{"title":"病毒感染过程中泛素介导的自噬调节。","authors":"Joydeep Nag, Janvi Patel, 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":null,"pages":null},"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":"{\"title\":\"Ubiquitin-Mediated Regulation of Autophagy During Viral Infection.\",\"authors\":\"Joydeep Nag, Janvi Patel, 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\":null,\"pages\":null},\"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}","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}
Ubiquitin-Mediated Regulation of Autophagy During Viral Infection.
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.
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.