Marek's disease (MD) is a lymphoproliferative disease of domestic chickens that is caused by a highly cell-associated oncogenic α-herpesvirus, Marek's disease virus (MDV). MDV replicates in chicken lymphocytes and establishes a latent infection within CD4 T cells. MD is characterized by bursal and thymic atrophy and rapid onset of T cell lymphomas that infiltrate lymphoid tissues, visceral organs, and peripheral nerves with severe clinical symptoms that include transient paralysis, anemia, weight loss, and neurologic disorders. The cecal tonsils (CT) are considered the largest lymphoid aggregates of avian gut-associated lymphoid tissue (GALT). Along with Peyer's patches, CT elicits protective immune responses against bacterial and viral pathogens in the intestinal tract of avian species. In this study we investigated the effect of MDV infection on CT structural changes and cytokine gene expression in two MD-susceptible and resistant chicken lines. The histopathologic analysis revealed 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 cytolytic infection. The lymphoid depletion, however, recovered approximately 2 wk postinfection but the loss of germinal centers persisted during the latent phase of infection in both lines. The atrophy of this important GALT was transient and there were no visible differences between the CT of the infected and control birds of either line by 21 days postinfection. Of the genes tested, IFN-β and IFN-γ were up regulated in the CT of both infected lines during lytic infection. The expression levels of both genes were much higher in the susceptible line than in the resistant line. A similar pattern of expression was observed for IL-6, IL-10, IL-13, and iNOS. IL-12 was up regulated in the CT of birds of the susceptible line during all three phases of infection. An over expression of IL-18 was also observed in CT of the susceptible line during lytic and latent phases of infection. IL-8 was the only cytokine expressed at higher levels in the CT of the resistant line during the lytic and reactivation phases of infection. The histopathologic observations and gene expression profiling are further discussed.

Atrofia transitoria de las tonsilas cecales inducida por el virus de la enfermedad de Marek.

La enfermedad de Marek (MD) es una enfermedad linfoproliferativa de los pollos domésticos que es causada por un α-herpesvirus oncogénico altamente asociado a células, denominado virus de la enfermedad de Marek (MDV). El virus de la enfermedad de Marek se replica en los linfocitos de pollo y establece una infección latente en las células T CD4 . El virus de Marek se caracteriza por producir bursitis, atrofia del timo y rápida aparición de linfomas de células T que se infiltran en los tejidos linfoides, en los órganos viscerales y en los nervios periféricos, produciendo signos clínicos severos que incluyen parálisis transitoria, anemia, pérdida de peso y trastornos neurológicos. Las tonsilas cecales se consideran los agregados de tejido linfoide más grandes asociados al intestino aviar (con las siglas en inglés GALT). Junto con las placas de Peyer, las tonsilas cecales inducen respuestas inmunes protectoras contra patógenos bacterianos y virales en el tracto intestinal de las especies aviares. En este estudio se investigó el efecto de la infección por el virus de Marek en los cambios estructurales de las tonsilas cecales y en la expresión genética de citocinas en dos líneas de pollos, una susceptible y la otra resistente al virus de Marek. El análisis histopatológico reveló que el virus de Marek provoca la pérdida de los centros germinales foliculares dentro de las tonsilas cecales de la línea resistente, mientras que induce una despoblación linfoide severa y casi total en la línea susceptible durante la infección