|Petkov, D -|
|Linneman, E -|
|Sellers, H -|
Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 1, 2009
Publication Date: September 6, 2009
Repository URL: http://handle.nal.usda.gov/10113/37256
Citation: Petkov, D.I., Linneman, E.G., Kapczynski, D.R., Sellers, H.S. 2009. Identification and characterization of two distinct bursal B-cell subpopulations following infectious bursal disease virus infection of White Leghorn chickens. Avian Diseases. 53(3):347-355. Interpretive Summary: Protection of poultry against disease caused by avian viruses relies on induction of immunity. Many viruses have developed mechanisms to inhibit the host immune response by interfering with immune function. Infectious bursal disease virus (IBDV) has been shown to suppress immunity in birds. The objectives of the present study were to extend the knowledge of immune suppression in chickens by examining the impact of IBDV on different immune cell populations. Results indicate infection of chickens with IBDV decreases select members of host cells responsible for antibody production, while unaffecting others. This is the first report identifying and characterizing two distinct subpopulations of immune cells, one resistant and one susceptible, to IBDV infection.
Technical Abstract: Infectious bursal disease virus (IBDV) is an immunosuppressive virus which primarily infects IgM, B-cells in the bursa of Fabricius. Flow cytometric analysis was used to phenotype B-cell populations in the bursa and spleen following IBDV infection. In the bursa, two IgM B-cell subpopulations, designated as A and B, were identified based on cell size and granularity. While both subpopulations differentially expressed IgM and Bu1b surface markers, both groups displayed major histocompatibility (MHC) class II surface antigens at equal levels. Following IBDV-challenge of non vaccinated birds, the B subpopulation was significantly reduced between 7 and 21 days-post-challenge compared to either non-challenged birds or vaccinated-challenged birds. However, the reduction of subpopulation B in the bursa following IBDV exposure did not reduce the levels of total serum IgA, IgG, and IgM immunoglobulins nor did it affect IgG and IgA B-cells in the spleen. Phenotypic analysis of the subpopulations identified differential expression of Lewis-x, IgM, Bu1b, MUI36, and MUI78 surface antigens between the subpopulations. An age-related decrease in the proportion of subpopulation A, and an increase in subpopulation B were observed in non-vaccinated non-challenged birds after approximately 90 days of age. Overall these are the first studies to identify two distinct IgM B-cell subpopulations in the chicken bursa, and describe the decrease in the IgM B-cell population relative to IgA and IgG B-cells following IBDV infection.