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Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
Published on: August 24, 2015
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Echovirus 1 internalization negatively regulates epidermal growth factor receptor downregulation
Moona Huttunen1, Paula Turkki1, Anita Mäki1
1Department of Biological and Environmental Science/NanoScience Center, University of Jyväskylä, Jyväskylä, Finland.
Cellular Microbiology
|September 26, 2016
Summary
Echovirus 1 (EV1) infection inhibits epidermal growth factor receptor (EGFR) downregulation, promoting viral spread. This specific interference with EGFR trafficking benefits EV1 infection and enhances cell viability.
Area of Science:
- Cell Biology
- Virology
- Molecular Biology
Background:
- Echovirus 1 (EV1) utilizes a distinct internalization pathway separate from the epidermal growth factor receptor (EGFR) pathway.
- EV1 and EGFR pathways exhibit close proximity but different degradation kinetics.
Purpose of the Study:
- To investigate the interaction between EV1 and EGFR trafficking pathways.
- To determine if EV1 affects EGFR downregulation and cellular processes.
Main Methods:
- Live and confocal microscopy to track EV1 and EGFR vesicles.
- Analysis of EGFR levels and localization in infected cells.
- Assessment of EV1 infection and cell viability under different treatment conditions.
Main Results:
- EV1 inhibits EGFR downregulation, leading to EGFR accumulation in cytoplasmic endosomes.
- EV1 does not broadly disrupt cellular trafficking or transferrin recycling.
- EGFR pathway activation enhances EV1 infection and cell survival.
- EV1-induced EGFR phenotype may involve protein kinase C alpha activation.
Conclusions:
- EV1 specifically interferes with EGFR trafficking, hindering its downregulation.
- This specific interaction benefits EV1 infection by enhancing viral spread and cell viability.
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