Risser R, Horowitz J M, McCubrey J
Annu Rev Genet. 1983;17:85-121. doi: 10.1146/annurev.ge.17.120183.000505.
The earlier demonstration that genes of the mouse greatly influenced the spontaneous incidence of lymphoma was among the more persistent barriers to general acceptance of a viral etiology of this disease. We now can be fairly certain that some of those mouse genes are the DNA life phase of a class of retrovirus known as murine leukemia virus. These MuLV, although related in sequence to each other, are a collection of viruses that show diverse patterns of host range and tissue tropisms. The host-range properties of MuLV serve as means of classifying them into related families known as ecotropic, xenotropic, and amphotropic, and are probably dictated by determinants on gp70. The preferential abilities to replicate in different tissues, on the other hand, may be dictated by the controlling sequences located at the 3' end of the genome, known as U3. MuLV genomes are located at many different sites in the mouse genome. The viral genomes found at those sites can be induced to be expressed with different efficiencies spontaneously in vivo, by chemicals in vitro, or by DNA transfection. Certain MuLV genomes can also interact to increase expression perhaps by recombination or trans complementation. Although the molecular mechanisms that explain these phenomena are not yet clear, the phenomenon of differential expression has important pathological consequences, particularly in the development of lymphoma. The complex process by which endogenous MuLV induce leukemia appears to involve the expression and interaction of multiple MuLV genomes. It seems apparent that expression of an MCF-like gp70 is an invariant aspect of this process, and that observation suggests that this molecule, like the SFFV gp52, may indeed serve to stimulate cell proliferation. The most common means of expressing such a molecule at elevated levels appears to involve recombining it into an ecotropic genome that replicates with high efficiency. Thus, the viral requirements for leukemogenesis may depend on both efficient and perhaps tissue tropic replication as well as on the expression of a particular gp70.(ABSTRACT TRUNCATED AT 400 WORDS)
早期关于小鼠基因极大影响淋巴瘤自发发病率的证明，是该疾病病毒病因被普遍接受的较为持久的障碍之一。我们现在可以相当确定，其中一些小鼠基因是一类称为鼠白血病病毒的逆转录病毒的DNA生命阶段。这些鼠白血病病毒（MuLV）虽然在序列上彼此相关，但却是一组显示出不同宿主范围和组织嗜性模式的病毒。MuLV的宿主范围特性是将它们分类为嗜亲性、异嗜性和双嗜性相关家族的手段，并且可能由gp70上的决定簇决定。另一方面，在不同组织中优先复制的能力可能由位于基因组3'端的控制序列（称为U3）决定。MuLV基因组位于小鼠基因组的许多不同位点。在这些位点发现的病毒基因组可以在体内自发地、在体外通过化学物质或通过DNA转染以不同效率被诱导表达。某些MuLV基因组也可能通过重组或反式互补相互作用以增加表达。虽然解释这些现象的分子机制尚不清楚，但差异表达现象具有重要的病理后果，特别是在淋巴瘤的发展中。内源性MuLV诱导白血病的复杂过程似乎涉及多个MuLV基因组的表达和相互作用。很明显，MCF样gp70的表达是这个过程不变的一个方面，并且该观察结果表明该分子，就像SFFV gp52一样，可能确实起到刺激细胞增殖的作用。以高水平表达这种分子的最常见方式似乎涉及将其重组到高效复制的嗜亲性基因组中。因此，白血病发生的病毒要求可能既取决于高效且可能具有组织嗜性的复制，也取决于特定gp70的表达。（摘要截短至400字）
