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Herpes simplex virus glycoprotein D relocates nectin-1 from intercellular contacts.
Arjun K Bhargava1, Paul W Rothlauf2, Claude Krummenacher3
1Department of Biochemistry, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Virology
|October 11, 2016
Summary
Herpes simplex virus glycoprotein D disrupts nectin-1 interactions, affecting its cell junction localization. This viral mechanism impacts how the virus enters cells, offering insights into herpes simplex virus (HSV) infection pathways.
Area of Science:
- Virology
- Cell Biology
- Molecular Interactions
Background:
- Herpes simplex virus (HSV) utilizes nectin-1, a cell adhesion molecule, for entry into neurons and epithelial cells.
- Viral glycoprotein D (gD) acts as a ligand for nectin-1, binding to a site that overlaps with nectin-1's homophilic interaction site.
Purpose of the Study:
- To investigate how HSV gD binding affects nectin-1's localization and interactions at cell junctions.
- To determine if nectin-1's interaction with afadin is necessary for gD-mediated effects.
Main Methods:
- Observing the effect of HSV gD on nectin-1 redistribution from cell junctions.
- Assessing the role of afadin in nectin-1 redistribution and virion surfing.
- Analyzing nectin-1 accumulation on gD-coated surfaces.
Main Results:
- HSV gD disrupts nectin-1's intercellular homophilic trans-interaction and causes its redistribution from cell junctions.
- Nectin-1 redistribution and virion surfing are independent of afadin.
- Cells on gD-coated surfaces show reduced nectin-1 accumulation at cell contacts.
Conclusions:
- HSV gD directly interacts with nectin-1, altering its localization and function.
- The interaction of HSV gD with nectin-1 influences nectin-1 globally through signaling pathways.
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