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Updated: Aug 7, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Immune evasion mechanisms of varicella-zoster virus
1Stanford University School of Medicine, California 94305, USA.
Abstract:
Varicella-zoster virus can to modulate the expression of class I and class II major histocompatibility (MHC) molecules. MHC class I expression is downregulated in VZV-infected T cells as well as in fibroblasts. VZV-infected cells do not respond to exposure to interferon-gamma (IFN-gamma) by upregulation of MHC class II expression. However, MHC class II expression is induced when cells are treated with IFN-gamma before VZV infection. These effects on MHC class I and class II expression can be expected to interfere transiently with adaptive immune responses of the host, mediated by CD4 and CD8 T cells, ensuring that the virus has sufficient opportunity for transmission to susceptible contracts.
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