Abstract
Primary varicella-zoster virus (VZV) infection commonly causes chickenpox. After control of the primary infection, VZV lies dormant within the sensory ganglia. When immunity is decreased, VZV can reactivate and replicate itself massively in neurons, then spread to skin through neuritis and cause herpes zoster. The body has a powerful immune surveillance system, which can timely eradicate mutational or virus-infected cells. In order to replicate itself, spread and cause skin lesions, or remain latent in ganglia for a long time, VZV must encode the capability to escape from immune surveillance system. This review summarizes multiple immune escape mechanisms of VZV, including limitation on host immune recognition, down-regulation of expressions of related immune molecules, interference with antigen presentation, etc. Key words: Herpesvirus 3, human; Immunity; Escape reaction; Interferons; NF-kappa B
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