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Home / Equine Research Bank / Viruses / Cell Surface Vimentin Is an Attachment Factor That Facilitat...
Viruses2026; 18(1); 113; doi: 10.3390/v18010113

Cell Surface Vimentin Is an Attachment Factor That Facilitates Equine Arteritis Virus Infection In Vitro.

Abstract: Our laboratory identified the susceptible allelic variant of equine CXCL16 protein (EqCXCL16S) as an entry receptor for equine arteritis virus (EAV). However, EAV has a broad host cell tropism and infects cells that lack EqCXCL16S. Thus, we hypothesized that EAV interacts with other host cell protein(s) that facilitate EAV infection. A virus overlay protein-binding assay in combination with a Far-Western blot from EAV-susceptible equine pulmonary artery endothelial cells (EECs) and equine dermal fibroblasts (E. Derm) identified a 57 kDa protein, present in the membrane fraction of the protein lysate, as a possible EAV-binding protein. Subsequent LC-MS/MS analysis identified this 57 kDa protein as vimentin. Screening of different mammalian cell lines has shown that only cells expressing vimentin are susceptible to EAV infection. Pre-treatment of EECs with an anti-vimentin polyclonal antibody and Withaferin A partially inhibit EAV infection. Finally, the overexpression of equine vimentin (EqVim) in HEK-293 cells increases their susceptibility to EAV infection. Overall, our data strongly indicate that EAV binds to the host cell protein equine vimentin, which actively participates in EAV infection, potentially serving as an attachment factor. The data suggest that EAV interacts with various host cell proteins to achieve its diverse cell tropism.
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Publication Date: 2026-01-15 PubMed ID: 41600875PubMed Central: PMC12846471DOI: 10.3390/v18010113Google Scholar: Lookup
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  • Journal Article

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

Overview

  • This research identifies the host cell protein vimentin as a key factor that facilitates the infection of cells by equine arteritis virus (EAV), expanding understanding beyond the previously known receptor.

Background

  • Equine arteritis virus (EAV) is a virus that infects horses and has a broad range of susceptible host cell types (broad cell tropism).
  • Previous studies found that a specific variant of the equine CXCL16 protein (EqCXCL16S) acts as an entry receptor for EAV, allowing the virus to infect certain cells.
  • However, EAV can infect cells that do not express EqCXCL16S, suggesting there are additional cellular factors involved in viral entry or infection.

Research Hypothesis

  • The researchers hypothesized that other proteins on the host cell surface might interact with EAV to facilitate infection.
  • Identifying such proteins could explain the virus’s ability to infect a wide variety of cells beyond those expressing EqCXCL16S.

Methods

  • A virus overlay protein-binding assay combined with a Far-Western blot was used to detect proteins that bind to EAV on the surface of equine cells known to be susceptible to infection (equine pulmonary artery endothelial cells and equine dermal fibroblasts).
  • This approach identified a 57 kDa membrane-associated protein that could potentially bind EAV.
  • Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was then used to accurately identify this protein as vimentin.
  • Various mammalian cell lines were screened to determine the correlation between vimentin expression and susceptibility to EAV infection.
  • Experimental interventions included pre-treating cells with anti-vimentin antibodies and Withaferin A (a compound known to inhibit vimentin function) to assess their effects on infection rate.
  • Additionally, overexpression of equine vimentin (EqVim) in HEK-293 cells (a human cell line normally less susceptible to EAV) was performed to observe changes in susceptibility.

Key Findings

  • The 57 kDa protein that interacts with EAV was identified as vimentin, a type of intermediate filament protein commonly found inside cells but also present on the cell surface in some contexts.
  • Cells expressing vimentin were found to be permissive to EAV infection, whereas cells lacking vimentin were resistant.
  • Pre-treatment with anti-vimentin antibodies or Withaferin A partially blocked EAV infection, indicating that vimentin plays an active role in viral entry or attachment.
  • Overexpression of equine vimentin in HEK-293 cells increased their susceptibility to EAV, reinforcing the role of vimentin as an attachment factor facilitating infection.

Conclusions and Implications

  • The study reveals that equine vimentin on the cell surface can act as an attachment factor for EAV, helping the virus bind to host cells and facilitate infection.
  • This expands the understanding of how EAV infects a broad spectrum of cells, showing that the virus uses multiple host cell proteins beyond the previously identified receptor EqCXCL16S.
  • Targeting vimentin or its interaction with EAV could represent a potential therapeutic strategy to limit or prevent equine arteritis virus infection.
  • The findings suggest a complex mechanism where EAV exploits various host proteins to achieve its wide cell tropism, a strategy that might be shared by other viruses as well.

Cite This Article

APA
Thieulent CJ, Sarkar S, Carossino M, Bhowmik M, Zhu H, Balasuriya UBR. (2026). Cell Surface Vimentin Is an Attachment Factor That Facilitates Equine Arteritis Virus Infection In Vitro. Viruses, 18(1), 113. https://doi.org/10.3390/v18010113

Publication

Viruses
ISSN: 1999-4915
NlmUniqueID: 101509722
Country: Switzerland
Language: English
Volume: 18
Issue: 1
PII: 113

Researcher Affiliations

Thieulent, Côme J
  • Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA.
Sarkar, Sanjay
  • Infectious Disease Research, Southern Research, 2000 9th Avenue S, Birmingham, AL 35205, USA.
Carossino, Mariano
  • Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA.
  • Louisiana Animal Disease Diagnostic Laboratory, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA.
Bhowmik, Mouli
  • Department of Pediatrics, University of Alabama at Birmingham Heersink School of Medicine, Birmingham, LA 53233, USA.
Zhu, Haining
  • Department of Pharmacology and Toxicology, R Ken Coit College of Pharmacy, University of Arizona, Skaggs Pharmaceutical Sciences Center, 1703 E. Mabel Street, Tucson, AZ 85721, USA.
Balasuriya, Udeni B R
  • Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA.

MeSH Terms

  • Animals
  • Vimentin / metabolism
  • Vimentin / genetics
  • Horses
  • Equartevirus / physiology
  • Endothelial Cells / virology
  • Endothelial Cells / metabolism
  • Humans
  • HEK293 Cells
  • Arterivirus Infections / virology
  • Arterivirus Infections / veterinary
  • Arterivirus Infections / metabolism
  • Virus Attachment
  • Fibroblasts / virology
  • Receptors, Virus / metabolism
  • Virus Internalization
  • Horse Diseases / virology
  • Horse Diseases / metabolism
  • Cell Line

Grant Funding

  • IK6 BX006316 / BLRD VA
  • PG002150, PG002207, and PG008671 / Self-generated funds
  • AWD-47990-1 / NIH-USDA NIFA R01 Research Grant Program Dual Purpose with Dual Benefit: Research in Bi-omedicine and Agriculture Using Agriculturally Important Domestic Animal Species grant number 2019-67016-29102

Conflict of Interest Statement

The authors declare no conflicts of interest.

References

This article includes 70 references
  1. Kuhn J.H., Lauck M., Bailey A.L., Shchetinin A.M., Vishnevskaya T.V., Bào Y., Ng T.F.F., LeBreton M., Schneider B.S., Gillis A.. Reorganization and Expansion of the Nidoviral Family Arteriviridae. Arch. Virol. 2016;161:755–768.
    doi: 10.1007/s00705-015-2672-zpmc: PMC5573231pubmed: 26608064google scholar: lookup
  2. Brinton M.A., Gulyaeva A.A., Balasuriya U.B.R., Dunowska M., Faaberg K.S., Goldberg T., Leung F.C.C., Nauwynck H.J., Snijder E.J., Stadejek T.. ICTV Virus Taxonomy Profile: Arteriviridae 2021. J. Gen. Virol. 2021;102:001632.
    doi: 10.1099/jgv.0.001632pmc: PMC8513641pubmed: 34356005google scholar: lookup
  3. Bryans J.T., Crowe M.E., Doll E.R., McCollum W.H.. Isolation of a Filterable Agent Causing Arteritis of Horses and Abortion by Mares; Its Differentiation from the Equine Abortion (Influenza) Virus. Cornell Vet. 1957;47:3–41.
    pubmed: 13397177
  4. Doll E.R., Knappenberger R.E., Bryans J.T.. An Outbreak of Abortion Caused by the Equine Arteritis Virus. Cornell Vet. 1957;47:69–75.
    pubmed: 13397180
  5. Balasuriya U.B.R., Carossino M., Timoney P.J.. Equine Viral Arteritis: A Respiratory and Reproductive Disease of Significant Economic Importance to the Equine Industry. Equine Vet. Educ. 2018;30:497–512.
    doi: 10.1111/eve.12672google scholar: lookup
  6. Timoney P.J., McCollum W.H.. Equine Viral Arteritis. Vet. Clin. N. Am. Equine Pract. 1993;9:295–309.
    doi: 10.1016/S0749-0739(17)30397-8pmc: PMC7134676pubmed: 8395325google scholar: lookup
  7. Balasuriya U.B.R., Snijder E.J., Heidner H.W., Zhang J., Zevenhoven-Dobbe J.C., Boone J.D., McCollum W.H., Timoney P.J., MacLachlan N.J.. Development and Characterization of an Infectious cDNA Clone of the Virulent Bucyrus Strain of Equine Arteritis Virus. J. Gen. Virol. 2007;88:918–924.
    doi: 10.1099/vir.0.82415-0pubmed: 17325365google scholar: lookup
  8. Balasuriya U.B., Snijder E.J., van Dinten L.C., Heidner H.W., Wilson W.D., Hedges J.F., Hullinger P.J., MacLachlan N.J.. Equine Arteritis Virus Derived from an Infectious cDNA Clone Is Attenuated and Genetically Stable in Infected Stallions. Virology 1999;260:201–208.
    doi: 10.1006/viro.1999.9817pubmed: 10405372google scholar: lookup
  9. Balasuriya U.B.R., Go Y.Y., MacLachlan N.J.. Equine Arteritis Virus. Vet. Microbiol. 2013;167:93–122.
    doi: 10.1016/j.vetmic.2013.06.015pmc: PMC7126873pubmed: 23891306google scholar: lookup
  10. Balasuriya U.B.R.. Equine Viral Arteritis. Vet. Clin. N. Am. Equine Pract. 2014;30:543–560.
    doi: 10.1016/j.cveq.2014.08.011pubmed: 25441113google scholar: lookup
  11. Campos J.R., Breheny P., Araujo R.R., Troedsson M.H.T., Squires E.L., Timoney P.J., Balasuriya U.B.R.. Semen Quality of Stallions Challenged with the Kentucky 84 Strain of Equine Arteritis Virus. Theriogenology 2014;82:1068–1079.
    doi: 10.1016/j.theriogenology.2014.07.004pubmed: 25156969google scholar: lookup
  12. Vairo S., Vandekerckhove A., Steukers L., Glorieux S., Van den Broeck W., Nauwynck H.. Clinical and Virological Outcome of an Infection with the Belgian Equine Arteritis Virus Strain 08P178. Vet. Microbiol. 2012;157:333–344.
    doi: 10.1016/j.vetmic.2012.01.014pubmed: 22306037google scholar: lookup
  13. Carossino M., Loynachan A.T., Canisso I.F., Cook R.F., Campos J.R., Nam B., Go Y.Y., Squires E.L., Troedsson M.H.T., Swerczek T.. Equine Arteritis Virus Has Specific Tropism for Stromal Cells and CD8 + T and CD21 + B Lymphocytes but Not for Glandular Epithelium at the Primary Site of Persistent Infection in the Stallion Reproductive Tract. J. Virol. 2017;91:e00418-17.
    doi: 10.1128/JVI.00418-17pmc: PMC5469258pubmed: 28424285google scholar: lookup
  14. Cole J.R., Hall R.F., Gosser H.S., Hendricks J.B., Pursell A.R., Senne D.A., Pearson J.E., Gipson C.A.. Transmissibility and Abortogenic Effect of Equine Viral Arteritis in Mares. J. Am. Vet. Med. Assoc. 1986;187:769–771.
    doi: 10.2460/javma.1986.189.07.769pubmed: 3021696google scholar: lookup
  15. Vaala W.E., Hamir A.N., Dubovi E.J., Timoney P.J., Ruiz B.. Fatal, Congenitally Acquired Infection with Equine Arteritis Virus in a Neonatal Thoroughbred. Equine Vet. J. 1992;24:155–158.
    doi: 10.1111/j.2042-3306.1992.tb02803.xpubmed: 1316264google scholar: lookup
  16. Carossino M, Dini P, Kalbfleisch T.S, Loynachan A.T, Canisso I.F, Cook R.F, Timoney P.J, Balasuriya U.B.R. Equine Arteritis Virus Long-Term Persistence Is Orchestrated by CD8+ T Lymphocyte Transcription Factors, Inhibitory Receptors, and the CXCL16/CXCR6 Axis. PLoS Pathog 2019;15:e1007950.
    doi: 10.1371/journal.ppat.1007950pmc: PMC6692045pubmed: 31356622google scholar: lookup
  17. Carossino M, Wagner B, Loynachan A.T, Cook R.F, Canisso I.F, Chelvarajan L, Edwards C.L, Nam B, Timoney J.F, Timoney P.J. Equine Arteritis Virus Elicits a Mucosal Antibody Response in the Reproductive Tract of Persistently Infected Stallions. Clin Vaccine Immunol 2017;24:e00215-17.
    doi: 10.1128/CVI.00215-17pmc: PMC5629664pubmed: 28814389google scholar: lookup
  18. Go Y.Y, Zhang J, Timoney P.J, Cook R.F, Horohov D.W, Balasuriya U.B.R. Complex Interactions between the Major and Minor Envelope Proteins of Equine Arteritis Virus Determine Its Tropism for Equine CD3 + T Lymphocytes and CD14 + Monocytes. J Virol 2010;84:4898–4911.
    doi: 10.1128/JVI.02743-09pmc: PMC2863813pubmed: 20219931google scholar: lookup
  19. Go Y.Y, Bailey E, Cook D.G, Coleman S.J, MacLeod J.N, Chen K.-C, Timoney P.J, Balasuriya U.B.R. Genome-Wide Association Study among Four Horse Breeds Identifies a Common Haplotype Associated with In Vitro CD3+ T Cell Susceptibility/Resistance to Equine Arteritis Virus Infection. J Virol 2011;85:13174–13184.
    doi: 10.1128/JVI.06068-11pmc: PMC3233183pubmed: 21994447google scholar: lookup
  20. Go Y.Y, Bailey E, Timoney P.J, Shuck K.M, Balasuriya U.B.R. Evidence That In Vitro Susceptibility of CD3+ T Lymphocytes to Equine Arteritis Virus Infection Reflects Genetic Predisposition of Naturally Infected Stallions To Become Carriers of the Virus. J Virol 2012;86:12407–12410.
    doi: 10.1128/JVI.01698-12pmc: PMC3486460pubmed: 22933293google scholar: lookup
  21. Sarkar S, Chelvarajan L, Go Y.Y, Cook F, Artiushin S, Mondal S, Anderson K, Eberth J, Timoney P.J, Kalbfleisch T.S. Equine Arteritis Virus Uses Equine CXCL16 as an Entry Receptor. J Virol 2016;90:3366–3384.
    doi: 10.1128/JVI.02455-15pmc: PMC4794689pubmed: 26764004google scholar: lookup
  22. Sarkar S, Bailey E, Go Y.Y, Cook R.F, Kalbfleisch T, Eberth J, Chelvarajan R.L, Shuck K.M, Artiushin S, Timoney P.J. Allelic Variation in CXCL16 Determines CD3+ T Lymphocyte Susceptibility to Equine Arteritis Virus Infection and Establishment of Long-Term Carrier State in the Stallion. PLoS Genet 2016;12:e1006467.
    doi: 10.1371/journal.pgen.1006467pmc: PMC5145142pubmed: 27930647google scholar: lookup
  23. Doll E.R, Bryans J.T, Wilson J.C. Immunization against Equine Viral Arteritis Using Modified Live Virus Propagated in Cell Cultures of Rabbit Kidney. Cornell Vet 1968;48:497–524.
    pubmed: 4971878
  24. Radwan A.I, Burger D. The Complement-Requiring Neutralization of Equine Arteritis Virus by Late Antisera. Virology 1973;51:71–77.
    doi: 10.1016/0042-6822(73)90366-8pubmed: 4630828google scholar: lookup
  25. Konishi S, Akashi H, Sentsui H, Ogata M. Studies on Equine Viral Arteritis I. Characterization of the Virus and Trial Survey on Antibody with Vero Cell Cultures. Jap J Vet Sci 1975;37:259–267.
    doi: 10.1292/jvms1939.37.5_259pubmed: 172689google scholar: lookup
  26. Harry T.O, McCollum W.H. Stability of Viability and Immunizing Potency of Lyophilized, Modified Equine Arteritis Live-Virus Vaccine. Am J Vet Res 1981;42:1501–1505.
    doi: 10.2460/ajvr.1981.42.09.1501pubmed: 6275755google scholar: lookup
  27. Van Berlo M.F, Horzinek M.C, Van der Zeijst B.A.M. Equine Arteritis Virus-Infected Cells Contain Six Polyadenylated Virus-Specific RNAs. Virology 1982;118:345–352.
    doi: 10.1016/0042-6822(82)90354-3pmc: PMC7130458pubmed: 6283728google scholar: lookup
  28. Zhang J, Timoney P.J, MacLachlan N.J, McCollum W.H, Balasuriya U.B.R. Persistent Equine Arteritis Virus Infection in HeLa Cells. J Virol 2008;82:8456–8464.
    doi: 10.1128/JVI.01249-08pmc: PMC2519626pubmed: 18579588google scholar: lookup
  29. Lu Z, Zhang J, Huang C.M, Go Y.Y, Faaberg K.S, Rowland R.R.R, Timoney P.J, Balasuriya U.B.R. Chimeric Viruses Containing the N-Terminal Ectodomains of GP5 and M Proteins of Porcine Reproductive and Respiratory Syndrome Virus Do Not Change the Cellular Tropism of Equine Arteritis Virus. Virology 2012;432:99–109.
    doi: 10.1016/j.virol.2012.05.022pubmed: 22739441google scholar: lookup
  30. Metz G, Abeyá M, Serena M, Panei C, Echeverría M. Evaluation of Apoptosis Markers in Different Cell Lines Infected with Equine Arteritis Virus. Biotech Histochem 2019;94:115–125.
    doi: 10.1080/10520295.2018.1521989pubmed: 30350720google scholar: lookup
  31. Maloney S.M, Shaw T.M, Nennig K.M, Larsen M.S, Shah A, Kumar A, Marcotrigiano J, Grove J, Snijder E.J, Kirchdoerfer R.N. CD81 Is a Receptor for Equine Arteritis Virus (Family: Arteriviridae). mBio 2025;16:e0062325.
    doi: 10.1128/mbio.00623-25pmc: PMC12239600pubmed: 40422661google scholar: lookup
  32. Asagoe T, Inaba Y, Jusa E.R, Kouno M, Uwatoko K, Fukunaga Y. Effect of Heparin on Infection of Cells by Equine Arteritis Virus. J Vet Med Sci 1997;59:727–728.
    doi: 10.1292/jvms.59.727pubmed: 9300374google scholar: lookup
  33. Lu Z, Sarkar S, Zhang J, Balasuriya U.B.R. Conserved Arginine Residues in the Carboxyl Terminus of the Equine Arteritis Virus E Protein May Play a Role in Heparin Binding but May Not Affect Viral Infectivity in Equine Endothelial Cells. Arch Virol 2016;161:873–886.
    doi: 10.1007/s00705-015-2733-3pubmed: 26739582google scholar: lookup
  34. Hedges J.F, Demaula C.D, Moore B.D, Mclaughlin B.E, Simon S.I, Maclachlan N.J. Characterization of Equine E-Selectin. Immunology 2001;103:498–504.
    doi: 10.1046/j.1365-2567.2001.01262.xpmc: PMC1783268pubmed: 11529941google scholar: lookup
  35. Moore B.D, Balasuriya U.B.R, Hedges J.F, MacLachlan N.J. Growth Characteristics of a Highly Virulent, a Moderately Virulent, and an Avirulent Strain of Equine Arteritis Virus in Primary Equine Endothelial Cells Are Predictive of Their Virulence to Horses. Virology 2002;298:39–44.
    doi: 10.1006/viro.2002.1466pubmed: 12093171google scholar: lookup
  36. Go Y.Y, Li Y, Chen Z, Han M, Yoo D, Fang Y, Balasuriya U.B.R. Equine Arteritis Virus Does Not Induce Interferon Production in Equine Endothelial Cells: Identification of Nonstructural Protein 1 as a Main Interferon Antagonist. BioMed Res Int 2014;2014:420658.
    doi: 10.1155/2014/420658pmc: PMC4055586pubmed: 24967365google scholar: lookup
  37. Mondal S.P, Cook R.F, Chelvarajan R.L, Henney P.J, Timoney P.J, Balasuriya U.B.R. Development and Characterization of a Synthetic Infectious cDNA Clone of the Virulent Bucyrus Strain of Equine Arteritis Virus Expressing mCherry (Red Fluorescent Protein). Arch Virol 2016;161:821–832.
    doi: 10.1007/s00705-015-2633-6pubmed: 26711457google scholar: lookup
  38. Wagner H.M, Balasuriya U.B.R, James MacLachlan N. The Serologic Response of Horses to Equine Arteritis Virus as Determined by Competitive Enzyme-Linked Immunosorbent Assays (c-ELISAs) to Structural and Non-Structural Viral Proteins. Comp Immunol Microbiol Infect Dis 2003;26:251–260.
    doi: 10.1016/S0147-9571(02)00054-1pubmed: 12676125google scholar: lookup
  39. Balasuriya U.B, Rossitto P.V, DeMaula C.D, MacLachlan N.J. A 29K Envelope Glycoprotein of Equine Arteritis Virus Expresses Neutralization Determinants Recognized by Murine Monoclonal Antibodies. J Gen Virol 1993;74:2525–2529.
    doi: 10.1099/0022-1317-74-11-2525pubmed: 7504076google scholar: lookup
  40. Yang L, Gal J, Chen J, Zhu H. Self-Assembled FUS Binds Active Chromatin and Regulates Gene Transcription. Proc Natl Acad Sci USA 2014;111:17809–17814.
    doi: 10.1073/pnas.1414004111pmc: PMC4273402pubmed: 25453086google scholar: lookup
  41. Thieulent C, Hue E.S, Sutton G, Fortier C, Dallemagne P, Zientara S, Munier-Lehmann H, Hans A, Paillot R, Vidalain P.-O. Identification of Antiviral Compounds against Equid Herpesvirus-1 Using Real-Time Cell Assay Screening: Efficacy of Decitabine and Valganciclovir Alone or in Combination. Antivir Res 2020;183:104931.
    doi: 10.1016/j.antiviral.2020.104931pubmed: 32926887google scholar: lookup
  42. Sarkar S, Balasuriya U.B.R, Horohov D.W, Chambers T.M. The Neuropathogenic T953 Strain of Equine Herpesvirus-1 Inhibits Type-I IFN Mediated Antiviral Activity in Equine Endothelial Cells. Vet Microbiol 2016;183:110–118.
    doi: 10.1016/j.vetmic.2015.12.011pubmed: 26790943google scholar: lookup
  43. Thieulent C.J, Carossino M, Balasuriya U.B.R, Graves K, Bailey E, Eberth J, Canisso I.F, Andrews F.M, Keowen M.L, Go Y.Y. Development of a TaqMan® Allelic Discrimination qPCR Assay for Rapid Detection of Equine CXCL16 Allelic Variants Associated with the Establishment of Long-Term Equine Arteritis Virus Carrier State in Stallions. Front Genet 2022;13:871875.
    doi: 10.3389/fgene.2022.871875pmc: PMC9043104pubmed: 35495124google scholar: lookup
  44. Perkins D.N, Pappin D.J.C, Creasy D.M, Cottrell J.S. Probability-Based Protein Identification by Searching Sequence Databases Using Mass Spectrometry Data. Electrophoresis 1999;20:3551–3567.
    doi: 10.1002/(SICI)1522-2683(19991201)20:18<3551::AID-ELPS3551>3.0.CO;2-2pubmed: 10612281google scholar: lookup
  45. Bargagna-Mohan P, Hamza A, Kim Y, Khuan (Abby) Ho Y, Mor-Vaknin N, Wendschlag N, Liu J, Evans R.M, Markovitz D.M, Zhan C.-G. The Tumor Inhibitor and Antiangiogenic Agent Withaferin A Targets the Intermediate Filament Protein Vimentin. Chem Biol 2007;14:623–634.
    doi: 10.1016/j.chembiol.2007.04.010pmc: PMC3228641pubmed: 17584610google scholar: lookup
  46. Shaw T.M, Huey D, Mousa-Makky M, Compaleo J, Nennig K, Shah A.P, Jiang F, Qiu X, Klipsic D, Rowland R.R.R. The Neonatal Fc Receptor (FcRn) Is a Pan-Arterivirus Receptor. Nat Commun 2024;15:6726.
    doi: 10.1038/s41467-024-51142-xpmc: PMC11306234pubmed: 39112502google scholar: lookup
  47. Dutour-Provenzano G, Etienne-Manneville S. Intermediate Filaments. Curr Biol 2021;31:R522–R529.
    doi: 10.1016/j.cub.2021.04.011pubmed: 34033784google scholar: lookup
  48. Arrindell J, Desnues B. Vimentin: From a Cytoskeletal Protein to a Critical Modulator of Immune Response and a Target for Infection. Front Immunol 2023;14:1224352.
    doi: 10.3389/fimmu.2023.1224352pmc: PMC10354447pubmed: 37475865google scholar: lookup
  49. Ramos I, Stamatakis K, Oeste C.L, Pérez-Sala D. Vimentin as a Multifaceted Player and Potential Therapeutic Target in Viral Infections. Int J Mol Sci 2020;21:4675.
    doi: 10.3390/ijms21134675pmc: PMC7370124pubmed: 32630064google scholar: lookup
  50. Mor-Vaknin N, Punturieri A, Sitwala K, Markovitz D.M. Vimentin Is Secreted by Activated Macrophages. Nat Cell Biol 2003;5:59–63.
    doi: 10.1038/ncb898pubmed: 12483219google scholar: lookup
  51. Päll T, Pink A, Kasak L, Turkina M, Anderson W, Valkna A, Kogerman P. Soluble CD44 Interacts with Intermediate Filament Protein Vimentin on Endothelial Cell Surface. PLoS ONE 2011;6:e29305.
    doi: 10.1371/journal.pone.0029305pmc: PMC3244446pubmed: 22216242google scholar: lookup
  52. Kim J.-K, Fahad A.-M, Shanmukhappa K, Kapil S. Defining the Cellular Target(s) of Porcine Reproductive and Respiratory Syndrome Virus Blocking Monoclonal Antibody 7G10. J Virol 2006;80:689–696.
    doi: 10.1128/JVI.80.2.689-696.2006pmc: PMC1346842pubmed: 16378972google scholar: lookup
  53. Yu Y.T.-C, Chien S.-C, Chen I.-Y, Lai C.-T, Tsay Y.-G, Chang S.C, Chang M.-F. Surface Vimentin Is Critical for the Cell Entry of SARS-CoV. J Biomed Sci 2016;23:14.
    doi: 10.1186/s12929-016-0234-7pmc: PMC4724099pubmed: 26801988google scholar: lookup
  54. Amraei R, Xia C, Olejnik J, White M.R, Napoleon M.A, Lotfollahzadeh S, Hauser B.M, Schmidt A.G, Chitalia V, Mühlberger E. Extracellular Vimentin Is an Attachment Factor That Facilitates SARS-CoV-2 Entry into Human Endothelial Cells. Proc Natl Acad Sci USA 2022;119:e2113874119.
    doi: 10.1073/pnas.2113874119pmc: PMC8833221pubmed: 35078919google scholar: lookup
  55. Lalioti V, González-Sanz S, Lois-Bermejo I, González-Jiménez P, Viedma-Poyatos Á, Merino A, Pajares M.A, Pérez-Sala D. Cell Surface Detection of Vimentin, ACE2 and SARS-CoV-2 Spike Proteins Reveals Selective Colocalization at Primary Cilia. Sci Rep 2022;12:7063.
    doi: 10.1038/s41598-022-11248-ypmc: PMC9052736pubmed: 35487944google scholar: lookup
  56. Zhang Y, Zhao S, Li Y, Feng F, Li M, Xue Y, Cui J, Xu T, Jin X, Jiu Y. Host Cytoskeletal Vimentin Serves as a Structural Organizer and an RNA-Binding Protein Regulator to Facilitate Zika Viral Replication. Proc Natl Acad Sci USA 2022;119:e2113909119.
    doi: 10.1073/pnas.2113909119pmc: PMC8872754pubmed: 35193960google scholar: lookup
  57. Yang J, Zou L, Yang Y, Yuan J, Hu Z, Liu H, Peng H, Shang W, Zhang X, Zhu J. Superficial Vimentin Mediates DENV-2 Infection of Vascular Endothelial Cells. Sci Rep 2016;6:38372.
    doi: 10.1038/srep38372pmc: PMC5133558pubmed: 27910934google scholar: lookup
  58. Schäfer G, Graham L.M, Lang D.M, Blumenthal M.J, Bergant Marušič M, Katz A.A. Vimentin Modulates Infectious Internalization of Human Papillomavirus 16 Pseudovirions. J Virol 2017;91:e00307-17.
    doi: 10.1128/JVI.00307-17pmc: PMC5533935pubmed: 28566373google scholar: lookup
  59. Das S, Ravi V, Desai A. Japanese Encephalitis Virus Interacts with Vimentin to Facilitate Its Entry into Porcine Kidney Cell Line. Virus Res 2011;160:404–408.
    doi: 10.1016/j.virusres.2011.06.001pubmed: 21798293google scholar: lookup
  60. Liang J.-J, Yu C.-Y, Liao C.-L, Lin Y.-L. Vimentin Binding Is Critical for Infection by the Virulent Strain of Japanese Encephalitis Virus: Virulent JEV Binds Vimentin for Infection. Cell Microbiol 2011;13:1358–1370.
    doi: 10.1111/j.1462-5822.2011.01624.xpubmed: 21707907google scholar: lookup
  61. Du N, Cong H, Tian H, Zhang H, Zhang W, Song L, Tien P. Cell Surface Vimentin Is an Attachment Receptor for Enterovirus 71. J Virol 2014;88:5816–5833.
    doi: 10.1128/JVI.03826-13pmc: PMC4019121pubmed: 24623428google scholar: lookup
  62. Song T, Fang L, Wang D, Zhang R, Zeng S, An K, Chen H, Xiao S. Quantitative Interactome Reveals That Porcine Reproductive and Respiratory Syndrome Virus Nonstructural Protein 2 Forms a Complex with Viral Nucleocapsid Protein and Cellular Vimentin. J Proteom 2016;142:70–81.
    doi: 10.1016/j.jprot.2016.05.009pubmed: 27180283google scholar: lookup
  63. Liang Z, Li P, Wang C, Singh D, Zhang X. Visualizing the Transport of Porcine Reproductive and Respiratory Syndrome Virus in Live Cells by Quantum Dots-Based Single Virus Tracking. Virol Sin 2020;35:407–416.
    doi: 10.1007/s12250-019-00187-0pmc: PMC7462959pubmed: 31872331google scholar: lookup
  64. Zheng X, Li R, Qiao S, Chen X, Zhang L, Lu Q, Xing G, Zhou E, Zhang G. Vimentin Rearrangement by Phosphorylation Is Beneficial for Porcine Reproductive and Respiratory Syndrome Virus Replication In Vitro. Vet Microbiol 2021;259:109133.
    doi: 10.1016/j.vetmic.2021.109133pubmed: 34087674google scholar: lookup
  65. Tanaka S, Kobayashi W, Haraguchi M, Ishihata K, Nakamura N, Ozawa M. Snail1 Expression in Human Colon Cancer DLD-1 Cells Confers Invasive Properties without N-Cadherin Expression. Biochem Biophys Rep 2016;8:120–126.
    doi: 10.1016/j.bbrep.2016.08.017pmc: PMC5613769pubmed: 28955947google scholar: lookup
  66. Liu C.-Y., Lin H.-H., Tang M.-J., Wang Y.-K.. Vimentin Contributes to Epithelial-Mesenchymal Transition Cancer Cell Mechanics by Mediating Cytoskeletal Organization and Focal Adhesion Maturation.. Oncotarget 2015;6:15966–15983.
    doi: 10.18632/oncotarget.3862pmc: PMC4599250pubmed: 25965826google scholar: lookup
  67. Inada M., Izawa G., Kobayashi W., Ozawa M.. 293 Cells Express Both Epithelial as Well as Mesenchymal Cell Adhesion Molecules.. Int. J. Mol. Med. 2016;37:1521–1527.
    doi: 10.3892/ijmm.2016.2568pmc: PMC4866952pubmed: 27121032google scholar: lookup
  68. Grin B., Mahammad S., Wedig T., Cleland M.M., Tsai L., Herrmann H., Goldman R.D.. Withaferin A Alters Intermediate Filament Organization, Cell Shape and Behavior.. PLoS ONE 2012;7:e39065.
    doi: 10.1371/journal.pone.0039065pmc: PMC3376126pubmed: 22720028google scholar: lookup
  69. Sharma K.B., Subramani C., Ganesh K., Sharma A., Basu B., Balyan S., Sharma G., Ka S., Deb A., Srivastava M.. Withaferin A Inhibits Chikungunya Virus nsP2 Protease and Shows Antiviral Activity in the Cell Culture and Mouse Model of Virus Infection.. PLoS Pathog. 2024;20:e1012816.
    doi: 10.1371/journal.ppat.1012816pmc: PMC11723598pubmed: 39775571google scholar: lookup
  70. Arrindell J., Abou Atmeh P., Jayet L., Sereme Y., Mege J.-L., Desnues B.. Vimentin Is an Important ACE2 Co-Receptor for SARS-CoV-2 in Epithelial Cells.. iScience 2022;25:105463.
    doi: 10.1016/j.isci.2022.105463pmc: PMC9618295pubmed: 36338433google scholar: lookup

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