Respiratory syncytial virus infection of human respiratory epithelial cells enhances both muscarinic and beta2-adrenergic receptor gene expression.

The possible changes in transcriptional activities of the M1 muscarinic acetylcholine receptor (mAChR) and beta2-adrenergic receptor (AR) genes in respiratory syncytial virus (RSV)-infected human type 2 alveolar epithelial cells (A549 cells) were analyzed semiquantitatively by reverse transcription-polymerase chain reaction (RT-PCR). RSV enhanced M1 mAChR gene expression significantly at 4 hrs post infection (p.i.), and this enhancement persisted until 10 hrs, after peaking at 7 hrs. Beta2-AR gene expression also increased significantly as early as at 1 hr p.i. and persisted for more than 10 hrs. These transcriptional enhancements were observed in cells treated with live but not with inactivated virus. Our observations suggest that RSV infection of human respiratory epithelial cells may enhance the expression of both parasympathetic and sympathetic receptors. The upregulated M1 mAChR gene in virus-infected cells may correlate with temporal airway hyperresponsiveness in subjects with RSV or other respiratory virus infection. The enhanced beta2-AR gene expression in peripheral lungs might explain the excessive mucus secretion observed during viral pneumonitis.