Marek's disease virus influences the expression of genes associated with IFN-gamma-inducible MHC class II expression.

Chickens infected with Marek's disease virus (MDV) become lifelong carriers regardless of their susceptibility to clinical disease. Therefore various viral immune-evasive mechanisms must play a role in MDV-host interactions. MDV has previously been shown to influence the expression of major histocompatibility complex (MHC) class II molecules. However, little is known about the underlying mechanisms of this phenomenon. In the present study, we studied the effect of MDV infection on the expression of several genes associated with IFN-gamma-inducible MHC class II expression at 4, 7, 14, and 21 days post-infection (dpi). There was a significant (p <or= 0.05) downregulation of MHC class II beta chain expression throughout the experiment, while other components of the MHC class II heterotrimer (i.e., alpha chain and the invariant chain) were significantly downregulated only at 4 and 21 dpi. Furthermore, the expression of components of the IFN-gamma-receptor complex was significantly downregulated at 4 dpi. In contrast, a number of other IFN-gamma-signaling molecules, including signal transducer and activator of transcription 1 (STAT1), interferon-responsive factor 1 (IRF-1), and class II transactivator (CIITA) were significantly upregulated at most time points. The results of this study shed light on the possible mechanisms by which MDV may evade host immunosurveillance.