Herpes simplex virus infection can occur without involvement of the fibroblast growth factor receptor.

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Basic fibroblast growth factor (bFGF) has been reported to block uptake of herpes simplex virus type 1 (HSV-1) and plaque formation on arterial smooth muscle cells, suggesting a role for the bFGF receptor in HSV entry (R. J. Kaner, A. Baird, A. Mansukhani, C. Basilico, B. D. Summers, R. Z. Florkiewicz, and D. P. Hajjar, Science 248:1410-1413, 1990). We confirmed the effect of bFGF on infection of this cell type with HSV-1 and HSV-2 and found the same result with umbilical vein endothelial cells. However, bFGF does not inhibit plaque formation on any other cell type we tested. Furthermore, there is no correlation between the level of expression of the bFGF receptor and the effect of bFGF. HEp-2 and A431 cells express barely detectable levels of receptor, and yet they are fully permissive for HSV infection in a bFGF-insensitive manner. Thus, interaction of virus with the bFGF receptor is not required for infection of many cell types. In addition, infection of smooth muscle cells is not prevented by incubation of virus with an anti-bFGF antibody, arguing against the hypothesis that virion-associated bFGF acts as a bridge between virus and receptor (A. Baird, R. Z. Florkiewicz, P. A. Maher, R. J. Kaner, and D. P. Hajjar, Nature [London] 348:344-346, 1990).

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