Respiratory syncytial virus (RSV) suppression of glucocorticoid receptor phosphorylation does not account for repression of transactivation

• GR N-terminus is essential for RSV suppression of GR-induced transactivation.
• RSV infection inhibits dexamethasone-induced GR phosphorylation.
• Protein phosphatase inhibitor reverses RSV suppression of GR phosphorylation.
• Protein phosphatase inhibition does not reverse RSV effects on GR function.
• Mutation of GR phosphorylation sites does not reverse RSV effects on GR function.

Respiratory syncytial virus (RSV)-induced bronchiolitis in infants, although inflammatory in nature, is not responsive to glucocorticoids. We have recently shown that RSV-infected lung epithelial cells have impaired glucocorticoid receptor (GR)-mediated transactivation. In this study, we show that the N-terminal region of GR is required for RSV repression of GR transactivation and that RSV infection of lung epithelial cells reduces ligand-dependent GR phosphorylation at serine 211 and serine 226. However, we also show that these changes in GR phosphorylation do not account for the RSV repression of GR transactivation suggesting other regions of the GR N-terminus must also be involved.