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ARS Home » Southeast Area » Athens, Georgia » U.S. National Poultry Research Center » Avian Disease and Oncology Research » Research » Publications at this Location » Publication #303765
Title: Marek’s disease virus induces transient atrophy of cecal tonsils

Author
item Heidari, Mohammad
item FITZGERALD, SCOTT - Michigan State University
item Zhang, Huanmin

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 7/20/2014
Publication Date: 7/20/2014
Citation: Heidari, M., Fitzgerald, S.D., Zhang, H. 2014. Marek’s disease virus induces transient atrophy of cecal tonsils [abstract]. In: Proceeding for 10th International Symposium on Marek's Disease and Avian Herpesviruses, July 20-23, 2014, East Lansing, Michigan. p. 43.

Interpretive Summary:

Technical Abstract: Marek’s disease (MD) is a lymphoproliferative disease of domestic chickens caused by an immunosupperessive alpha herpesvirus, Marek’s disease virus (MDV). Clinical signs of MD include bursal/thymic atrophy and neurological disorders. The cecal tonsils (CT) are the largest lymphoid aggregates of avian gut-associated lymphoid tissue. Along with Peyer’s patches, CT provides immunity against bacterial and viral infections in the intestinal tract of avian species. We investigated the role of MDV infection on the atrophy of CT and cytokine gene expression pattern in the MD-susceptible and resistant lines of chickens. MDV causes the loss of germinal follicular centers within the CT of the resistant line while inducing a near total lymphoid depletion in the susceptible line during lytic infection. Although the loss of germinal centers persisted during the latent phase of infection in both lines, the lymphoid depletion recovered approximately 14 days post infection (dpi). The atrophy of CT was transient as there was no visible differences between the CT of infected and control birds of either line by 21 dpi. Cytokine gene expression profiling revealed that IL-6, IL-10, IL-13, IFN-beta, IFN-gamma, and iNOS were all up regulated in the CT of both lines during lytic infection. The expression levels of these genes, however, were higher in the susceptible line than the resistant line. IL-12 had higher transcriptional activity 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 over expressed in the CT of the resistant line during lytic and latent phases of infection.