Gonzalez R, Matsiota P, Torchy C, De Kinkelin P, Avrameas S
Unité d'Immunocytochimie, CNRS URA 359, Institut Pasteur.
Res Immunol. 1989 Sep;140(7):675-84. doi: 10.1016/0923-2494(89)90021-7.
Normal and viral-infected rainbow trout (RT) were tested for serum antibody activity against self and nonself antigens. Particularly high titres of anti-trinitrophenyl (TNP) antibodies were noted, as in other fish species. To analyse this, the anti-TNP antibodies were isolated by affinity chromatography and their capacity to interfere with viral infection in vitro was studied. We selected RT fibroblasts as target cells, and two common pathogenic viruses in trout, a rhabdovirus, viral haemorrhagic septicaemia virus (VHS) and a birnavirus, the infectious pancreatic necrosis virus (IPN). Anti-TNP antibodies were examined for their capacity to neutralize VHS and IPN viruses. Data obtained show that the anti-TNP antibodies, even at high concentrations, only partially neutralized virus. In contrast, when anti-TNP antibodies were assayed for their protective activity using RT fibroblast cells infected with VHS or IPN viruses, results showed high protective activity, regardless of serum origin or of the virus used, when the antibodies were added to the cell culture after viral infection. Therefore, our experiments indicate that the protective activity does not seem to be due to a direct interaction of the antibodies with the viruses. It is suggested that virus-modified cell surface self structures exhibit new epitopes which interact with the anti-TNP antibodies. Such an interaction would allow anti-TNP antibodies to participate in a non-specific defence mechanism against viral infection.
对正常和病毒感染的虹鳟鱼(RT)进行了针对自身和非自身抗原的血清抗体活性测试。与其他鱼类一样,发现其抗三硝基苯基(TNP)抗体的滴度特别高。为了对此进行分析,通过亲和层析分离出抗TNP抗体,并研究了它们在体外干扰病毒感染的能力。我们选择虹鳟鱼成纤维细胞作为靶细胞,以及虹鳟鱼中两种常见的致病病毒,一种弹状病毒,即病毒性出血性败血症病毒(VHS)和一种双RNA病毒,即传染性胰腺坏死病毒(IPN)。检测抗TNP抗体中和VHS和IPN病毒的能力。获得的数据表明,即使在高浓度下,抗TNP抗体也只能部分中和病毒。相反,当使用感染了VHS或IPN病毒的虹鳟鱼成纤维细胞检测抗TNP抗体的保护活性时,结果显示,在病毒感染后将抗体添加到细胞培养物中时,无论血清来源或所用病毒如何,都具有很高的保护活性。因此,我们的实验表明,保护活性似乎不是由于抗体与病毒的直接相互作用。有人提出,病毒修饰的细胞表面自身结构会呈现出新的表位,这些表位会与抗TNP抗体相互作用。这种相互作用将使抗TNP抗体参与针对病毒感染的非特异性防御机制。