Host cell components affect the sensitivity of HIV type 1 to complement-mediated virolysis.
Host cell components affect the sensitivity of HIV type 1 to complement-mediated virolysis.
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宿主细胞成分影响 1 型 HIV 对补体介导的病毒裂解的敏感性。
DOI：
10.1089/aid.1994.10.829
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发表时间：
1994
影响因子：
1.5
通讯作者：
Spear,GT
中科院分区：
文献类型：
--
作者：
Saifuddin,M;Ghassemi,M;Patki,C;Parker,CJ;Spear,GT
感染能力，全长HIV-1克隆（pNL 4 -3）在7个人细胞系和外周血单核细胞中表达，以评估宿主细胞组分对游离病毒与补体系统相互作用的贡献。在H9细胞系中表达的HIV-1在HIV抗体阳性患者血清和抗V3单克隆抗体的存在下对补体介导的病毒裂解相对敏感，H9细胞系常用于体外感染。在宿主细胞上评估补体受体1、2和3、补体控制蛋白反应性裂解膜抑制剂（MIRL，CD 59）和衰变加速因子（CD 55）以及HLA-DR的表达。病毒对补体的敏感性与MIRL和IgG 2细胞的表达量呈负相关。还评价了来自JY细胞系和突变体JY 33细胞系的HIV的补体介导的病毒溶解，所述突变体JY 33细胞系缺乏磷脂酰肌醇（PI）连接蛋白（包括MIRL和RIRL）的表达。在突变细胞系中表达的病毒比在野生型细胞中表达的病毒对抗体非依赖性以及抗体依赖性补体介导的病毒裂解更敏感。通过显示抗MIRL或抗ESTV抗体诱导补体介导的病毒裂解，直接证明病毒表面存在MIRL和ESTV。这些实验表明，宿主细胞类型可以显著影响HIV对补体介导的病毒裂解的易感性，并表明PI连接的补体控制蛋白在这种抗性中起重要作用。
An infection-competent, full-length HIV-1 clone (pNL4-3) was expressed in seven human cell lines and in peripheral blood mononuclear cells in order to assess the contribution of host cell components toward interaction of free virus with the complement system. HIV-1 expressed in the H9 cell line, which is frequently used forin vitroinfection, was relatively susceptible to complement-mediated virolysis in the presence of both HIV antibody-positive patient serum and an anti-V3 monoclonal antibody. Expression of complement receptors 1, 2, and 3, complement control proteins membrane inhibitor of reactive lysis (MIRL, CD59) and decay-accelerating factor (DAF, CD55), and HLA-DR was assessed on host cells. There was an inverse relationship between the sensitivity of virus to complement and the amount of expression of MIRL and DAF on cells. HIV derived from the JY cell line and the mutant JY33 cell line, which is deficient in expression of phosphatidylinositol (PI)-linked proteins including MIRL and DAF, were also evaluated for complement-mediated virolysis. Virus expressed in the mutant cell line was more sensitive to antibody-independent as well as antibody-dependent complement-mediated virolysis than virus expressed in the wild-type cells. Direct demonstration of the presence of MIRL and DAF on the viral surface was obtained by showing that anti-MIRL or anti-DAF antibody induced complement-mediated virolysis. These experiments show that the host cell type can substantially influence the susceptibility of HIV to complement-mediated virolysis and suggest that PI-linked complement control proteins play an important role in this resistance.