Immune Responses to Marek’s Disease Virus Infection

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Marek’s disease (MD), a herpesvirus-induced lymphomatous disease in chickens, has attracted the interest of immunologists since MD virus (MDV) was isolated in 1968 and vaccines became available shortly afterwards (Witter 1985,Witter 2000). The pathogenesis of MD has been reviewed extensively (Calnek 1986,Calnek 1998,Calnek 2000; Schat 1987b). Infection of chickens with MDV is characterized by several distinct phases in which innate and acquired immune responses play important roles. The first phase is characterized by the replication of MDV in lymphoid cells, which are mostly B lymphocytes. The consequence of the lytic infection is that T lymphocytes become activated. Only activated, but not resting, T cells can be infected with MDV. Schat and Xing (2000) hypothesized recently that a viral homologue of interleukin (IL)-8 (vIL-8) (LIu et al. 1999) may be involved in attracting the activated T cells to the infected B cells (see Sects. 2.1, 6.2) to facilitate the transfer of virus. Intimate contact between B and T cells is important for the transfer of infectious virus from cell to cell (Kaleta 1977), because MDV is highly cell-associated (Schat 1984). Temporal immunosuppression of the humoral immune responses is often one of the consequences of the lytic infection in B lymphocytes. During the second phase, a latent infection is normally established in these activated T cells, although some activated CD4+ and CD8+ T cells may undergo a lytic infection (Baigent et al. 1998). The actual process of establishment and maintenance of latency has not been elucidated, but it is likely that a complex set of interactions, including immune responses and specific cellular and viral genes, is responsible.