The Abelson Murine Leukemia Virus Oncogene

Abstract

Abelson murine leukemia virus (A-MuLV) is an acute transforming retrovirus which induces a rapid lymphosarcoma in mice. The virus arose in one of a series of mice that were treated with prednisolone and infected with the replication-competent retrovirus Moloney murine leukemia virus (M-MuLV) (1, 2). One such mouse developed a non-thymic tumor; the cause was shown to be a virus when it was demonstrated that filtered extracts from this tumor were capable of inducing similar tumors in animals. These tumors were quite distinct from the thymic tumors normally induced by the parental M-MuLV, suggesting that a new virus had arisen in the course of the infection. This new virus, termed A-MuLV, has been the subject of intensive study in recent years. The analysis of the structure of the viral genome has had profound effects on our thinking about the mechanisms by which oncogenic gene structures can arise. This review will describe the biology of the virus, its genetic structure, current models for the origin of the virus, and the properties of the cellular gene from which it arose. Several other reviews describing these and other aspects of the virus have been published (3–8).

Biology of A-MuLV. Infection of experimental animals with A-MuLV preparations results in the rapid onset of disease. Neonatal mice injected with the virus develop an invariably fatal lymphosarcoma 3 to 5 weeks after injection; the first neoplastic cells appear in the bone marrow as early as 15 to 20 days after infection. The cells spread rapidly to the meninges and to selected lymph nodes, often resulting in localized lymphadenopathy. The tumor cells, exhibiting a characteristic lymphoblastic morphology, can be adapted to growth in vitro and cloned. These cultures have allowed a detailed characterization of the tumor cells. More importantly, primary explants from various tissues can be prepared and transformed in vitro by infection with the virus (9, 10).