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J Gen Virol 73 (1992), 1845-1848; DOI 10.1099/0022-1317-73-7-1845
© 1992 Society for General Microbiology
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Herpes simplex virus type 1 infection of mouse astrocytes treated with basic fibroblast growth factor

Richard D. Dix1,2,3,, Lisa Hurst1 and Robert W. Keane4

1 Department of Ophthalmology
2 Department of Microbiology and Immunology
3 Department of Neurology
and4 Physiology and Biophysics, P.O. Box 016880, Bascom Palmer Eye Institute, University of Miami School of Medicine, Miami, Florida 33101, U.S.A.

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.

Received 29 January 1992; accepted 17 March 1992.




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