Abstract
BackgroundAvian influenza virus (AIV) induced proinflammatory cytokine expression is believed to contribute to the disease pathogenesis following infection of poultry. However, there is limited information on the avian immune response to infection with low pathogenic avian influenza virus (LPAIV).MethodsTo gain a better understanding of the early viral-host interactions of LPAIV in chickens, primary chicken embryo hepatocytes (CEH) 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.ResultsCEH can support growth of the tested LPAIVs when with trypsin supplementation. 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.ConclusionThe 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.
Highlights
Avian influenza (AI) infection in poultry can result in high morbidity and mortality, and negatively affect international trade [1]
LPAI viruses have the potential to evolve into highly pathogenic (HP) Avian influenza virus (AIV) and this has been documented in many poultry outbreaks
Growth kinetics of viruses on chicken embryo hepatocytes (CEH) To investigate the replication of different virus strains, CEHs were infected with H5N9, H5N3, H7N2 and H9N2 viruses at multiplicity of infection (MOI) of 1 and the viral titers in the supernatants were determined as log10EID50/ml
Summary
Avian influenza (AI) infection in poultry can result in high morbidity and mortality, and negatively affect international trade [1]. H5 and H7 subtypes, have been associated with HPAI mutation [4,5] This has led to a new proposed definition of avian influenza to extend all infections caused by H5 and H7 viruses regardless of their virulence as notifiable avian influenza (NAI) [6]. The H9N2 subtype was first reported to infect turkeys in the United States in 1966 and has seriously affected the poultry industry of the Asia and Middle East since the mid-1990s [7,8,9]. This subtype is considered one of the most likely candidates to cause a new influenza pandemic in humans [10]. There is limited information on the avian immune response to infection with low pathogenic avian influenza virus (LPAIV)
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