The TET3 inflammasome senses unique long HSV-1 proteins for virus particle budding from the nucleus.

IF 21.8 1区 医学 Q1 IMMUNOLOGY
Qiannv Liu, Weitao Li, Yan Qian, Chunlei Wang, Chun Kong, Mengqian Li, Liangliang Sun, Lang Sun, Yanli Pang, Changtao Jiang, Shuo Wang, Pengyan Xia
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引用次数: 0

Abstract

Inflammasomes play important roles in resisting infections caused by various pathogens. HSV-1 is a highly contagious virus among humans. The process by which HSV-1 particles bud from the nucleus is unique to herpes viruses, but the specific mechanism is still unclear. Here, we screened genes involved in HSV-1 replication. We found that TET3 plays an essential role in HSV-1 infection. TET3 recognizes the UL proteins of HSV-1 and, upon activation, can directly bind to caspase-1 to activate an ASC-independent inflammasome in the nucleus. The subsequent cleavage of GSDMD in the nucleus is crucial for the budding of HSV-1 particles from the nucleus. Inhibiting the perforation ability of GSDMD on the nuclear membrane can significantly reduce the maturation and spread of HSV-1. Our results may provide a new approach for the treatment of HSV-1 in the future.

TET3 炎症体感知独特的 HSV-1 长蛋白,以便病毒粒子从细胞核出芽。
炎症体在抵抗各种病原体感染方面发挥着重要作用。HSV-1 是一种在人类中具有高度传染性的病毒。HSV-1 颗粒从细胞核中萌发的过程是疱疹病毒所独有的,但具体机制尚不清楚。在这里,我们筛选了参与 HSV-1 复制的基因。我们发现 TET3 在 HSV-1 感染中扮演着重要角色。TET3能识别HSV-1的UL蛋白,激活后可直接与caspase-1结合,激活细胞核中不依赖于ASC的炎性体。随后,GSDMD 在细胞核中的裂解对 HSV-1 颗粒从细胞核中出芽至关重要。抑制 GSDMD 在核膜上的穿孔能力可以显著减少 HSV-1 的成熟和传播。我们的研究结果可能会为未来治疗HSV-1提供一种新方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
31.20
自引率
1.20%
发文量
903
审稿时长
1 months
期刊介绍: Cellular & Molecular Immunology, a monthly journal from the Chinese Society of Immunology and the University of Science and Technology of China, serves as a comprehensive platform covering both basic immunology research and clinical applications. The journal publishes a variety of article types, including Articles, Review Articles, Mini Reviews, and Short Communications, focusing on diverse aspects of cellular and molecular immunology.
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