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HSV-2 disrupts gap junctional intercellular communication between mammalian cells in vitro
N O Fischer1, G N Mbuy, R I Woodruff
1Department of Biology, West Chester University, West Chester, PA 19383-8102, USA.
Journal of Virological Methods
|February 13, 2001
Summary
Herpes simplex virus-2 (HSV-2) infection rapidly disrupts cell-to-cell communication in African green monkey kidney cells. This viral infection significantly impairs gap junctions, affecting both dye and electrical coupling.
Area of Science:
- Virology
- Cell Biology
- Neuroscience
Background:
- Gap junctions facilitate intercellular communication via dye and electrical coupling.
- Herpes simplex virus-2 (HSV-2) is a significant human pathogen.
- Understanding viral disruption of cellular functions is crucial for disease research.
Purpose of the Study:
- To investigate the impact of HSV-2 infection on gap junction communication in Vero cells.
- To determine the temporal relationship between HSV-2 infection and gap junction dysfunction.
Main Methods:
- Vero cells were infected with HSV-2.
- Lucifer yellow CH dye spread was used to assess dye coupling.
- Intracellular electrophysiological measurements quantified ionic coupling coefficients.
Main Results:
- HSV-2 infection progressively reduced gap junction coupling.
- Dye coupling was abolished within 24 hours post-infection.
- Ionic coupling coefficients decreased from 0.4 in control cells to <0.08 at 24 hours post-infection.
Conclusions:
- HSV-2 infection rapidly and severely impairs gap junction function in Vero cells.
- Gap junction disruption occurs early in infection, preceding visible cytopathic effects.
- HSV-2 effectively disables intercellular communication pathways.