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Humoral Immune Response to Chicken Pox (Varicella)

VZV can productively infect mature human DCs and that infection results in the downregulation of specific cell surface immune molecules together with impaired T-cell-stimulatory capacity. Given the importance of mature DCs in initiating antiviral immune responses, VZV interference with mature DC function represents an immune evasion mechanism which is likely to confer a survival advantage on the virus by inhibiting or reducing the consequences of a DC-initiated immune response. It was previously demonstrated that VZV encodes two separate immune evasion strategies of specifically downregulating cell surface MHC class I and inhibiting the upregulation of gamma interferon-induced MHC class II expression during productive infection of primary HFFs. These VZV-encoded immunomodulatory effects are likely to delay the initial clonal amplification of VZV-specific CD8+ and CD4+ T lymphocytes and at least transiently enhance the ability of VZV to replicate at cutaneous sites. There is also 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.

VZV can productively infect immature DCs and subsequently transfer infectious virus to autologous T lymphocytes. The ability of VZV to infect immature DCs and transfer virus to T lymphocytes has provided a model for virus dissemination during primary infection. In this instance, after initial infection of the human host, the virus encounters immature DCs of the respiratory mucosa which subsequently transport virus to the T-lymphocyte-rich draining lymph nodes, resulting in T-lymphocyte infection and subsequent dissemination of virus to other sites. Thus, it appears that VZV is DC tropic and can target two distinct aspects of DC function represented by immature and mature DCs. This ability to infect both DC types confers upon the virus the potential to both increase virus dissemination in the host and evade the immune response.

Mature DC function relies not only on the recognition of antigenic peptides in association with MHC molecules but also on the interaction with several other immune molecules including CD40, CD54, CD80, CD83, and CD86. With the exception of MHC class II, all of the molecules of MHC class I, CD80, CD83, and CD86 were downregulated on VZV-infected mature DCs. These indicates that the mechanism by which VZV alters immune molecule expression on mature DCs appears novel, since the pattern of immune molecule alteration differs from that of other viruses which infect and alter mature DCs.

At a mean of 5 years after vaccination, 93% of children and 94% of adults had IgG antibodies to VZV as determined by ELISA.