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Updated: May 9, 2026

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
The intermediate filament network protein, vimentin, is required for parvoviral infection
1Department of Zoology, University of British Columbia, 6270 University Boulevard, Vancouver, British Columbia, Canada V6T 1Z4.
Abstract:
Intermediate filaments (IFs) have recently been shown to serve novel roles during infection by many viruses. Here we have begun to study the role of IFs during the early steps of infection by the parvovirus minute virus of mice (MVM). We found that during early infection with MVM, after endosomal escape, the vimentin IF network was considerably altered, yielding collapsed immunofluorescence staining near the nuclear periphery. Furthermore, we found that vimentin plays an important role in the life cycle of MVM. The number of cells, which successfully replicated MVM, was reduced in infected cells in which the vimentin network was genetically or pharmacologically modified; viral endocytosis, however, remained unaltered. Perinuclear accumulation of MVM-containing vesicles was reduced in cells lacking vimentin. Our data suggests that vimentin is required for the MVM life cycle, presenting possibly a dual role: (1) following MVM escape from endosomes and (2) during endosomal trafficking of MVM.
Insights
Vimentin intermediate filaments are crucial for the minute virus of mice (MVM) life cycle. Disrupting vimentin hinders viral replication and intracellular trafficking after MVM escapes endosomes.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Intermediate filaments (IFs) are increasingly recognized for their roles in viral infections.
- The specific involvement of IFs in the early stages of parvovirus infection remains underexplored.
Purpose of the Study:
- To investigate the role of vimentin intermediate filaments in the early infection steps of the minute virus of mice (MVM).
Main Methods:
- Utilized immunofluorescence microscopy to observe vimentin network alterations post-MVM endosomal escape.
- Employed genetic and pharmacological methods to modify the vimentin network in infected cells.
- Assessed viral replication, endocytosis, and vesicle trafficking.
Main Results:
- MVM infection significantly altered the vimentin network, causing collapse near the nuclear periphery.
- Reduced MVM replication occurred in cells with modified vimentin, while endocytosis remained unaffected.
- Vimentin-deficient cells showed decreased perinuclear accumulation of MVM-containing vesicles.
Conclusions:
- Vimentin plays a critical role in the MVM life cycle, likely in two phases: post-endosomal escape and during endosomal trafficking.
- Vimentin is essential for efficient MVM replication and intracellular transport.
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