Published online by Cambridge University Press: 24 December 2009
Varicella zoster virus (VZV) like the other herpesvirus family members is a highly successful and ubiquitous human pathogen. In order for VZV to persist in the human population, the virus has evolved strategies to avoid immune detection and potentially promote viral pathogenesis. We have demonstrated that VZV encodes two separate immune evasion strategies by specifically down-regulating cell-surface MHC class I (Abendroth et al., 2001a) and inhibiting the up-regulation of interferon-γ-induced MHC class II expression (Abendroth et al., 2000) during productive infection of primary human foreskin fibroblasts (HFFs). Given that VZV appears to evade host recognition by T-cells during the prolonged, 10–21 day incubation period, viral genes encoding immunomodulatory proteins are likely to delay the initial clonal amplification of VZV specific CD4+ and CD8+ T-lymphocytes and at least transiently enhance the ability of VZV to replicate at cutaneous sites. Recently we have studied the interaction of VZV with human dendritic cells (DCs) and T-lymphocytes. VZV has the ability to infect immature DCs and transfer virus to T-lymphocytes (Abendroth et al., 2001b). VZV also readily infects tonsil T-cells (Ku et al., 2002). The analysis of VZV interactions with T-cells during viral pathogenesis is described in Chapter 37. These capacities of VZV to infect DC and T-cells provide new models of viral dissemination during primary and recurrent VZV infections. Further studies assessing mature DCs have revealed a third immune evasion mechanism for VZV whereby the virus is able to productively infect a specialized immune cell (representing the most potent antigen presenting cell type), and in doing so impairs its ability to function properly.