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Updated: Sep 27, 2026

Measurement of BK-polyomavirus Non-Coding Control Region Driven Transcriptional Activity Via Flow Cytometry
Published on: July 13, 2019
Cell penetration and trafficking of polyomavirus
Joanna M Gilbert1, Ilya G Goldberg, Thomas L Benjamin
1Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Armenise-233, Boston, MA 02115, USA. jgilbert@hms.harvard.edu
Abstract:
The murine polyomavirus (Py) enters mouse fibroblasts and kidney epithelial cells via an endocytic pathway that is caveola-independent (as well as clathrin-independent). In contrast, uptake of simian virus 40 into the same cells is dependent on caveola. Following the initial uptake of Py, both microtubules and microfilaments play roles in trafficking of the virus to the nucleus. Colcemid, which disrupts microtubules, inhibits the ability of Py to reach the nucleus and replicate. Paclitaxel, which stabilizes microtubules and prevents microtubule turnover, has no effect, indicating that intact but not dynamic microtubules are required for Py infectivity. Compounds that disrupt actin filaments enhance Py uptake while stabilization of actin filaments impedes Py infection. Virus particles are seen in association with actin in cells treated with microfilament-disrupting or filament-stabilizing agents at levels comparable to those in untreated cells, suggesting that a dynamic state of the microfilament system is important for Py infectivity.
Insights
Murine polyomavirus (Py) uses a unique endocytic pathway, distinct from simian virus 40. Both intact microtubules and dynamic microfilaments are crucial for Py trafficking and infection in host cells.
Area of Science:
- Cell Biology
- Virology
- Molecular Biology
Background:
- Murine polyomavirus (Py) is a pathogen that infects mouse cells.
- Viral entry mechanisms and intracellular trafficking are critical for understanding infection.
- Caveolae, clathrin, microtubules, and microfilaments are key cellular components involved in endocytosis and transport.
Purpose of the Study:
- To elucidate the endocytic pathway utilized by murine polyomavirus (Py) for cellular entry.
- To investigate the roles of microtubules and microfilaments in the intracellular trafficking of Py to the nucleus.
- To determine the specific requirements for microtubule and microfilament dynamics in Py infectivity.
Main Methods:
- Utilized mouse fibroblasts and kidney epithelial cells for infection studies.
- Employed pharmacological agents (Colcemid, Paclitaxel) to disrupt or stabilize microtubules.
- Used compounds to disrupt or stabilize actin filaments (microfilaments).
- Observed viral association with cellular components using microscopy.
Main Results:
- Py entry is independent of caveolae and clathrin, unlike simian virus 40.
- Intact, but not dynamic, microtubules are necessary for Py nuclear transport and replication.
- Disruption of actin filaments enhances Py uptake, while stabilization impedes infection, highlighting the importance of microfilament dynamics.
Conclusions:
- Murine polyomavirus employs a distinct endocytic route compared to other polyomaviruses.
- Efficient Py infection relies on intact microtubules for transport and a dynamic microfilament system for entry and trafficking.
- Understanding these cellular interactions provides insights into viral pathogenesis and potential therapeutic targets.
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