ArticleJournal of virology2008
Foot-and-mouth disease virus, but not bovine enterovirus, targets the host cell cytoskeleton via the nonstructural protein 3Cpro.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- Foot-and-mouth disease virus 3C protease as virulence determinant plays multiple roles in cleaving viral polyprotein and host factors.Virulence · 2026Review
- The whole genome sequencing offers insights into the susceptibility to the foot-and-mouth disease virus carrier state.Veterinary research · 2026Article
- Development and immunogenicity of adenoviral Fc-fused FMDV virus-like particle vaccine in swine.The veterinary quarterly · 2025Article
- RSV-induced expanded ciliated cells contribute to bronchial wall thickening.Virus research · 2023Article
- Mechanosensitive extrusion of Enterovirus A71-infected cells from colonic organoids.Nature microbiology · 2023Article
- ROCK1/MLC2 inhibition induces decay of viral mRNA in BPXV infected cells.Scientific reports · 2022Article
- Adherent and suspension baby hamster kidney cells have a different cytoskeleton and surface receptor repertoire.PloS one · 2021Article
- Cellular Vimentin Interacts with Foot-and-Mouth Disease Virus Nonstructural Protein 3A and Negatively Modulates Viral Replication.Journal of virology · 2020Article
- Production and Purification of High-Titer Newcastle Disease Virus for Use in Preclinical Mouse Models of Cancer.Molecular therapy. Methods & clinical development · 2018Article
- Microtubule Regulation and Function during Virus Infection.Journal of virology · 2017Review
- Role of human rhinovirus in triggering human airway epithelial-mesenchymal transition.Respiratory research · 2017Article
- Article
- Protease 3C of hepatitis A virus induces vacuolization of lysosomal/endosomal organelles and caspase-independent cell death.BMC cell biology · 2015Article
- Comparison of strategies for the production of FMDV empty capsids using the baculovirus vector system.Molecular biotechnology · 2014Article
- Article
- A role for endoplasmic reticulum exit sites in foot-and-mouth disease virus infection.The Journal of general virology · 2013Article
- Foot-and-mouth disease virus 3C protease induces fragmentation of the Golgi compartment and blocks intra-Golgi transport.Journal of virology · 2013Article
- Cell susceptibility to baculovirus transduction and echovirus infection is modified by protein kinase C phosphorylation and vimentin organization.Journal of virology · 2013Article
- Foot-and-mouth disease virus modulates cellular vimentin for virus survival.Journal of virology · 2013Article
- Foot-and-mouth disease virus nonstructural protein 2C interacts with Beclin1, modulating virus replication.Journal of virology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Foot-and-mouth disease virus (FMDV), a member of the Picornaviridae, is a pathogen of cloven-hoofed animals and causes a disease of major economic importance. Picornavirus-infected cells show changes in cell morphology and rearrangement of cytoplasmic membranes, which are a consequence of virus replication. We show here, by confocal immunofluorescence and electron microscopy, that the changes in morphology of FMDV-infected cells involve changes in the distribution of microtubule and intermediate filament components during infection. Despite the continued presence of centrosomes in infected cells, there is a loss of tethering of microtubules to the microtubule organizing center (MTOC) region. Loss of labeling for gamma-tubulin, but not pericentrin, from the MTOC suggests a targeting of gamma-tubulin (or associated proteins) rather than a total breakdown in MTOC structure. The identity of the FMDV protein(s) responsible was determined by the expression of individual viral nonstructural proteins and their precursors in uninfected cells. We report that the only viral nonstructural protein able to reproduce the loss of gamma-tubulin from the MTOC and the loss of integrity of the microtubule system is FMDV 3C(pro). In contrast, infection of cells with another picornavirus, bovine enterovirus, did not affect gamma-tubulin distribution, and the microtubule network remained relatively unaffected.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.