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先天性免疫对猴痘病毒感染的反应:机制与免疫逃避。

Innate Immune Response to Monkeypox Virus Infection: Mechanisms and Immune Escape.

机构信息

Department of Virology, Faculty of Medicine, Lorestan University of Medical Sciences, Khorramabad, Iran.

Department of Veterinary, Faculty of Veterinary Medicine, Lorestan University, Khorramabad, Iran.

出版信息

J Innate Immun. 2024;16(1):413-424. doi: 10.1159/000540815. Epub 2024 Aug 13.

DOI:10.1159/000540815
PMID:39137733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11521483/
Abstract

BACKGROUND

The reemergence of monkeypox virus (Mpox, formerly monkeypox) in 2022 in non-endemic countries has raised significant concerns for global health due to its high transmissibility and mortality rate. A major challenge in combating Mpox is its ability to evade the host's innate immune system, the first line of defense against viral infections.

SUMMARY

Mpox encodes various proteins that interfere with key antiviral pathways and mechanisms, such as the nuclear factor kappa B signaling, cytokine production, complement and inflammasome activation, and chemokine binding. These proteins modulate the expression and function of innate immune mediators, such as interferons, interleukins, and Toll-like receptors, and impair the recruitment and activation of innate immune cells, such as natural killer cells. By suppressing or altering these innate immune responses, Mpox enhances its replication and infection in the host tissues and organs, leading to systemic inflammation, tissue damage, and organ failure.

KEY MESSAGES

This study reveals new insights into the molecular and cellular interactions between Mpox and the host's innate immune system. It identifies potential targets and strategies for antiviral interventions, highlighting the importance of understanding these interactions to develop effective treatments and improve global health responses to Mpox outbreaks.

摘要

背景

2022 年,猴痘病毒(Mpox,以前称为猴痘)在非流行国家重新出现,由于其高传染性和高死亡率,引起了全球健康的重大关注。对抗 Mpox 的一个主要挑战是其逃避宿主固有免疫系统的能力,固有免疫系统是抵御病毒感染的第一道防线。

摘要

Mpox 编码多种蛋白,这些蛋白干扰关键的抗病毒途径和机制,如核因子 kappa B 信号转导、细胞因子产生、补体和炎性小体激活以及趋化因子结合。这些蛋白调节固有免疫介质的表达和功能,如干扰素、白细胞介素和 Toll 样受体,并损害固有免疫细胞的募集和激活,如自然杀伤细胞。通过抑制或改变这些固有免疫反应,Mpox 增强了其在宿主组织和器官中的复制和感染,导致全身炎症、组织损伤和器官衰竭。

要点

本研究揭示了 Mpox 与宿主固有免疫系统之间的分子和细胞相互作用的新见解。它确定了抗病毒干预的潜在靶点和策略,强调了了解这些相互作用对于开发有效治疗方法和改善全球对 Mpox 爆发的健康反应的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/042e/11521483/fa2d3c662ac3/jin-2024-0016-0001-540815_F03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/042e/11521483/88ea46d61a6e/jin-2024-0016-0001-540815_F01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/042e/11521483/942522678d11/jin-2024-0016-0001-540815_F02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/042e/11521483/fa2d3c662ac3/jin-2024-0016-0001-540815_F03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/042e/11521483/88ea46d61a6e/jin-2024-0016-0001-540815_F01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/042e/11521483/942522678d11/jin-2024-0016-0001-540815_F02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/042e/11521483/fa2d3c662ac3/jin-2024-0016-0001-540815_F03.jpg

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