Journal
IMMUNITY
Volume 15, Issue 5, Pages 787-799Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(01)00226-6
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Funding
- NCI NIH HHS [P01-CA19014, 2-R01-CA58853, 2-R01-CA66519] Funding Source: Medline
- NIAID NIH HHS [T32-AI07419] Funding Source: Medline
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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.
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