|Kulkarni, Gururaj - Raj|
|Jiang, Haijun - China Agricultural University|
Submitted to: Biomed Central (BMC) Genomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/28/2011
Publication Date: 6/3/2011
Publication URL: http://handle.nal.usda.gov/10113/60748
Citation: Kapczynski, D.R., Liljebjelke, K.A., Kulkarni, G., Hunt, H.D., Jiang, H., Petkov, D. 2011. Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza. Biomed Central (BMC) Genomics. 5(4):S13.
Interpretive Summary: Avian influenza (AI) is an economically important virus of poultry that has significant impact on global trade. To protect birds against AI infection, a basic understanding of how the immune system recognizes and responds to AI is critical to developing new vaccines. One mechanism for recognizing AI is through cell-mediated immunity (CMI), which has been suggested to be an important factor to the development of protection in chickens against avian influenza. In these studies we demonstrate that CMI against one subtype of AI will cross react against a different subtype of AI. These studies further our knowledge of cross reactive CMI against AI.
Technical Abstract: Avian influenza (AI) infection in poultry can result in high morbidity and mortality, and negatively affect international trade. Because most AI vaccines used for poultry are inactivated, our knowledge of immunity against AI is based largely on humoral immune responses. In fact, little is known about cellular immunity following a primary AI infection in poultry, especially regarding cytotoxic T lymphocytes (CTL's). In these studies, major histocompatibility complex (MHC)-defined (B2/B2) chickens were infected with low pathogenic AI (LPAI) H9N2 and clinical signs of disease were monitored over a two weeks period. Splenic lymphocytes from infected and naïve birds were examined for cross reactivity against homologous and heterologous (H7N2) LPAI by ex vivo stimulation. Cellular immunity was determined by cytotoxic lysis of B2/B2 infected lung target cells and proliferation of T cells following exposure to LPAI. Infection with H9N2 resulted in statistically significant weight loss compared to sham-infected birds. Splenic lymphocytes derived from H9N2-infected birds displayed lysis of both homologous (H9N2) and heterologous (H7N2) infected target cells, whereas lymphocytes obtained from sham-infected birds did not. T cell proliferation was determined to be highest when exposed to the homologous virus. Taken together these data extend the findings that cellular immunity, including CTL's, is cross reactive against heterologous isolates of AI and contribute to protection following infection.