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猴痘病毒感染的人永生化角质形成细胞的特征。

Characterization of Human Immortalized Keratinocyte Cells Infected by Monkeypox Virus.

机构信息

State Key Laboratory of Analytical Chemistry for Life Science & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing 210093, China.

Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, State Key Laboratory of Pathogen and Biosecurity, Key Laboratory of Jilin Province for Zoonosis Prevention and Control, Changchun 130118, China.

出版信息

Viruses. 2024 Jul 26;16(8):1206. doi: 10.3390/v16081206.

Abstract

Monkeypox virus (MPXV) can induce systemic skin lesions after infection. This research focused on studying MPXV proliferation and the response of keratinocytes. Using transmission electron microscopy (TEM), we visualized different stages of MPXV development in human immortalized keratinocytes (HaCaT). We identified exocytosis of enveloped viruses as the exit mechanism for MPXV in HaCaT cells. Infected keratinocytes showed submicroscopic changes, such as the formation of vesicle-like structures through the recombination of rough endoplasmic reticulum membranes and alterations in mitochondrial morphology. Transcriptome analysis revealed the suppressed genes related to interferon pathway activation and the reduced expression of antimicrobial peptides and chemokines, which may facilitate viral immune evasion. In addition, pathway enrichment analysis highlighted systemic lupus erythematosus pathway activation and the inhibition of the Toll-like receptor signaling and retinol metabolism pathways, providing insights into the mechanisms underlying MPXV-induced skin lesions. This study advances our understanding of MPXV's interaction with keratinocytes and the complex mechanisms leading to skin lesions.

摘要

猴痘病毒(MPXV)感染后可引起全身性皮肤损伤。本研究专注于研究 MPXV 的增殖和角质形成细胞的反应。我们使用透射电子显微镜(TEM)观察了人永生化角质形成细胞(HaCaT)中 MPXV 不同发育阶段。我们发现,出芽病毒的胞吐作用是 MPXV 从 HaCaT 细胞中释放的机制。受感染的角质形成细胞表现出亚微观变化,例如通过粗面内质网膜的重组形成囊泡样结构,以及线粒体形态的改变。转录组分析显示,与干扰素途径激活相关的基因受到抑制,抗菌肽和趋化因子的表达减少,这可能有助于病毒的免疫逃逸。此外,途径富集分析强调了系统性红斑狼疮途径的激活以及 Toll 样受体信号和视黄醇代谢途径的抑制,为理解 MPXV 诱导皮肤损伤的机制提供了线索。本研究增进了我们对 MPXV 与角质形成细胞相互作用以及导致皮肤损伤的复杂机制的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c91/11359611/42116175fc51/viruses-16-01206-g001.jpg

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