|JIANG, HAIJUN - China Agricultural University|
|YU, KANGZHEN - China Agricultural University|
Submitted to: Virology Journal
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/14/2013
Publication Date: 11/19/2013
Citation: Jiang, H., Yu, K., Kapczynski, D.R. 2013. Transcription factor regulation and cytokine expression following in vitro infection of primary chicken cell culture with low pathogenic avian influenza virus. Virology Journal. 10:342. DOI: 10.1186/1743-422X-10-342.
Interpretive Summary: Avian influenza causes significant economic losses to the poultry industry worldwide. While the highly pathogenic form of avian influenza causes rapid mortality in birds, the low pathogenic form is responsible for significant morbidity, and some of these viruses have demonstrated the ability to mutate into a highly pathogenic form. Relatively little information exists on the immune response of poultry to infection with low pathogenic avian influenza virus. In these studies we determined the early immune response of primary chicken cells to infection with low pathogenic avian influenza. Our results demonstrate that a potent anti-viral response was quickly up regulated following infection and increased with viral growth. Overall, these studies demonstrate the contribution of the immune response of poultry to avian influenza virus.
Technical Abstract: Avian influenza virus (AIV) induced proinflammatory cytokine expression is believed to contribute to the disease pathogenesis following infection. However, there is limited information on the avian immune response to infection with low pathogenic avian influenza virus (LPAIV). To gain a better understanding of the early viral-host interactions of LPAIV in chickens, primary chicken embryo liver (CELi) cells were infected with four different LPAIVs of U.S. origin. Kinetics of virus replication, transcription factor (c-Jun, p50 and IRF-3) activation and immune response gene (IL-6, IL-1beta, IFN-alpha and Mx) expression were studied at four different time points (6, 12, 24 and 48 hours) post infection and compared to non-infected controls. Results demonstrate that CELi cells can provide efficient support growth of the tested LPAIVs when supplemented with trypsin. All four immune response genes tested were upregulated following infection as were transcription factors c-Jun, p50 and IRF-3. Amplification of these genes was dependant on virus replication (e.g. inclusion of trypsin), such that immune response genes and transcription factors were upregulated as viral titers increased. The results of these studies demonstrate the requirement of virus replication for innate immune regulation and broaden our understanding of transcription factor responses related to LPAIV infection in chickens.