O'Brien S J, Simonson J M, Boone C W
J Gen Virol. 1976 Nov;33(2):355-60. doi: 10.1099/0022-1317-33-2-355.
We have used a quantitative radiolabelled antibody procedure to measure the amount of certain virus structural antigens on the surface of BALB/c RAG cells producing endogenous B-tropic type C virus. RAG cells expressed group specificities of MuLV p30 on their cell surface but did not express gp70 group specificities. However, type specificities of gp70 were expressed on BALB/c cell lines infected with Moloney leukaemia virus. The majority of p30 antigens detected on the RAG cell surface were removed by trypsin and their reappearance was prevented by cycloheximide, even in the presence of 'conditioned medium' containing MuLV. Passive adsorption of exogenous MuLV p30 to the surface of virus negative BALB/c fibroblasts reached a maximum of 20% of the protein detectable on virus producing RAG cells. These data support the hypothesis that much, but not all, of the surface p30 is expressed de novo on the cell membrane and not derived from passive adsorption of p30 released from shed virus or as a by-product of virus infection of a cell.
我们采用了一种定量放射性标记抗体方法，来测量产生内源性B嗜性C型病毒的BALB/c RAG细胞表面特定病毒结构抗原的量。RAG细胞在其细胞表面表达了莫洛尼白血病病毒（MuLV）p30的群特异性，但未表达gp70群特异性。然而，在感染了莫洛尼白血病病毒的BALB/c细胞系上表达了gp70的型特异性。在RAG细胞表面检测到的大多数p30抗原可被胰蛋白酶去除，并且即使在含有MuLV的“条件培养基”存在的情况下，放线菌酮也能阻止其再次出现。外源性MuLV p30被动吸附到病毒阴性的BALB/c成纤维细胞表面，其吸附量最高可达产生病毒的RAG细胞上可检测到蛋白质的20%。这些数据支持了这样一种假说，即细胞表面的p30大部分（但不是全部）是在细胞膜上重新合成的，并非来自脱落病毒释放的p30的被动吸附，也不是细胞病毒感染的副产物。
