[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-461952-105":59,"doc-detail-461952-en":130},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":123,"head_meta":125,"extra_data":127,"updated_unix":129},105,"en","vimentin-dynamics-in-viral-infection-shield-or-sabotage","Vimentin Dynamics in Viral Infection - Shield or Sabotage?","","Vimentin is a type III intermediate filament protein that preserves cellular integrity, organelle positioning, and mechanical resilience, while also undergoing dynamic changes during viral infection. Viral invasion drives vimentin filament disassembly into soluble oligomers with hydrophobic and acidic interfaces that promote viral attachment and entry as co-receptors. After entry, virus-induced post-translational modifications reshape intracellular vimentin, enabling oligomer-to-cage-like reassembly that encloses viral replication complexes. Whether these cages enhance replication or reflect host defense remains unresolved.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/vimentin-dynamics-in-viral-infection-shield-or-sabotage/461952/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/vimentin-dynamics-in-viral-infection-shield-or-sabotage/461952.png","ImageObject",300,407,{"name":92,"@type":93},"Noah","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-30","2026-09-30",true,{"@type":102,"interactionType":103,"userInteractionCount":52},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"How does viral infection change vimentin structure during entry?","Question",{"text":112,"@type":113},"Viral infection causes vimentin filament disassembly into soluble oligomers. These oligomers are recruited to the cell surface and function as viral co-receptors that facilitate attachment and entry.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"What happens to intracellular vimentin after viral entry?",{"text":117,"@type":113},"After entry, viral proteins trigger post-translational modifications in intracellular vimentin. Vimentin is rearranged from oligomers into cage-like structures that encapsulate viral replication complexes.",{"name":119,"@type":110,"acceptedAnswer":120},"Do vimentin cage-like structures protect the virus or the host?",{"text":121,"@type":113},"The document states the outcome is open and context-dependent. These structures may promote replication by providing physical protection and spatial organization, or they may represent host-imposed defense that disrupts trafficking and enhances apoptosis.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},461952,1791432852,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":52,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145,"preview_page_count":4},8796095462418,"https://ap-avatar.wpscdn.com/avatar/80000253c1241d02b47?x-image-process=image/resize,m_fixed,w_180,h_180&k=1778826106357471780","Review  \nVimentin Dynamics in Viral Infection: Shield or Sabotage?  \nYing Ling 1,2, *, Xuanyi Ling 3 and Zaixin Liu 4,5, *  \nAcademic Editor: Luigi Rosa  \nReceived: 15 October 2025  \nRevised: 11 December 2025  \nAccepted: 12 December 2025  \nPublished: 30 December 2025  \nCopyright: © 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.  \n1 School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK  \n2 Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China  \n3 Academic Center for Exploratory Students, University of Connecticut, Storrs, CT 06269, USA; [ugi24002@uconn.edu](ugi24002@uconn.edu)  \n4 State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China  \n5 National Foot and Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China  \n* [Correspondence: yxl1887@student.bham.ac.uk](Correspondence: yxl1887@student.bham.ac.uk) (Y.L.); [zaixinliucaas@163.com](zaixinliucaas@163.com) (Z.L.)  \nAbstract  \nVimentin is a type III intermediate filament protein that maintains cellular integrity, organelle positioning, and resilience to mechanical stress, but it is increasingly recognized for its dynamic change in viral infection. Viral infection causes vimentin filament disassembly into soluble oligomers with hydrophobic and acidic interfaces conducive to viral binding. These oligomers are recruited to the cell surface, where they act as viral co-receptors, facilitating viral attachment and entry. Upon entry, the viral protein induces post-translational modifications in intracellular vimentin filaments undergoing rearrangement processes, including disassembly into oligomers and then reassembly into cage-like structures that encapsulate viral replication complexes. Whether these structures promote viral replication or represent a host-imposed defense remains open. Our findings highlight the pro-viral“shield” and anti-viral “sabotage” role, a context-dependent role of vimentin during viral infection. Importantly, we offer a perspective encompassing structural biology and molecular and cellular signaling insights into vimentin dynamics, an approach that has not been explored in the current literature. We further propose that targeting vimentin is an innovative strategy for anti-viral intervention.  \nKeywords: vimentin; virus; co-receptor; PTMs; vimentin cage; viral replication complexes  \n1. Introduction  \nIntermediate filaments (IFs) are a family of tissue-and context-specific cytoskeletal proteins [1–3] . Vimentin is a type III IF protein predominantly expressed in mesenchymal cells [4] . Structurally, vimentin comprises an intrinsically disordered N-terminal head domain, a central α-helical rod domain responsible for coiled-coil dimer formation, anda flexible C-terminal tail domain that contributes to filament assembly and interaction specificity [5] . These domains enable vimentin to assemble into dynamic hierarchically organized filament networks that sustain cellular plasticity, anchor organelles, and provide mechanical stability. Beyond its structural role, vimentin participates in a wide range of cellular processes through signaling pathways and gene regulatory networks, including wound healing, cellular remodeling, and tissue repair [6] . Vimentin is increasingly recognized as a central mediator of cell activation, with emerging roles in inflammation, apoptosis, and cellular signaling [7–9] . Vimentin exists in both extracellular and intracellular forms. Furthermore, extracellular vimentin can be divided into cell surface vimentin  \n(CSV), which remains anchored to the cell membrane, and secreted vimentin, which is released into the extracellular environment. CSV represents a dynamic form of","cbCaithqpZRTGdi7","https://ap.wps.com/l/cbCaithqpZRTGdi7","pdf",4520115,22,"English","# Introduction\n## Vimentin structure and forms\n## Post-translational modifications and filament remodeling\n## Vimentin cages and viral replication complexes\n## Pro-viral shield versus anti-viral sabotage roles","[{\"question\":\"How does viral infection change vimentin structure during entry?\",\"answer\":\"Viral infection causes vimentin filament disassembly into soluble oligomers. These oligomers are recruited to the cell surface and function as viral co-receptors that facilitate attachment and entry.\"},{\"question\":\"What happens to intracellular vimentin after viral entry?\",\"answer\":\"After entry, viral proteins trigger post-translational modifications in intracellular vimentin. Vimentin is rearranged from oligomers into cage-like structures that encapsulate viral replication complexes.\"},{\"question\":\"Do vimentin cage-like structures protect the virus or the host?\",\"answer\":\"The document states the outcome is open and context-dependent. These structures may promote replication by providing physical protection and spatial organization, or they may represent host-imposed defense that disrupts trafficking and enhances apoptosis.\"}]","Vimentin Dynamics in Viral Infection - Shield or Sabotage? | PDF",1790762860,55]