Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15224, USA.
Center for Microbial Pathogenesis, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA 15224, USA.
Viruses. 2020 Sep 25;12(10):1074. doi: 10.3390/v12101074.
Enteroviruses manipulate host membranes to form replication organelles, which concentrate viral and host factors to allow for efficient replication. However, this process has not been well-studied in living cells throughout the course of infection. To define the dynamic process of enterovirus membrane remodeling of major secretory pathway organelles, we have developed plasmid-based reporter systems that utilize viral protease-dependent release of a nuclear-localized fluorescent protein from the endoplasmic reticulum (ER) membrane during infection, while retaining organelle-specific fluorescent protein markers such as the ER and Golgi. This system thus allows for the monitoring of organelle-specific changes induced by infection in real-time. Using long-term time-lapse imaging of living cells infected with coxsackievirus B3 (CVB), we detected reporter translocation to the nucleus beginning ~4 h post-infection, which correlated with a loss of Golgi integrity and a collapse of the peripheral ER. Lastly, we applied our system to study the effects of a calcium channel inhibitor, 2APB, on virus-induced manipulation of host membranes. We found that 2APB treatment had no effect on the kinetics of infection or the percentage of infected cells. However, we observed aberrant ER structures in CVB-infected cells treated with 2APB and a significant decrease in viral-dependent cell lysis, which corresponded with a decrease in extracellular virus titers. Thus, our system provides a tractable platform to monitor the effects of inhibitors, gene silencing, and/or gene editing on viral manipulation of host membranes, which can help determine the mechanism of action for antivirals.
肠道病毒通过操纵宿主膜来形成复制细胞器,这些细胞器集中了病毒和宿主因子,以实现高效复制。然而,在感染过程中,整个过程在活细胞中尚未得到很好的研究。为了定义肠道病毒对主要分泌途径细胞器的膜重塑过程,我们开发了基于质粒的报告系统,该系统利用病毒蛋白酶在感染过程中从内质网(ER)膜上释放核定位荧光蛋白,同时保留细胞器特异性荧光蛋白标记物,如 ER 和高尔基体。因此,该系统允许实时监测感染引起的细胞器特异性变化。通过对感染柯萨奇病毒 B3(CVB)的活细胞进行长期延时成像,我们检测到报告蛋白在感染后约 4 小时转移到细胞核,这与高尔基体完整性的丧失和外周 ER 的崩溃相关。最后,我们应用我们的系统来研究钙通道抑制剂 2APB 对病毒诱导的宿主膜操作的影响。我们发现 2APB 处理对感染的动力学或感染细胞的百分比没有影响。然而,我们观察到在 2APB 处理的 CVB 感染细胞中出现异常的 ER 结构,并且病毒依赖性细胞裂解显著减少,这与细胞外病毒滴度的降低相对应。因此,我们的系统为监测抑制剂、基因沉默和/或基因编辑对病毒操纵宿主膜的影响提供了一个可行的平台,这有助于确定抗病毒药物的作用机制。