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首页> 外文期刊>Journal of Virology >Sendai Virus Envelopes Can Mediate Epstein-Barr Virus Binding to and Penetration into Epstein-Barr Virus Receptor-Negative Cells
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Sendai Virus Envelopes Can Mediate Epstein-Barr Virus Binding to and Penetration into Epstein-Barr Virus Receptor-Negative Cells

机译：仙台病毒信封可以将Epstein-Barr病毒介绍并渗透到Epstein-Barr病毒受体阴性细胞中

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Epstein-Barr virus (EBV) receptor-negative cells were treated with UV-inactivated Sendai virus (SV) or with reconstituted SV envelopes having a low hemolytic activity and then assayed for EBV binding or for susceptibility to EBV infection. EBV binding was assessed by using both unlabeled and fluoresceinated EBV preparations. It was found that SV or SV envelope treatment renders these cells able to bind EBV. Various experiments were performed to clarify the mechanism of this SV-induced binding. The EBV receptor-negative 1301 cells were treated with SV either at 0°C or at both 0 and 37°C successively and then examined for EBV binding at 0°C. It was thus found that when SV treatment was performed exclusively at 0°C, the target cells showed higher fluorescence intensity after their incubation with fluoresceinated EBV. In addition, Clostridium perfringens neuraminidase treatment of 1301 cells did not induce any EBV binding to these cells. These data indicate that EBV binding is not due to the disturbance of the cell membrane by SV envelope fusion or to the uncovering of EBV binding sites on the cells after the enzymatic action of SV neuraminidase. Moreover, bound EBV was partly eluted from SV-treated 1301 cells at 37°C, and the treatment of EBV with C. perfringens neuraminidase inhibited its SV-mediated binding. These data indicate that EBV binds to the hemagglutinin-neuraminidase of SV on the target cell surface and that a fraction of the bound EBV becomes irreversibly associated with the SV-treated cell membrane. Our data also show that EBV can penetrate into 1301 cells which have incorporated SV envelopes into their membrane, as demonstrated by the induction of the EBV-determined nuclear antigen by B95-8 EBV in SV envelope-treated 1301 cells.
机译：用UV - 灭活的仙台病毒（SV）处理Epstein-Barr病毒（EBV）受体阴性细胞，或者具有低溶血活性的重构的SV包络，然后测定EBV结合或易受EBV感染的敏感性。通过使用未标记和荧光的EBV制剂来评估EBV结合。发现SV或SV包络处理使得能够结合EBV的这些细胞。进行各种实验以阐明该血液诱导的结合的机制。将EBV受体阴性1301细胞连续用SV或在0℃和37℃下均匀处理，然后在0℃下检查EBV结合。因此发现，当SV处理完全在0℃下进行时，靶细胞与荧光沸腾的EBV孵育后呈较高的荧光强度。此外，梭菌菌株 Neuraminidase治疗1301细胞的治疗并未诱导任何与这些细胞的EBV结合。这些数据表明EBV结合不是由于细胞膜通过SV包络融合的干扰或在细胞上露出细胞上的EBV结合位点之后的SV神经氨酸酶的酶促作用。此外，将结合的EBV在37℃下部分从SV处理的1301个细胞中洗脱，并用 C处理EBV。 perfringens 神经氨酸酶抑制其SV介导的结合。这些数据表明EBV与靶细胞表面上的SV的血凝素 - 神经氨酸酶结合，并且结合的EBV的一部分与SV处理的细胞膜不可逆地相关。我们的数据还表明，EBV可以渗透到1301个细胞中，该细胞已将SV包络掺入膜中，如通过在SV包膜处理的1301个细胞中诱导EBV确定的核抗原的诱导。

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