Microtubules in Polyomavirus Infection
Language English Country Switzerland Media electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
31963741
PubMed Central
PMC7019765
DOI
10.3390/v12010121
PII: v12010121
Knihovny.cz E-resources
- Keywords
- T antigens, VP1 capsid protein, cell cycle block, dynein, kinesin, microtubules, molecular motors, polyomavirus, virus, virus trafficking,
- MeSH
- Cell Nucleus virology MeSH
- Cytosol virology MeSH
- Endoplasmic Reticulum virology MeSH
- Endosomes virology MeSH
- Host-Pathogen Interactions * MeSH
- Humans MeSH
- Microtubules physiology virology MeSH
- Mice MeSH
- Polyomavirus genetics pathogenicity MeSH
- Virus Replication MeSH
- Protein Binding MeSH
- Capsid Proteins genetics metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Capsid Proteins MeSH
- VP1 protein, polyomavirus MeSH Browser
Microtubules, part of the cytoskeleton, are indispensable for intracellular movement, cell division, and maintaining cell shape and polarity. In addition, microtubules play an important role in viral infection. In this review, we summarize the role of the microtubules' network during polyomavirus infection. Polyomaviruses usurp microtubules and their motors to travel via early and late acidic endosomes to the endoplasmic reticulum. As shown for SV40, kinesin-1 and microtubules are engaged in the release of partially disassembled virus from the endoplasmic reticulum to the cytosol, and dynein apparently assists in the further disassembly of virions prior to their translocation to the cell nucleus-the place of their replication. Polyomavirus gene products affect the regulation of microtubule dynamics. Early T antigens destabilize microtubules and cause aberrant mitosis. The role of these activities in tumorigenesis has been documented. However, its importance for productive infection remains elusive. On the other hand, in the late phase of infection, the major capsid protein, VP1, of the mouse polyomavirus, counteracts T-antigen-induced destabilization. It physically binds microtubules and stabilizes them. The interaction results in the G2/M block of the cell cycle and prolonged S phase, which is apparently required for successful completion of the viral replication cycle.
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Mouse polyomavirus infection induces lamin reorganisation
The interactions between PML nuclear bodies and small and medium size DNA viruses
The Interplay between Viruses and Host DNA Sensors
Nuclear Cytoskeleton in Virus Infection