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Herpes simplex virus type 1 infection of mouse astrocytes treated with basic fibroblast growth factor
1Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine, Florida 33101.
Abstract:
We explored a possible role for the basic fibroblast growth factor (FGF) receptor during herpes simplex virus type 1 (HSV-1) infection of primary mouse astrocytes, glial cells of the central nervous system known to express FGF receptors. Plaque reduction experiments showed that treatment of astrocyte monolayers with human recombinant basic FGF failed to inhibit HSV-1 infectivity, although treatment with either heparin or poly-L-lysine reduced it by approximately 100%. Identical results were obtained when monolayers of human embryonic lung fibroblasts or African green monkey kidney cells were treated with FGF, heparin or poly-L-lysine prior to HSV-1 infection. We conclude that the basic FGF receptor is not involved in the uptake of HSV-1 during productive infection of astrocytes. Our findings suggest that this molecule is not the predominant cellular receptor for HSV-1 among vertebrate cells and plays no role in defining HSV-1 neurotropism in vivo.
Insights
The basic fibroblast growth factor (FGF) receptor is not involved in herpes simplex virus type 1 (HSV-1) entry into astrocytes. This study indicates FGF receptor is not a primary cellular receptor for HSV-1.
Area of Science:
- Virology
- Cell Biology
- Neuroscience
Background:
- Herpes simplex virus type 1 (HSV-1) infects various cell types, including astrocytes in the central nervous system.
- Astrocytes express basic fibroblast growth factor (FGF) receptors, suggesting a potential role in HSV-1 infection.
- Understanding HSV-1 cellular receptors is crucial for elucidating its neurotropism.
Purpose of the Study:
- To investigate the role of the basic fibroblast growth factor (FGF) receptor in herpes simplex virus type 1 (HSV-1) infection of primary mouse astrocytes.
- To determine if FGF receptor mediates HSV-1 entry into glial cells.
- To assess the involvement of FGF receptor in HSV-1 infectivity and neurotropism.
Main Methods:
- Plaque reduction assays were performed on primary mouse astrocyte monolayers.
- Cells were treated with human recombinant basic FGF, heparin, or poly-L-lysine prior to HSV-1 infection.
- Experiments were replicated using human embryonic lung fibroblasts and African green monkey kidney cells.
Main Results:
- Treatment with basic FGF did not inhibit HSV-1 infectivity in astrocytes.
- Heparin and poly-L-lysine significantly reduced HSV-1 infectivity by approximately 100% in astrocytes.
- Similar results were observed in fibroblasts and kidney cells, where FGF failed to inhibit infection, while heparin and poly-L-lysine did.
Conclusions:
- The basic FGF receptor is not involved in the uptake of HSV-1 during productive infection of astrocytes.
- The basic FGF receptor is unlikely to be the predominant cellular receptor for HSV-1 in vertebrate cells.
- The basic FGF receptor does not play a role in defining HSV-1 neurotropism in vivo.