Location: Avian Disease and Oncology ResearchTitle: Marek’s disease virus induced transient atrophy of cecal tonsils
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 6/19/2014
Publication Date: 7/16/2014
Citation: Heidari, M., Fitzgerald, S., Zhang, H. 2014. Marek’s disease virus induced transient atrophy of cecal tonsils. Meeting Abstract. XIII Avain Immunology Research Group Conference 2014, July 16-19, 2014, University of Guelph, Guelph, Canada.
Technical Abstract: Although bursal and thymic atrophy associated with Marek’s disease (MD) is well established and characterized, the effect of Marek's disease virus (MDV) infection on lymphoid aggregates within the gut-associated lymphoid tissue (GALT) is not known. The cecal tonsils (CT) are the two largest lymphoid organs in the avian GALT that along with Peyer’s patches elicit protective immune responses against bacterial and viral infections in the intestinal tract of avian species. We investigated the role of Marek's disease virus (MDV) infection on the atrophy of CT and cytokine gene expression pattern in two Marek's disease susceptible and resistant chicken lines. The histopathological analysis indicated that MDV causes the loss of germinal follicular centers within the CT of the resistant line while inducing a severe near total lymphoid depletion in the susceptible line during lytic infection. The lymphoid depletion, however, recovered approximately 14 days post infection (dpi) but the loss of germinal centers persisted during the latent phase of infection in both lines. Unlike bursa and thymus, the atrophy of this important GALT was transient and there were no visible differences between the CT of infected and control birds of either line by 21 dpi. The immunohistochemical analysis of the infected tissues revealed that B and CD4+ T cells were severely depleted during the lytic infection but recovered by 21 dpi. Little to no changes was observed in the populations of other cell types. Gene expression profiling data showed an increase in transcriptional activities of IL-6, IL-10, IL-13, IFN-beta, IFN-gamma, and iNOS in the CT of both lines during lytic infection. The expression levels of these genes, however, were higher in the CT of the susceptible line than the resistant line. IL-12 expression was up regulated in the CT of susceptible line during all three phases of infection. IL-18 was also up regulated in the CT of the susceptible line during lytic and latent phases of infection. IL-8 was the only cytokine with higher transcriptional activity in the CT of the resistant line during lytic and latent phases of infection.