Induction of receptors for complement and immunoglobulins by herpesviruses of various species.

Cells infected with herpes simplex virus type 1 (HSV-1) express a viral glycoprotein on the cell surface, which can function as a receptor for a cleavage product of complement factor 3 (C3b), and it has been suggested that this has biological relevance in the infected host (Smiley et al., 1985, J. Virol. 19, 217). As herpesviruses of different species share common determinants on their glycoproteins, a possible conservation of biological function was investigated for bovine herpesviruses type 1 and 2 (BHV-1 and -2), equine herpesvirus type 1 (EHV-1) and HSV-1 and -2, respectively. Only HSV-1 and EHV-1 induced C3b-receptors on infected cells. Nevertheless, BHV-1 infected cells could be killed by complement-dependent neutrophil mediated cytotoxicity (CDNC) as could EHV-1-infected cells. HSV-1-infected cells were not killed by this mechanism, but were highly susceptible to direct C-lysis. Four different scenarios for interaction between herpesvirus-infected cells and the nonspecific host defense system are presented.