Restrictions That Influence Avian Leukosis Virus-Induced Lymphoid Leukosis
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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 Virus Haploid Genome Lymphoid Tumor Preneoplastic Lesion Avian Leukosis Virus
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