The fibroblast growth factor receptor is not required for herpes simplex virus type 1 infection.
The early events mediating herpes simplex virus type 1 (HSV-1) infection include virion attachment to cell surface heparan sulfates and subsequent penetration. Recent evidence has suggested that the high-affinity fibroblast growth factor (FGF) receptor mediates HSV-1 entry. This report presents three lines of experimental evidence showing that the high-affinity FGF receptor is not required for HSV-1 infection. First, rat L6 myoblasts lacking FGF receptors were as susceptible to HSV-1 infection as L6 cells genetically engineered to express the FGF receptor. Second, a soluble FGF receptor fragment that inhibited FGF binding and receptor activation did not inhibit HSV-1 infection. Finally, basic FGF (but not acidic FGF) inhibited HSV-1 infection in L6 cells lacking FGF receptors, presumably by blocking cell surface heparan sulfates also required for HSV-1 infection. These results show that the high-affinity FGF receptor is not required for HSV-1 infection but instead that specific low-affinity basic FGF binding sites are used for HSV-1 infection.
Mirda
D P
DP
Cancer Research Institute, University of California, San Francisco 94143-0724.
Navarro
D
D
Paz
P
P
Lee
P L
PL
Pereira
L
L
Williams
L T
LT
D000818:Animals; D002460:Cell Line; D005346:Fibroblast Growth Factors / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D051381:Rats; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*; D017468:Receptors, Fibroblast Growth Factor; D018139:Simplexvirus / Q000378:metabolism* / Q000502:physiology; D012995:Solubility; D014162:Transfection; D014709:Vero Cells; D014779:Virus Replication
D011956:Receptors, Cell Surface; D017468:Receptors, Fibroblast Growth Factor; D005346:Fibroblast Growth Factors