Our previous research has suggested that IE1, an immediate-early protein encoded by the white spot syndrome virus (WSSV), may modulate the shrimp integrin-FAK signaling pathway. However, the specific molecular mechanism and role of IE1 in regulating this signaling pathway remain unclear. In this study, we demonstrated that IE1 competes for binding to the cytoplasmic tail of Penaeus vannamei integrin-α5, resulting in the inhibition of the integrin-α5-FAK interaction, thereby suppressing FAK activation and cell adhesion. Furthermore, we observed a significant increase in the expression of P. vannamei integrin-α5 and FAK following WSSV infection. Additionally, knockdown of integrin-α5 or FAK through RNA interference has been shown to reduce cell adhesion and enhance WSSV infection. In conclusion, our findings reveal that IE1 disrupts integrin-FAK signaling to inhibit cell adhesion, ultimately promoting WSSV infection in shrimp.