Porcine epidemic diarrhea virus (PEDV) invades porcine intestinal epithelial cells (IECs) and causes diarrhea and dehydration in pigs. In the present study, we showed a suppression of PEDV infection in porcine jejunum intestinal epithelial cells (IPEC-J2) by an increase in autophagy. Autophagy was activated by rapamycin at a dose that does not affect cell viability and tight junction permeability. The induction of autophagy was examined by LC3I/LC3II conversion. To confirm the autophagic-flux (entire autophagy pathway), autophagolysosomes were examined by an immunofluorescence assay. Pre-treatment with rapamycin significantly restricted not only a 1 h infection but also a longer infection (24 h) with PEDV, while this effect disappeared when autophagy was blocked. Co-localization of PEDV and autophagosomes suggests that PEDV could be a target of autophagy. Moreover, alleviation of PEDV-induced cell death in IPEC-J2 cells pretreated with rapamycin demonstrates a protective effect of rapamycin against PEDV-induced epithelial cell death. Collectively, the present study suggests an early prevention against PEDV infection in IPEC-J2 cells via autophagy that might be an effective strategy for the restriction of PEDV, and opens up the possibility of the use of rapamycin in vivo as an effective prophylactic and prevention treatment.

猪流行性腹泻病毒（PEDV）侵袭猪肠道上皮细胞（IEC），并引起猪的腹泻和脱水。在本研究中，我们显示自噬增加可抑制猪空肠肠道上皮细胞（IPEC-J2）中的PEDV感染。雷帕霉素以不影响细胞生存力和紧密连接通透性的剂量激活自噬。通过LC3I / LC3II转化检查自噬的诱导。为了确认自噬通量（整个自噬途径），通过免疫荧光测定法检查了自噬溶酶体。雷帕霉素预处理不仅显着限制了PEDV感染1小时，而且延长了感染时间（24小时），而自噬被阻断后，这种作用消失了。PEDV和自噬体的共定位表明PEDV可能是自噬的目标。此外，用雷帕霉素预处理的IPEC-J2细胞中PEDV诱导的细胞死亡的减轻证明雷帕霉素对PEDV诱导的上皮细胞死亡具有保护作用。总体而言，本研究表明通过自噬早期预防IPEC-J2细胞中PEDV感染，这可能是限制PEDV的有效策略，并开辟了雷帕霉素使用的可能性体内作为一种有效的预防和预防治疗。