Porcine epidemic diarrhea virus E protein causes endoplasmic reticulum stress and up-regulates interleukin-8 expression

Abstract

BackgroundPorcine epidemic diarrhea virus (PEDV) is an important pathogen in swine and is responsible for substantial economic losses. Previous studies suggest that the PEDV E protein plays an important role in the viral assembly process. However, the subcellular localization and other functions of PEDV E protein still require more research.MethodsThe subcellular localization and function of PEDV E protein were investigated by examining its effects on cell growth, cell cycle progression, interleukin-8 (IL-8) expression and cell survival.ResultsThe results show that plenty of PEDV E protein is localized in the ER, with small quantities localized in the nucleus. The PEDV E protein has no effect on the intestinal epithelial cells (IEC) growth, cell cycle and cyclin A expression. The cells expressing PEDV E protein express higher levels of IL-8 than control cells. Further studies show that PEDV E protein induced endoplasmic reticulum (ER) stress and activated NF-κB which is responsible for the up-regulation of IL-8 and Bcl-2 expression.ConclusionsThis study shows that the PEDV E protein is localized in the ER and the nucleus and it can cause ER stress. The PEDV E protein had no effect on the IEC growth and cell cycle. In addition, the PEDV E protein is able to up-regulate IL-8 and Bcl-2 expression.

Rapamycin-induced autophagy restricts porcine epidemic diarrhea virus infectivity in porcine intestinal epithelial cells

“…When PEDV infects porcine IECs, its entrance is mediated by receptors such as aminopeptidase N protein (Belouzard et al, 2012) or sugars (Deng et al, 2016;Liu et al, 2015) expressed on porcine IECs (Cong et al, 2015;Jung and Saif, 2015). It has been reported that the virus infected epithelium results in barrier dysfunction by downregulation of tight junction proteins (Zhao et al, 2014) and an increase in interleukin (IL)-8 (Xu et al, 2013) and necrotic cell death . However, the mechanism that defends against PEDV infection in porcine IECs is unknown.…”

Porcine epidemic diarrhea virus N protein prolongs S-phase cell cycle, induces endoplasmic reticulum stress, and up-regulates interleukin-8 expression

“…The cell cycle was measured by using propidium iodide staining as described previously (Xu et al, 2013;Tang et al, 2010). Briefly, approximately 2 Â 10 6 cells of the stable cell lines and control cells were treated with trypsin, washed with phosphate-buffered saline (PBS) for twice, resuspended in 75% ethanol and fixed at 4 8C for 3 days.…”

“…The procedures of Real-time quantitative PCR were described previously (Xu et al, 2013). Briefly, total RNA was extracted from cells using TRIzol agent (Invitrogen, California, USA), and 2 mg each RNA sample was reversetranscribed using First-strand cDNA synthesis kit (Invitrogen, California, USA).…”

Vaccines for porcine epidemic diarrhea virus and other swine coronaviruses

“…The M protein is the most abundant virion component and also contains conserved linear B-cell epitopes (Zhang et al, 2012). The E protein is responsible for the assembly of virion, and it causes endoplasmic reticulum stress and interleukin-8 expression up-regulation (Xu et al, 2013a). Accessory genes are dispensable for virus growth in vitro, but they may play an important role in the virus survival in the infected host.…”