Immune evasion during varicella zoster virus infection of keratinocytes.

T cells are sensitized during varicella-zoster virus (VZV) infection and are important for control of viral spread and reactivation. In this report, we show that human keratinocytes infected with VZV inhibited upregulation of major histocompatibility complex (MHC) class I, MHC class II and intercellular adhesion molecule-1 after interferon (IFN)-gamma treatment. The ability of keratinocytes to upregulate MHC class I in response to IFN-alpha, tumour necrosis factor (TNF)-alpha and Toll-like receptor (TLR)-3 ligand was also diminished upon VZV infection. VZV-infected keratinocytes treated with IFN-gamma had significantly reduced capacity to stimulate antigen-specific T cells compared with uninfected cells. Interference with IFN-alpha, TNF-alpha, IFN-gamma and TLR-3 signalling in keratinocytes by VZV may contribute to immune evasion of the adaptive immune response