PDF(Pubmed)
Abstract：
UNASSIGNED: Chikungunya virus (CHIKV) infection is associated with acute clinical manifestations and chronic joint inflammation. CHIKV has emerged as a significant causative agent of central nervous system (CNS) complications, including encephalitis and related sequelae. Microglial cells, crucial for immune responses and tissue repair in the CNS, play a vital role in the host response to viral infections, with their activation potentially leading to either protection or pathology. In this study, the infection biology of CHIKV in the C20 human microglial cell line was investigated.
UNASSIGNED: The permissiveness of C20 cells to CHIKV infection was assessed, and viral replication kinetics were compared to Vero E6 cells. Cytopathic effects of CHIKV infection on C20 cells were examined, along with ultrastructural changes using transmission electron microscopy. Additionally, apoptosis induction, mitochondrial membrane potential, and alterations in cell surface marker expression were evaluated by flow cytometry.
UNASSIGNED: CHIKV infection demonstrated permissiveness in C20 cells, similar to Vero cells, resulting in robust viral replication and cytopathic effects. Ultrastructural analysis revealed viral replication, mature virion formation, and distinctive cytoplasmic and nuclear changes in infected C20 cells. CHIKV infection induced significant apoptosis in C20 cells, accompanied by mitochondrial membrane depolarization and altered expression of cell surface markers such as CD11c, CD14, and HLA-DR. Notably, decreased CD14 expression was observed in CHIKV-infected C20 cells.
UNASSIGNED: The study findings suggest that CHIKV infection induces apoptosis in C20 microglial cells via the mitochondrial pathway, with significant alterations in cell surface marker expression, particularly CD14 that is linked with apoptosis induction. These observations provide valuable insights into the role of human microglial cells in the host response to CHIKV infection and contribute to the knowledge on the neuropathogenesis of this virus.
UNASSIGNED: The permissiveness of C20 cells to CHIKV infection was assessed, and viral replication kinetics were compared to Vero E6 cells. Cytopathic effects of CHIKV infection on C20 cells were examined, along with ultrastructural changes using transmission electron microscopy. Additionally, apoptosis induction, mitochondrial membrane potential, and alterations in cell surface marker expression were evaluated by flow cytometry.
UNASSIGNED: CHIKV infection demonstrated permissiveness in C20 cells, similar to Vero cells, resulting in robust viral replication and cytopathic effects. Ultrastructural analysis revealed viral replication, mature virion formation, and distinctive cytoplasmic and nuclear changes in infected C20 cells. CHIKV infection induced significant apoptosis in C20 cells, accompanied by mitochondrial membrane depolarization and altered expression of cell surface markers such as CD11c, CD14, and HLA-DR. Notably, decreased CD14 expression was observed in CHIKV-infected C20 cells.
UNASSIGNED: The study findings suggest that CHIKV infection induces apoptosis in C20 microglial cells via the mitochondrial pathway, with significant alterations in cell surface marker expression, particularly CD14 that is linked with apoptosis induction. These observations provide valuable insights into the role of human microglial cells in the host response to CHIKV infection and contribute to the knowledge on the neuropathogenesis of this virus.
摘要：
■基孔肯雅病毒（CHIKV）感染与急性临床表现和慢性关节炎症有关。CHIKV已成为中枢神经系统（CNS）并发症的重要病原体，包括脑炎和相关后遗症。小胶质细胞,对于中枢神经系统的免疫反应和组织修复至关重要，在宿主对病毒感染的反应中起着至关重要的作用，它们的激活可能导致保护或病理。在这项研究中,研究了CHIKV在C20人小胶质细胞系中的感染生物学。
■评估了C20细胞对CHIKV感染的宽容，将病毒复制动力学与VeroE6细胞进行比较。检查了CHIKV感染对C20细胞的细胞病变作用，以及使用透射电子显微镜的超微结构变化。此外,凋亡诱导，线粒体膜电位，通过流式细胞术评估细胞表面标志物表达的改变。
■CHIKV感染在C20细胞中表现出宽容，类似于Vero细胞，导致强大的病毒复制和细胞病变效应。超微结构分析显示病毒复制，成熟的病毒体形成，以及感染的C20细胞中独特的细胞质和细胞核变化。CHIKV感染诱导C20细胞显著凋亡,伴随着线粒体膜去极化和细胞表面标志物如CD11c的表达改变，CD14和HLA-DR。值得注意的是,在CHIKV感染的C20细胞中观察到CD14表达降低。
■研究结果表明，CHIKV感染通过线粒体途径诱导C20小胶质细胞凋亡，细胞表面标记表达的显著改变，特别是与细胞凋亡诱导相关的CD14。这些观察结果为人类小胶质细胞在宿主对CHIKV感染的反应中的作用提供了有价值的见解，并有助于了解该病毒的神经发病机理。
■评估了C20细胞对CHIKV感染的宽容，将病毒复制动力学与VeroE6细胞进行比较。检查了CHIKV感染对C20细胞的细胞病变作用，以及使用透射电子显微镜的超微结构变化。此外,凋亡诱导，线粒体膜电位，通过流式细胞术评估细胞表面标志物表达的改变。
■CHIKV感染在C20细胞中表现出宽容，类似于Vero细胞，导致强大的病毒复制和细胞病变效应。超微结构分析显示病毒复制，成熟的病毒体形成，以及感染的C20细胞中独特的细胞质和细胞核变化。CHIKV感染诱导C20细胞显著凋亡,伴随着线粒体膜去极化和细胞表面标志物如CD11c的表达改变，CD14和HLA-DR。值得注意的是,在CHIKV感染的C20细胞中观察到CD14表达降低。
■研究结果表明，CHIKV感染通过线粒体途径诱导C20小胶质细胞凋亡，细胞表面标记表达的显著改变，特别是与细胞凋亡诱导相关的CD14。这些观察结果为人类小胶质细胞在宿主对CHIKV感染的反应中的作用提供了有价值的见解，并有助于了解该病毒的神经发病机理。
