Human rhinovirus and influenza virus infections of the upper airway lead to colds and the flu and can trigger exacerbations of lower airway diseases including asthma and chronic obstructive pulmonary disease. Novel diagnostic and therapeutic targets are still needed to differentiate between the cold and the flu, since the clinical course of influenza can be severe while that of rhinovirus is usually more mild. In our investigation of influenza and rhinovirus infection of human respiratory epithelial cells, we used a systems approach to identify the temporally changing patterns of host gene expression from these viruses. After infection of human bronchial epithelial cells (BEAS-2B) with rhinovirus, influenza virus or co-infection with both viruses, we studied the time-course of host gene expression changes over three days. We modeled host responses to these viral infections with time and documented the qualitative and quantitative differences in innate immune activation and regulation. Highlights • Human bronchial epithelial cells (BEAS-2B) were infected with rhinovirus (RV16), influenza A virus (H1N1) or both viruses. • Steady-state RNA was profiled from five biological replicate samples by microarray hybridization at multiple times over three days. • The changing patterns of key biological processes for each virus or both viruses together were analyzed. • The data reveal similarities and differences in innate immune responses, cytokine activation, regulation of apoptosis as well as other processes that have implications for host recovery from viral infection.
【저자키워드】 Influenza virus, rhinovirus, Co-infection, epithelial cell, Gene expression time-course,