Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
J Med Virol. 2017 Dec;89(12):2188-2195. doi: 10.1002/jmv.24846. Epub 2017 Aug 29.
Absent in melanoma 2 (AIM2) inflammasome is a multiprotein complex which plays a pivotal role in the host immune response to multiple pathogens. The role of AIM2 in human cytomegalovirus (HCMV) infection is poorly studied. Thus, using a small inference RNA (siRNA) approach and THP-1 derived macrophage cells infected with HCMV AD169 strain, we investigated the impact of HCMV infection on AIM2-mediated molecular events. Compared to wild-type cells, AIM2-defiecient macrophages showed a limited ability to activate caspase-1, process IL-1β, and induce cell death. In addition, AIM2-defiecient cells were unable to efficiently control HCMV infection, as the transcription of virus DNA polymerase gene UL54 and major tegument protein gene UL83 were higher compared to wild-type cells. In conclusion, HCMV infection induces an AIM2 inflammasome response, which negatively influences viral life cycle.
缺失黑色素瘤 2(AIM2)炎性小体是一种多蛋白复合物,在宿主对多种病原体的免疫反应中起着关键作用。AIM2 在人类巨细胞病毒(HCMV)感染中的作用研究甚少。因此,我们使用小干扰 RNA(siRNA)方法和感染 HCMV AD169 株的 THP-1 衍生巨噬细胞,研究了 HCMV 感染对 AIM2 介导的分子事件的影响。与野生型细胞相比,AIM2 缺陷型巨噬细胞激活 caspase-1、加工 IL-1β 和诱导细胞死亡的能力有限。此外,AIM2 缺陷型细胞无法有效控制 HCMV 感染,因为病毒 DNA 聚合酶基因 UL54 和主要被膜蛋白基因 UL83 的转录水平高于野生型细胞。总之,HCMV 感染诱导 AIM2 炎性小体反应,从而对病毒生命周期产生负面影响。