Inhibition of IFN-gamma signaling by an Epstein-Barr virus immediate-early protein.
Viruses have evolved elaborate mechanisms to target many aspects of the host's immune response. The cytokine IFN-gamma plays a central role in resistance of the host to infection via direct antiviral effects as well as modulation of the immune response. In this study, we demonstrate that the Epstein-Barr virus (EBV) immediate-early protein, BZLF1, inhibits the IFN-gamma signaling pathway. BZLF1 decreases the ability of IFN-gamma to activate a variety of important downstream target genes, such as IRF-1, p48, and CIITA, and prevents IFN-gamma- induced class II MHC surface expression. Additionally, BZLF1 inhibits IFN-gamma- induced STAT1 tyrosine phosphorylation and nuclear translocation. Finally, we demonstrate that BZLF1 decreases expression of the IFN-gamma receptor, suggesting a mechanism by which EBV may escape antiviral immune responses during primary infection.[1]References
- Inhibition of IFN-gamma signaling by an Epstein-Barr virus immediate-early protein. Morrison, T.E., Mauser, A., Wong, A., Ting, J.P., Kenney, S.C. Immunity (2001) [Pubmed]
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