Congenital varicella-zoster virus infection and the failure to establish virus-specific cell-mediated immunity.

Varicella-zoster virus (VZV) is one of the six human herpesviruses. The viral genome encodes five glycoproteins among its 70 open reading frames; these have been designated gpI to gpV. VZV causes the primary disease chickenpox, usually in children, after which the virus remains latent in the dorsal root ganglia. Later in life, VZV reactivates and causes the disease zoster. VZV can also infect the fetus of a pregnant woman who contracts chickenpox. The fetopathy is unusual in that it more closely resembles zoster than chickenpox. To determine whether the intrauterine immune response is impaired following VZV infection, the humoral and cellular immune responses were first defined in healthy children and adults following chickenpox. All produced virus-specific antibody responses to the viral glycoproteins; in addition, their lymphocytes proliferated when stimulated by both crude VZV antigen and purified glycoprotein products. The fetal immune system generated immunoglobulin M-specific antibodies to the individual VZV glycoproteins. However, no lymphocyte proliferative response was detected. Thus, these studies suggest that the fetus may not be able to mount a cell-mediated response to VZV antigens and that this impaired immunity may contribute to the severe sequelae.