GENETIC ASPECTS OF VIRAL ONCOGENESIS IN MICES

对病毒引起的肿瘤性疾病的遗传学研究已经导致了 许多参与这些过程的染色体基因的鉴定。许多 影响对病毒或病毒诱导疾病易感性的小鼠基因， 在各种近交实验室菌株中被鉴定出来，我们已经 将这些研究扩展到包括野生小鼠种群，因为它们 更大的遗传多样性。我们发现并描述了一部小说 野生小鼠病毒，HoMuLV，分离自东欧小鼠。这种病毒 是致病性的，尽管有不同的包膜，但具有嗜亲性寄主范围 gag基因与其它小鼠白血病病毒的不同之处还在于它的gag基因。 在其他实验中，我们描述了新的致癌序列， 由有缺陷的致病性野生小鼠病毒转导。了两本这本 在小鼠基因组中鉴定出了两种癌基因，其中一种是假基因。 我们还证明了哈维ras癌基因的激活是 与T细胞白血病的发展有关， 激活是通过病毒整合和染色体整合完成的。 重排最后，我们定位了编码亲嗜性MULV的基因， 细胞表面受体，并表征了相关的基因组序列， 可能代表嗜热MuLV受体基因。

Genetic studies on virus-induced neoplastic disease have led to the identification of many chromosomal genes involved in these processes. Many mouse genes affecting susceptibility to virus or virus-induced disease have been identified in the various inbred laboratory strains, and we have expanded these studies to include wild mouse populations because of their greater genetic diversity. We have identified and characterized a novel wild mouse virus, HoMuLV, isolated from Eastern European mice. This virus is pathogenic, has ecotropic host range despite its different envelope gene, and also differs from other murine leukemic viruses in its gag gene. In other experiments, we characterized the novel oncogenic sequence transduced by a defective pathogenic wild mouse virus. Two copies of this oncogene were identified in the mouse genome, one of which is a pseudogene. We also demonstrated that activation of the Harvey ras oncogene was associated with the development of a T cell leukemia and that this activation was accomplished by viral integration and chromosomal rearrangement. Finally, we positioned the gene encoding the ecotropic MULV cell surface receptor and characterized a related genomic sequence which may represent the amphotropic MuLV receptor gene.