Modulation of host CD59 expression by varicella-zoster virus in human xenografts in vivo

• MeWo-derived VZV is proved suitable as the CD59-free viral inoculum for our study.
• CD59 expression is not affected by VZV infection in human skin.
• CD59 expression is significantly increased in VZV-infected human thy/liv tissue.
• CD59 expression is markedly increased in VZV-infected human DRG.

Varicella-zoster virus (VZV) is the causative agent of both chickenpox (varicella) and shingles (zoster). VZV survives host defenses, even with an intact immune system, and disseminates in the host before causing disease. To date, several diverse immunomodulatory strategies used by VZV to undermine host immunity have been identified; however, few studies have addressed the complement evasion strategies used by this virus. Here, we show that expression of CD59, which is a key member of host regulators of complement activation (RCA), is significantly upregulated in response to VZV infection in human T cells and dorsal root ganglia (DRG) but not in human skin xenografts in SCID-hu mice in vivo. This is the first report demonstrating that VZV infection upregulates host CD59 expression in a tissue-specific manner in vivo, which may aid VZV in complement evasion and pathogenesis.