PDF(Pubmed)
Abstract：
The infection caused by porcine epidemic diarrhea virus (PEDV) is associated with high mortality in piglets worldwide. Host factors involved in the efficient replication of PEDV, however, remain largely unknown. Our recent proteomic study in the virus-host interaction network revealed a significant increase in the accumulation of CALML5 (EF-hand protein calmodulin-like 5) following PEDV infection. A further study unveiled a biphasic increase of CALML5 in 2 and 12 h after viral infection. Similar trends were observed in the intestines of piglets in the early and late stages of the PEDV challenge. Moreover, CALML5 depletion reduced PEDV mRNA and protein levels, leading to a one-order-of-magnitude decrease in virus titer. At the early stage of PEDV infection, CALML5 affected the endosomal trafficking pathway by regulating the expression of endosomal sorting complex related cellular proteins. CALML5 depletion also suppressed IFN-β and IL-6 production in the PEDV-infected cells, thereby indicating its involvement in negatively regulating the innate immune response. Our study reveals the biological function of CALML5 in the virology field and offers new insights into the PEDV-host cell interaction.
摘要：
猪流行性腹泻病毒（PEDV）引起的感染与世界范围内仔猪的高死亡率有关。参与PEDV有效复制的宿主因子，然而,基本上是未知的。我们最近在病毒-宿主相互作用网络中的蛋白质组学研究表明，PEDV感染后CALML5（EF-hand蛋白钙调蛋白样5）的积累显着增加。进一步的研究揭示了在病毒感染后2和12小时内CALML5的双相增加。在PEDV攻击的早期和晚期阶段，在仔猪的肠道中观察到了类似的趋势。此外，CALML5耗竭降低PEDVmRNA和蛋白水平，导致病毒滴度下降一个数量级。在PEDV感染的早期,CALML5通过调节内体分选复合物相关细胞蛋白的表达影响内体运输途径。CALML5耗竭还抑制了PEDV感染细胞中IFN-β和IL-6的产生，从而表明其参与负调节先天免疫应答。我们的研究揭示了CALML5在病毒学领域的生物学功能，并为PEDV-宿主细胞相互作用提供了新的见解。
