Gaur Arti, Green William R
Department of Microbiology and Immunology, and the Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA.
Viral Immunol. 2003;16(2):203-12. doi: 10.1089/088282403322017938.
In genetically susceptible strains, such as C57BL/6 (B6) mice, LP-BM5 causes murine AIDS (MAIDS). LP-BM5 is a complex mixture of murine leukemia viruses (MuLV) that includes replication competent ecotropic (BM5eco) and mink cell focus inducing (MCF), and replication defective (BM5d) MuLV. At present, for the BM5eco virus, sequence information on only the gag region is available. In this paper, we describe for the first time the sequencing of the entire BM5eco viral genome as well as analysis of homology with two other previously sequenced and well-characterized MuLVs, Emv-11 and Emv-2, the latter constituting the parental virus for BM5eco. We propose that the detailed sequence comparisons herein provide cogent evidence that BM5eco utilizes variations in cytotoxic T lymphocytes (CTL) epitopes as an immune escape mechanism. This CTL evasion mechanism may contribute substantially to the underlying prototypic susceptibility of B6 mice to LP-BM5-induced MAIDS.
在基因易感品系中，如C57BL/6（B6）小鼠，LP - BM5可引发鼠类获得性免疫缺陷综合征（MAIDS）。LP - BM5是一种鼠白血病病毒（MuLV）的复杂混合物，包括具有复制能力的亲嗜性（BM5eco）和貂细胞集落形成诱导（MCF）病毒，以及复制缺陷型（BM5d）MuLV。目前，对于BM5eco病毒，仅可获得gag区域的序列信息。在本文中，我们首次描述了整个BM5eco病毒基因组的测序，以及与另外两种先前测序且特征明确的MuLV（Emv - 11和Emv - 2）的同源性分析，后者是BM5eco的亲本病毒。我们提出，本文详细的序列比较提供了有力证据，表明BM5eco利用细胞毒性T淋巴细胞（CTL）表位的变异作为一种免疫逃逸机制。这种CTL逃避机制可能在很大程度上导致B6小鼠对LP - BM5诱导的MAIDS具有潜在的典型易感性。
