Preliminary biochemical characterization of the factors(s) responsible for herpesvirus-induced exogenous fusion

Abstract

Cell-free extracts prepared from herpes simplex virus[HSV]-infected BHK-21 [baby hamster kidney] cells rapidly induced exogenous fusion when incubated with indicator monolayers of uninfected BHK-21 cells. Fusion was first observed at 1 h, and peak activity was reached by 4 h. Divalent cations were required for activity. Inhibition of indicator cell macromolecular synthesis with metabolic inhibitors [cycloheximide, actinomycin D, mitomycin C and cytosine arabinoside] failed to prevent formation of cell-free extract-induced polykaryocytes. Removal of virus particles from the cell-free extract by velocity sedimentation centrifugation did not affect cell-free extract exogenous fusion activity. Studies using molecular probes, i.e., glycosidases, lectins and antiserum (directed against HSV envelope or capsid proteins), suggest that the factor(s) responsible for herpesvirus fusion is a fucosylated glycoprotein that is not a structural component of the virion.