Varicella-zoster virus (VZV) is the first human herpesvirus to be attenuated and then approved in 1995 as a live vaccine for children. Within a few years after its administration in the United States, small outbreaks of breakthrough varicella were observed in vaccinees. Several risk factors were determined. But now a new investigation suggests another risk factor, namely, a deficiency in antibody responses to a specific individual VZV glycoprotein called gC (ORF14; gpV) in the vaccinees. Antibody concentrations to 5 VZV protein antigens were measured in children who had either wild type varicella or varicella vaccination.
These proteins included two major glycoproteins called gE (ORF68; gpI) and gC (ORF14), both constituents of the viral envelope and therefore potentially important targets of the adaptive immune response. Of particular interest, the serum antibody responses to VZV gC antigen were significantly lower in vaccinees than in children who had wild type varicella. In contrast, the serum antibody responses to VZV gE antigen were comparable in both groups. These data implied that relatively little gC antigen was produced in children who were immunized. Since abundant gC protein is produced in skin vesicles during wild type varicella, the lack of a vesicular rash after vaccination may limit the amounts of some viral antigens required for an optimal antibody response.