Snyder H W, Stockert E, Fleissner E
J Virol. 1977 Aug;23(2):302-14. doi: 10.1128/JVI.23.2.302-314.1977.
The Gross cell surface antigen (GCSA), associated with expression of endogenous Gross-type murine leukemia virus (G-MuLV) in tissues of mice, is defined by the cytotoxic reaction of a C57BL/6 antiserum, anti-AKR spontaneous leukemia K36, with cells of the Gross virus-induced C57BL/6 leukemia, Emale symbolG2. Sequential lactoperoxidase-catalyzed radioiodination of Emale symbolG2 cells, Nonidet P-40 lysis, precipitation with anti-K36 serum, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis identified molecules with properties of polyproteins encoded by the gag region of the viral genome. These cell surface species could also be labeled by in vitro culturing of Emale symbolG2 with radioactive glucosamine. The viral specificity of these molecules and their participation in the GCSA typing system were established as follows. (i) Absorption of anti-K36 serum with GCSA(+), but not GCSA(-), leukemias led to a marked decrease in precipitation of these proteins. (ii) The same Emale symbolG2 cell surface proteins were also precipitated by antisera against the MuLV virion proteins p30 and p15. (iii) Anti-K36 was shown to possess antibodies against Gross virus p30 and p15. (iv) "Clearing" the Emale symbolG2 lysate of molecules reactive with anti-p30 or anti-p15 sera removed molecules reactive with anti-K36 serum. (v) Absorption of anti-K36 serum with disrupted G-MuLV virions or with Gross p30 or p15 removed GCSA cytotoxic antibodies; partial absorption was achieved with disrupted Rauscher-MuLV (R-MuLV) or with R-MuLV p30, and no absorption was found with R-MuLV p15. These data show that Emale symbolG2 cells express, on their surfaces, MuLV core polyproteins that apparently can be glycosylated and on which the determinants of GCSA are located.
与小鼠组织中内源性格罗斯型鼠白血病病毒（G-MuLV）表达相关的总细胞表面抗原（GCSA），由C57BL/6抗血清（抗AKR自发性白血病K36）与格罗斯病毒诱导的C57BL/6白血病（雌性符号G2）细胞的细胞毒性反应所定义。对雌性符号G2细胞进行连续的乳过氧化物酶催化的放射性碘化、Nonidet P-40裂解、用抗K36血清沉淀以及十二烷基硫酸钠-聚丙烯酰胺凝胶电泳，鉴定出具有病毒基因组gag区域编码的多聚蛋白特性的分子。这些细胞表面物质也可以通过用放射性葡糖胺体外培养雌性符号G2来标记。这些分子的病毒特异性及其在GCSA分型系统中的参与情况如下确定。（i）用GCSA（+）白血病而非GCSA（-）白血病吸收抗K36血清导致这些蛋白质沉淀明显减少。（ii）针对MuLV病毒粒子蛋白p30和p15的抗血清也沉淀出相同的雌性符号G2细胞表面蛋白。（iii）抗K36被证明含有针对格罗斯病毒p30和p15的抗体。（iv）“清除”雌性符号G2裂解物中与抗p30或抗p15血清反应的分子，会去除与抗K36血清反应的分子。（v）用破坏的G-MuLV病毒粒子或格罗斯p30或p15吸收抗K36血清可去除GCSA细胞毒性抗体；用破坏的劳斯氏肉瘤病毒（R-MuLV）或R-MuLV p30可实现部分吸收，而用R-MuLV p15未发现吸收。这些数据表明，雌性符号G2细胞在其表面表达MuLV核心多聚蛋白，这些蛋白显然可以被糖基化，并且GCSA的决定簇位于其上。
