Viral interactions with intermediate filaments: Paths less explored

Sripada, Samatha

doi:10.2147/chc.s8782

Cited by 7 publications

(7 citation statements)

References 35 publications

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“…This model allowed us to biochemically pull down cellular surface molecules that the FPC particles directly interacted with, potentially including the still-elusive non-HSPG secondary entry receptor ( 20 ). One of the most promising candidate molecules that was precipitated together with FPC HPV16-PsVs was identified as vimentin, which, in addition to its function as a cytoskeletal filament protein, plays important roles in entry of, infection with, and/or replication of several viruses ( 39 ). Although vimentin is primarily expressed intracellularly, we and others observed surface expression on a subpopulation of cultured cells displaying a particular punctuate expression pattern ( 40 ).…”

Section: Discussionmentioning

confidence: 99%

“…Vimentin is a type III intermediate filament (IF) protein and the major IF of mesenchymal cells and cells adapted to tissue culture as well as transformed cell lines ( 38 ). Unlike microfilaments and microtubules, IFs are a chemically heterogeneous group of structural proteins ( 39 ). Besides its traditionally assigned functions in maintaining the mechanical and structural properties of cells, vimentin also acts as a key organizer in the context of intracellular dynamics and architecture, such as cell adhesion, cell migration, and cell signaling ( 40 ).…”

Section: Introductionmentioning

confidence: 99%

“…Besides its traditionally assigned functions in maintaining the mechanical and structural properties of cells, vimentin also acts as a key organizer in the context of intracellular dynamics and architecture, such as cell adhesion, cell migration, and cell signaling ( 40 ). Interestingly, several viruses exploit vimentin during different phases of their life cycle, ranging from viral entry to replication, virus assembly, and egress ( 39 ). As one of the major components of the cytoskeleton, vimentin is primarily located in the cytoplasm, especially around the plasma membrane.…”

Section: Introductionmentioning

confidence: 99%

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Vimentin Modulates Infectious Internalization of Human Papillomavirus 16 Pseudovirions

Schäfer

Graham

Lang

et al. 2017

J Virol

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Human papillomavirus (HPV) infection is the most common viral infection of the reproductive tract, with virtually all cases of cervical cancer being attributable to infection by oncogenic HPVs. However, the exact mechanism and receptors used by HPV to infect epithelial cells are controversial. The current entry model suggests that HPV initially attaches to heparan sulfate proteoglycans (HSPGs) at the cell surface, followed by conformational changes, cleavage by furin convertase, and subsequent transfer of the virus to an as-yet-unidentified high-affinity receptor. In line with this model, we established an in vitro infection system using the HSPG-deficient cell line pgsD677 together with HPV16 pseudovirions (HPV16-PsVs). While pgsD677 cells were nonpermissive for untreated HPV16-PsVs, furin cleavage of the particles led to a substantial increase in infection. Biochemical pulldown assays followed by mass spectrometry analysis showed that furin-precleaved HPV16-PsVs specifically interacted with surface-expressed vimentin on pgsD677 cells. We further demonstrated that both furin-precleaved and uncleaved HPV16-PsVs colocalized with surface-expressed vimentin on pgsD677, HeLa, HaCaT, and NIKS cells, while binding of incoming viral particles to soluble vimentin protein before infection led to a substantial decrease in viral uptake. Interestingly, decreasing cell surface vimentin by small interfering RNA (siRNA) knockdown in HeLa and NIKS cells significantly increased HPV16-PsV infectious internalization, while overexpression of vimentin had the opposite effect. The identification of vimentin as an HPV restriction factor enhances our understanding of the initial steps of HPV-host interaction and may lay the basis for the design of novel antiviral drugs preventing HPV internalization into epithelial cells.IMPORTANCE Despite HPV being a highly prevalent sexually transmitted virus causing significant disease burden worldwide, particularly cancer of the cervix, cell surface events preceding oncogenic HPV internalization are poorly understood. We herein describe the identification of surface-expressed vimentin as a novel molecule not previously implicated in the infectious internalization of HPV16. Contrary to our expectations, vimentin was found to act not as a receptor but rather as a restriction factor dampening the initial steps of HPV16 infection. These results importantly contribute to our current understanding of the molecular events during the infectious internalization of HPV16 and open a new direction in the development of alternative drugs to prevent HPV infection.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Vimentin Modulates Infectious Internalization of Human Papillomavirus 16 Pseudovirions

Schäfer

Graham

Lang

et al. 2017

J Virol

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“…Apart from MTs and actin, the intermediate filament network (IFN) also plays an important role during viral infections [ 109 ]. The IFN protein vimentin is required by the incoming MVM particles during the endocytic trafficking and after endosomal escape in order to reach the perinuclear area.…”

Section: Trafficking and Interactions In The Cytosolmentioning

confidence: 99%

Protoparvovirus Cell Entry

Ros

Bayat

Wolfisberg

et al. 2017

Viruses

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The Protoparvovirus (PtPV) genus of the Parvoviridae family of viruses includes important animal pathogens and reference molecular models for the entire family. Some virus members of the PtPV genus have arisen as promising tools to treat tumoral processes, as they exhibit marked oncotropism and oncolytic activities while being nonpathogenic for humans. The PtPVs invade and replicate within the nucleus making extensive use of the transport, transcription and replication machineries of the host cells. In order to reach the nucleus, PtPVs need to cross over several intracellular barriers and traffic through different cell compartments, which limit their infection efficiency. In this review we summarize molecular interactions, capsid structural transitions and hijacking of cellular processes, by which the PtPVs enter and deliver their single-stranded DNA genome into the host cell nucleus. Understanding mechanisms that govern the complex PtPV entry will be instrumental in developing approaches to boost their anticancer therapeutic potential and improving their safety profile.

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“…However, the proper function of cytoskeleton for TBEV is still not fully understood. In DENV-infected cells, vimentin reorganisation was seen where a cage of vimentin is formed, and it has been shown that vimentin is involved in the assembly of DENV 2 particles [ 9 , 16 ]. Acrylamide, which is able to ruin the organisation of vimentin intermediate filaments [ 63 ], caused a reduction of colocalisation of DENV 2 antigen in host cell cytoplasm [ 9 ].…”

Section: The Involvement Of Cytoskeleton In Flavivirus mentioning

confidence: 99%

Interaction betweenFlavivirusand Cytoskeleton during Virus Replication

Foo

Chee

2015

BioMed Research International

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Flaviviruses are potentially human pathogens that cause major epidemics worldwide. Flavivirus interacts with host cell factors to form a favourable virus replication site. Cell cytoskeletons have been observed to have close contact with flaviviruses, which expands the understanding of cytoskeleton functions during virus replication, although many detailed mechanisms are still unclear. The interactions between the virus and host cytoskeletons such as actin filaments, microtubules, and intermediate filaments have provided insight into molecular alterations during the virus infection, such as viral entry, in-cell transport, scaffold assembly, and egress. This review article focuses on the utilization of cytoskeleton by Flavivirus and the respective functions during virus replication.

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Viral interactions with intermediate filaments: Paths less explored

Cited by 7 publications

References 35 publications

Vimentin Modulates Infectious Internalization of Human Papillomavirus 16 Pseudovirions

Vimentin Modulates Infectious Internalization of Human Papillomavirus 16 Pseudovirions

Protoparvovirus Cell Entry

Interaction betweenFlavivirusand Cytoskeleton during Virus Replication

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