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Pathogenesis, clinical disease, host response, and epidemiology: VZU
Ann Arvin, Departments of Pediatrics and Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA, USA,
Allison Abendroth, Centre for Virus Research, Westmead Millennium Institute and University of Sydney, Westmead, NSW, Australia
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.
Exposure of a susceptible individual to varicella-zoster virus (VZV) usually results in the clinical manifestations of varicella, in contrast to the other human herpesviruses, which are often acquired asymptomatically. Although symptoms of fever, malaise and vesicular rash occur in most cases, host responses play a critical role in limiting the progression of primary VZV infection. During the interval after mucosal inoculation, through the incubation period, the onset of varicella and the resolution of the acute illness, the virus first evades host clearance mechanisms and is then controlled by the induction of virus-specific immunity. VZV shares the characteristic of infectivity for cells of the host immune system that is common among viral pathogens. Like the human herpesviruses 6 and 7, VZV exhibits a tropism for T lymphocytes which is critical for the pathogenesis of primary infection (Moffat et al., 1995). Following mucosal inoculation, cell-associated viremia is presumed to be required for spread from regional lymph nodes to other sites of early viral replication in the liver, and viremia allows transport of VZV to cutaneous sites of replication during the late incubation period (Grose, 1981; Koropchak et al., 1989; Mainka et al.,1998).
Innate immunity may limit the initial spread of VZV within the host, but these defenses are usually not sufficient to prevent symptoms of illness before VZV specific adaptive immunity is elicited. Adaptive antiviral immunity consists of the clonal expansion of T lymphocytes and B lymphocytes that have the functional capacity to recognize specific VZV proteins and to interfere with viral replication and transfer of virions from infected to uninfected cells within the host.
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