Abstract
It has been suggested that fibroblast growth factor (FGF) receptors may mediate entry of herpes simplex virus (HSV) to susceptible cells. We investigated the possible modulation of acute lytic HSV infection of cultured rat neurons by basic FGF, using cell-specific markers and indirect immunostaining. Dissociated neural cell cultures were prepared from the medial septal region of the basal forebrain, the hippocampus and dorsal root ganglion (DRG). The proportion of neurons in the cultures was enhanced by the addition of cytosine arabinoside (2μM) in the hippocampal and DRG cultures and by inversion of the coverslips in septal cultures. The percentage of MAP2+ and neurofilament+ neurons in these cultures varied between 9 and 95%. Cultures were treated with basic FGF (4–5ng ml−1) ontinuously and infected with wild-type HSV-1, untreated uninfected cultures acting as controls. Both FGF binding and FGF receptors were demonstrated in hippocampal, and to a much lesser extent, DRG neurons. In repeated experiments it was found that FGF treatment did not have a significant effect on lytic infection in any of the neuronal populations studied as assessed by the development of viral antigen expression and comparison of identified neurons in FGF, treated versus untreated, infected cultures. Our data show that FGF does not have a ‘neuroprotective’ effect on HSV infection of either central or peripheral neurons.