Department of Microbiology, Boston University School of Medicine.
National Emerging Infectious Diseases Laboratories, Boston University, Massachusetts.
J Infect Dis. 2018 Nov 22;218(suppl_5):S403-S408. doi: 10.1093/infdis/jiy473.
Protein kinase R (PKR) is a key antiviral protein involved in sensing and restricting viral infections. Here we analyzed the ability of Marburg virus (MARV) viral protein 35 (VP35) to inhibit PKR activation in human and bat cells. Similar to the related Ebola and Lloviu viruses, MARV VP35 was able to inhibit PKR activation in 293T cells. In contrast, we found that MARV VP35 did not inhibit human or bat PKR activation in human glioblastoma U-251-MG cells or a Rousettus aegyptiacus cell line. Additional experiments revealed that PACT, a known PKR regulator, was insufficient to rescue the ability of VP35 to inhibit PKR activation in these cells. Taken together, this study indicates that the ability of VP35 to inhibit PKR is cell type specific, potentially explaining discrepancies between the ability of filoviruses to potently block innate immune responses, and the high levels of interferon and interferon-stimulated genes observed in filovirus patients.
蛋白激酶 R (PKR) 是一种参与感知和限制病毒感染的关键抗病毒蛋白。在这里,我们分析了马尔堡病毒 (MARV) 病毒蛋白 35 (VP35) 在人源和蝙蝠细胞中抑制 PKR 激活的能力。与相关的埃博拉病毒和 Lloviu 病毒类似,MARV VP35 能够抑制 293T 细胞中的 PKR 激活。相比之下,我们发现 MARV VP35 不能抑制人源神经胶质瘤 U-251-MG 细胞或 Rousettus aegyptiacus 细胞系中的人源或蝙蝠 PKR 激活。进一步的实验表明,PACT,一种已知的 PKR 调节剂,不足以挽救 VP35 抑制 PKR 激活的能力。综上所述,这项研究表明,VP35 抑制 PKR 的能力具有细胞类型特异性,这可能解释了丝状病毒强烈阻断先天免疫反应的能力与丝状病毒患者中干扰素和干扰素刺激基因水平较高之间的差异。