| Autor: |
Bakre AA; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia, USA., Jones LP; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia, USA., Murray J; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia, USA., Reneer ZB; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia, USA., Meliopoulos VA; Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis Tennessee., Cherry S; Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis Tennessee., Schultz-Cherry S; Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis Tennessee., Tripp RA; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia, USA. |
| Abstrakt: |
Swine influenza virus (SIV) can cause respiratory illness in swine. Swine contribute to influenza virus reassortment, as avian, human, and/or swine influenza viruses can infect swine and reassort, and new viruses can emerge. Thus, it is important to determine the host antiviral responses that affect SIV replication. In this study, we examined the innate antiviral cytokine response to SIV by swine respiratory epithelial cells, focusing on the expression of interferon (IFN) and interferon-stimulated genes (ISGs). Both primary and transformed swine nasal and tracheal respiratory epithelial cells were examined following infection with field isolates. The results show that IFN and ISG expression is maximal at 12 h postinfection (hpi) and is dependent on cell type and virus genotype. IMPORTANCE Swine are considered intermediate hosts that have facilitated influenza virus reassortment events that have given rise pandemics or genetically related viruses have become established in swine. In this study, we examine the innate antiviral response to swine influenza virus in primary and immortalized swine nasal and tracheal epithelial cells, and show virus strain- and host cell type-dependent differential expression of key interferons and interferon-stimulated genes. |
