Immune evasion as a pathogenic mechanism of varicella zoster virus

Abstract

Varicella zoster virus (VZV) is a human herpesvirus that causes varicella (chickenpox) during primary infection, establishes latency in dorsal root ganglia and may reactivate years later, producing herpes zoster. VZV must evade antiviral immunity during three important stages of viral pathogenesis, including the cell-associated viremia characteristic of primary infection, persistence in dorsal root ganglia during latency and the initial period of VZV reactivation. Our observations about the immunomodulatory effects of VZV document its capacity to interfere with adaptive immunity mediated by CD4 as well as CD8 T cells, ensuring the survival of the virus in the human population from generation to generation.