Abstract:
: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.
journal_name
Immunityjournal_title
Immunityauthors
Morrison TE,Mauser A,Wong A,Ting JP,Kenney SCdoi
10.1016/s1074-7613(01)00226-6keywords:
subject
Has Abstractpub_date
2001-11-01 00:00:00pages
787-99issue
5eissn
1074-7613issn
1097-4180pii
S1074-7613(01)00226-6journal_volume
15pub_type
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