Gras G S, Dormont D
Laboratoire de Neuropathologie Expérimentale et Neurovirologie, CRSSA, DSV/DPTE, Commissariat à l'Energie Atomique, Fontenay aux Roses, France.
J Virol. 1991 Jan;65(1):541-5. doi: 10.1128/JVI.65.1.541-545.1991.
A human Epstein-Barr virus-transformed B-cell line (IC.1) was characterized for cell surface antigen profile and permissivity to immunodeficiency virus (HIV) infection. According to cocultivation assay with MT2 cells, P24 release, and immunofluorescence assay, complement-sufficient serum enhanced in vitro infection of IC.1 cells. Enhancement occurs independently of the presence of HIV type 1-specific antibodies, although more efficiently when they are present. Blocking experiments with monoclonal antibodies demonstrated that complement receptor type 2 mediates this phenomenon and that the CD4 molecule is required for infection. Enhancement of in vitro infection on IC.1 cells appears closely related to previously described complement-mediated, antibody-dependent enhancement of HIV infection on the T-lymphoblastoid cell line MT2 (W. E. Robinson, Jr., D. C. Montefiori, and W. M. Mitchell, Lancet i:790-794, 1988).
一株人Epstein-Barr病毒转化的B细胞系(IC.1)对细胞表面抗原谱以及对免疫缺陷病毒(HIV)感染的易感性进行了特征分析。根据与MT2细胞的共培养试验、P24释放以及免疫荧光试验,补体充足的血清增强了IC.1细胞的体外感染。这种增强作用的发生与1型HIV特异性抗体的存在无关,不过当存在这些抗体时增强作用更有效。用单克隆抗体进行的阻断实验表明,2型补体受体介导了这一现象,并且感染需要CD4分子。IC.1细胞体外感染的增强似乎与先前描述的补体介导的、抗体依赖的HIV在T淋巴母细胞系MT2上感染的增强密切相关(小W. E. 罗宾逊、D. C. 蒙特菲奥里和W. M. 米切尔,《柳叶刀》i:790 - 794,1988)。