Hosaka Y, Fukami Y, Yasuda Y, Bonilla J A
Infect Immun. 1980 Feb;27(2):355-63. doi: 10.1128/iai.27.2.355-363.1980.
Complement-dependent antiviral antibody-mediated lysis of murine cells coated with Sendai virus or its envelope component (P815 mastocytoma cells and L929 cells) was studied with antiviral monospecific sera (anti-F and anti-HN sera). Three types of interactions different in terms of susceptibility of complement-dependent antibody-mediated lysis were distinguished: (i) fusion-positive Sendai viruses induced the susceptibility with both anti-F and anti-HN sera; (ii) fusion-negative envelope particles with F protein induced the susceptibility with only anti-F serum; (iii) noninfectious Sendai viruses with F0 protein induced no susceptibility. The lack of complement-dependent antibody-mediated cytolysis susceptibility in case (iii) was found to be due neither to detachment of cell-associated noninfectious virus in the presence of antiserum nor to antibody-mediated particular redistribution of cell surface virus antigens. Differences in virus or envelope component-cell association in these three cases were discussed.
利用抗病毒单特异性血清(抗F血清和抗HN血清)研究了补体依赖的抗病毒抗体介导的对涂有仙台病毒或其包膜成分的鼠细胞(P815肥大细胞瘤细胞和L929细胞)的裂解作用。根据补体依赖抗体介导裂解的敏感性,区分了三种不同类型的相互作用:(i)融合阳性仙台病毒在用抗F血清和抗HN血清时均诱导敏感性;(ii)带有F蛋白的融合阴性包膜颗粒仅在用抗F血清时诱导敏感性;(iii)带有F0蛋白的非感染性仙台病毒不诱导敏感性。发现情况(iii)中缺乏补体依赖抗体介导的细胞溶解敏感性既不是由于在抗血清存在下细胞相关非感染性病毒的脱离,也不是由于抗体介导的细胞表面病毒抗原的特定重新分布。讨论了这三种情况下病毒或包膜成分与细胞结合的差异。