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单纯疱疹病毒 2 型通过干扰素途径操纵自噬：病毒生存的一种策略。

HSV-2 Manipulates Autophagy through Interferon Pathway: A Strategy for Viral Survival.

机构信息

Division of Virology, ICMR-National Institute of Translational Virology and AIDS Research, Pune 411026, India.

出版信息

Viruses. 2024 Aug 29;16(9):1383. doi: 10.3390/v16091383.

DOI:10.3390/v16091383
PMID:39339859
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11437441/
Abstract

Autophagy, an evolutionarily conserved cellular process, influences the regulation of viral infections. While the existing understanding indicates that Herpes Simplex Virus type 2 (HSV-2) maintains a basal level of autophagy to support its viral yield, the precise pathways governing the induction of autophagy during HSV-2 infection remain unknown. Therefore, this study aims to explore the role of type I interferons (IFN-I) in modulating autophagy during HSV-2 infection and to decode the associated signaling pathways. Our findings revealed an interplay wherein IFN-I regulates the autophagic response during HSV-2 infection. Additionally, we investigated the cellular pathways modulated during this complex process. Exploring the intricate network of signaling events involved in autophagy induction during HSV-2 infection holds promising therapeutic implications. Identifying these pathways advances our understanding of host-virus interactions and holds the foundation for developing targeted therapeutic strategies against HSV-2. The insight gained from this study provides a platform for exploring potential therapeutic targets to restrict HSV-2 infections, addressing a crucial need in antiviral research.

摘要

自噬是一种进化上保守的细胞过程，影响病毒感染的调控。虽然现有研究表明单纯疱疹病毒 2 型 (HSV-2) 维持基础水平的自噬以支持其病毒产量，但在 HSV-2 感染期间诱导自噬的确切途径仍不清楚。因此，本研究旨在探讨 I 型干扰素 (IFN-I) 在调节 HSV-2 感染期间自噬中的作用，并解码相关的信号通路。我们的研究结果揭示了 IFN-I 在 HSV-2 感染期间调节自噬反应的相互作用。此外，我们还研究了在这个复杂过程中被调节的细胞途径。探索 HSV-2 感染期间诱导自噬的信号事件的复杂网络具有潜在的治疗意义。鉴定这些途径有助于我们理解宿主-病毒相互作用，并为开发针对 HSV-2 的靶向治疗策略奠定基础。本研究提供了一个探索限制 HSV-2 感染的潜在治疗靶点的平台，这是抗病毒研究的一个关键需求。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/b68dd456f5a5/viruses-16-01383-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/400688a2ec37/viruses-16-01383-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/66a61aace654/viruses-16-01383-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/39097b8c52f5/viruses-16-01383-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/30c890549e8c/viruses-16-01383-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/6be83c36c889/viruses-16-01383-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/d3da4bcf9254/viruses-16-01383-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/7b306d385679/viruses-16-01383-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/d35f695b1c8b/viruses-16-01383-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/b68dd456f5a5/viruses-16-01383-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/400688a2ec37/viruses-16-01383-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/66a61aace654/viruses-16-01383-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/39097b8c52f5/viruses-16-01383-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/30c890549e8c/viruses-16-01383-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/6be83c36c889/viruses-16-01383-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/d3da4bcf9254/viruses-16-01383-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/7b306d385679/viruses-16-01383-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/d35f695b1c8b/viruses-16-01383-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8e1/11437441/b68dd456f5a5/viruses-16-01383-g009.jpg

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The role of autophagy in viral infections.自噬在病毒感染中的作用。
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IRE1-mTOR-PERK Axis Coordinates Autophagy and ER Stress-Apoptosis Induced by P2X7-Mediated Ca Influx in Osteoarthritis.IRE1-雷帕霉素靶蛋白-蛋白激酶R（PKR）样内质网激酶轴协调骨关节炎中由P2X7介导的钙离子内流诱导的自噬和内质网应激-凋亡。
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