Ubiquitin-Mediated Regulation of Autophagy During Viral Infection.

IF 3.1 Q2 MICROBIOLOGY Current Clinical Microbiology Reports Pub Date : 2023-01-01 DOI:10.1007/s40588-022-00186-y
Joydeep Nag, Janvi Patel, Shashank Tripathi
{"title":"Ubiquitin-Mediated Regulation of Autophagy During Viral Infection.","authors":"Joydeep Nag,&nbsp;Janvi Patel,&nbsp;Shashank Tripathi","doi":"10.1007/s40588-022-00186-y","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose of review: </strong>Virus infections skew the host autophagic response to meet their replication and transmission demands by tapping into the critical host regulatory mechanisms that control the autophagic flux. This review is a compendium of previous reports highlighting the mechanisms that viruses adapt to hijack the host ubiquitination machinery to repurpose autophagy for their sustenance.</p><p><strong>Recent findings: </strong>Emerging evidence suggests a critical role of host ubiquitin machinery in the manifestation of the antiviral or proviral functions of autophagy. Lately, more emphasis has been laid to identify specific host E3 ubiquitin ligases, their targets (viral or host), and characterizing corresponding ubiquitin linkages by biochemical or genome-wide genetic screening approaches.</p><p><strong>Summary: </strong>Here, we highlight how viruses ingeniously engage and subvert the host ubiquitin-autophagy system to promote virus replication and antagonize intracellular innate immune responses.</p>","PeriodicalId":45506,"journal":{"name":"Current Clinical Microbiology Reports","volume":"10 1","pages":"1-8"},"PeriodicalIF":3.1000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9839220/pdf/","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Clinical Microbiology Reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s40588-022-00186-y","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
引用次数: 1

Abstract

Purpose of review: Virus infections skew the host autophagic response to meet their replication and transmission demands by tapping into the critical host regulatory mechanisms that control the autophagic flux. This review is a compendium of previous reports highlighting the mechanisms that viruses adapt to hijack the host ubiquitination machinery to repurpose autophagy for their sustenance.

Recent findings: Emerging evidence suggests a critical role of host ubiquitin machinery in the manifestation of the antiviral or proviral functions of autophagy. Lately, more emphasis has been laid to identify specific host E3 ubiquitin ligases, their targets (viral or host), and characterizing corresponding ubiquitin linkages by biochemical or genome-wide genetic screening approaches.

Summary: Here, we highlight how viruses ingeniously engage and subvert the host ubiquitin-autophagy system to promote virus replication and antagonize intracellular innate immune responses.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
病毒感染过程中泛素介导的自噬调节。
综述目的:病毒感染通过利用宿主控制自噬通量的关键调控机制来扭曲宿主的自噬反应,以满足其复制和传播的需要。这篇综述概述了以往的报道,强调了病毒适应劫持宿主泛素化机制以重新利用自噬来维持自身的机制。最新发现:新出现的证据表明宿主泛素机制在自噬的抗病毒或前病毒功能的表现中起关键作用。最近,更多的重点放在鉴定特异性宿主E3泛素连接酶及其靶点(病毒或宿主),并通过生化或全基因组遗传筛选方法表征相应的泛素连接。摘要:在这里,我们强调病毒如何巧妙地参与和破坏宿主泛素自噬系统,以促进病毒复制和对抗细胞内先天免疫反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
7.50
自引率
1.90%
发文量
9
期刊介绍: Current Clinical Microbiology Reports commissions expert reviews from leading scientists at the forefront of research in microbiology. The journal covers this broad field by dividing it into four key main areas of study: virology, bacteriology, parasitology, and mycology. Within each of the four sections, experts from around the world address important aspects of clinical microbiology such as immunology, diagnostics, therapeutics, antibiotics and antibiotic resistance, and vaccines. Some of the world’s foremost authorities in the field of microbiology serve as section editors and editorial board members. Section editors select topics for which leading researchers are invited to contribute comprehensive review articles that emphasize new developments and recently published papers of major importance, which are highlighted in annotated reference lists. These timely reviews of the literature examine the latest scientific discoveries and controversies as they emerge and are indispensable to both researchers and clinicians. The editorial board, composed of more than 20 internationally diverse members, reviews the annual table of contents, ensures that topics address all aspects of emerging research, and where applicable suggests topics of critical importance to various countries/regions.
期刊最新文献
SARS-CoV-2 Resistance to Small Molecule Inhibitors. Integrating Genomic Data with the Development of CRISPR-Based Point-of-Care-Testing for Bacterial Infections. Intimate Relationship Between Stress and Human Alpha‑Herpes Virus 1 (HSV‑1) Reactivation from Latency. Bacterial and Fungal Keratitis: Current Trends in Its Diagnosis and Management Engineered Therapeutic Antibody Against SARS-CoV-2
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1