Sheffield J B, Zacharchuk C M, Taraschi N, Daly T M
J Virol. 1976 Jul;19(1):255-66. doi: 10.1128/JVI.19.1.255-266.1976.
Undisrupted mouse mammary tumor virus (MuMTV) derived from the milk of of RIII mice has been analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and electron microscopy after treatment with insolubilized trypsin. No alterations were found in viral fine structure by either freeze-etch or negative-stain electron microscopy. No alterations were found in the ability of trypsinized virus to compete in a radioimmune assay for viral antigens. Infectivity experiments indicate no significant differences in the ability of treated virus to infect C57Bl mice. However, significant differences were observed in polypeptide composition. The intensely periodic acid-Schiff-positive band, gp140, was shown by galactose oxidase-borotritide labeling to be degraded into a fragment of 125,000 molecular weight. The major glycoprotein, gp55, was split into fragments of 36,000 and 23,000 molecular weight, both of which stained with periodic acid-Schiff stain. Gp68 was removed from the virus. Experiments with purified, iodinated gp55 showed that the trypsin-induced fragments of gp55 were immunologically active. We conclude that: (i) certain glycoproteins at the surface of MuMTV are accessible to an insoluble form of trypsin, (ii) the trypsin causes a nick in the polypeptide chain without affecting the configuration of the molecule; (iii) the nicked molecules remain bound to the virus; and (iv) the presence of these nicked molecules does not interfere with the biological or antigenic expression of virus function.
对源自RIII小鼠乳汁的未受干扰的小鼠乳腺肿瘤病毒(MuMTV),在用不溶性胰蛋白酶处理后,通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳和电子显微镜进行了分析。无论是冷冻蚀刻还是负染色电子显微镜检查,均未发现病毒精细结构有改变。在放射免疫分析中,经胰蛋白酶处理的病毒竞争病毒抗原的能力未发现改变。感染性实验表明,处理后的病毒感染C57Bl小鼠的能力没有显著差异。然而,在多肽组成上观察到了显著差异。经半乳糖氧化酶-硼氢化氚标记显示,强Periodic acid-Schiff阳性条带gp140被降解为分子量为125,000的片段。主要糖蛋白gp55被裂解为分子量为36,000和23,000的片段,二者均能被Periodic acid-Schiff染色。Gp68从病毒中去除。用纯化的碘化gp55进行的实验表明,胰蛋白酶诱导的gp55片段具有免疫活性。我们得出以下结论:(i)MuMTV表面的某些糖蛋白可被不溶性形式的胰蛋白酶作用;(ii)胰蛋白酶在多肽链上造成切口但不影响分子构型;(iii)有切口的分子仍与病毒结合;(iv)这些有切口的分子的存在不干扰病毒功能的生物学或抗原性表达。