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通过先天免疫途径控制 的登革病毒传播的 - 介导机制的综合评述。

A comprehensive review of -mediated mechanisms to control dengue virus transmission in through innate immune pathways.

机构信息

Department of Zoology, Faculty of Life Sciences, University of Okara, Okara, Pakistan.

出版信息

Front Immunol. 2024 Aug 8;15:1434003. doi: 10.3389/fimmu.2024.1434003. eCollection 2024.

DOI:10.3389/fimmu.2024.1434003
PMID:39176079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11338905/
Abstract

The Dengue virus (DENV), primarily spread by and also by in some regions, poses significant global health risks. Alternative techniques are urgently needed because the current control mechanisms are insufficient to reduce the transmission of DENV. Introducing into inhibits DENV transmission, however, the underlying mechanisms are still poorly understood. Innate immune effector upregulation, the regulation of autophagy, and intracellular competition between and DENV for lipids are among the theories for the mechanism of inhibition. Furthermore, mainly three immune pathways Toll, IMD, and JAK/STAT are involved in the host for the suppression of the virus. These pathways are activated by and DENV in the host and are responsible for the upregulation and downregulation of many genes in mosquitoes, which ultimately reduces the titer of the DENV in the host. The functioning of these immune pathways depends upon the , host, and virus interaction. Here, we summarize the current understanding of DENV recognition by the 's immune system, aiming to create a comprehensive picture of our knowledge. Additionally, we investigated how regulates the activation of multiple genes associated with immune priming for the reduction of DENV.

摘要

登革病毒(DENV)主要通过 和 在某些地区也通过 传播,对全球健康构成重大威胁。由于目前的控制机制不足以减少 DENV 的传播,因此迫切需要替代技术。将 引入 可抑制 DENV 的传播,但抑制机制仍知之甚少。先天免疫效应物的上调、自噬的调节以及 和 DENV 之间对脂质的细胞内竞争是抑制机制的理论之一。此外,主要有三条免疫途径 Toll、IMD 和 JAK/STAT 参与宿主对病毒的抑制。这些途径在宿主中被 和 DENV 激活,并负责蚊子中许多基因的上调和下调,最终降低宿主中 DENV 的滴度。这些免疫途径的功能取决于 的、宿主和病毒的相互作用。在这里,我们总结了 DENV 被 免疫系统识别的最新认识,旨在全面了解我们的知识。此外,我们还研究了 如何调节与免疫启动相关的多个基因的激活,以减少 DENV。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9ac/11338905/bd4fd973a3e6/fimmu-15-1434003-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9ac/11338905/3efacfabc169/fimmu-15-1434003-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9ac/11338905/cdc1f3981876/fimmu-15-1434003-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9ac/11338905/7a24c5040e1b/fimmu-15-1434003-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9ac/11338905/bd4fd973a3e6/fimmu-15-1434003-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9ac/11338905/3efacfabc169/fimmu-15-1434003-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9ac/11338905/cdc1f3981876/fimmu-15-1434003-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9ac/11338905/7a24c5040e1b/fimmu-15-1434003-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9ac/11338905/bd4fd973a3e6/fimmu-15-1434003-g004.jpg

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