A large number of retroviruses induce tumors at high frequency when injected into appropriate hosts. The regularity with which this cell-virus interactions leads to malignancy allows study of the events controlling the oncogenic process. One type of retrovirus, the acute leukemia virus, is particularly useful in such studies. These viruses all induce specific types of tumors after a very short latent period, indicating that these agents act by directly interfering with normal cellular growth and differentiation. In general, they have a similar genome structure, lacking most or all of the genes of replication-competent retroviruses. In place of these genes, they have acquired sequences closely related to sequences in normal cellular DNA. Current evidence suggests that the expression of these altered, host-derived sequences appears responsible for the virus' ability to induce tumors. Understanding the mechanism(s) by which this normal cellular information is subverted, leading to development of malignancy, has implications beyond retrovirus-cell interaction. To address this question, we have chosed to study Abelson murine leukemia virus, a member of the acute leukemia group that transforms lymphocytes, both in vitro and in vivo. Twomain lines of investigation are being pursued in an effort to understand virus-cell interaction in the neoplastic process: (1) studies to determine the virus genes responsible for lymphoid cell transformation and to elucidate their mechanism of action; (2) studies to define whether the virus interacts only with specific target cells at a certain state of differentiation and to determine the basis for this interaction.
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