Abstract

Infection of one day old White leghorn chicks with avian leukosis virus (ALV) usually results in the development of a bursal- dependent B-cell lymphoma (Purchase and Burmester, 1978). This tumor requires the bursal environment to develop and is characterized by the presence of cell surface immunoglobulin M (IgM) (Cooper et al., 1974). Integration of the ALV provirus within the normal c-myc locus of the target cell disrupts the expression of this locus and appears to be important in the development of the primary tumor (Hayward et al., 1981; Payne et al., 1982). However, alterations that influence the expression of the c-myc locus have been implicated in the development of a variety of lymphoid tumors in several species (Dalla-Favera et al., 1982; Shen-Ong et al., 1982; Corcoran et al., 1984; Levy et al., 1984). These lymphoid tumors exhibit considerable variation in their phenotype and include not only B-cell tumors that express IgM but also mature B-cell tumors that secrete IgG and T-cell tumors. It is not known why ALV infection produces such a restricted type of lymphoid tumor in the chicken. A variety of factors including (i) access of the virus to a particular type of target tissue, (ii) the abundance and proliferative capacity of different target cells at the time of virus replication and (iii) specific and non-specific host defense mechanisms could influence tumor development following ALV infection.KeywordsInfectious VirusHaploid GenomeLymphoid TumorPreneoplastic LesionAvian Leukosis VirusThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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