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首页> 美国卫生研究院文献>Journal of Virology >Factors involved in entry of the human immunodeficiency virus type 1 into permissive cells: lack of evidence of a role for CD26.
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Factors involved in entry of the human immunodeficiency virus type 1 into permissive cells: lack of evidence of a role for CD26.

机译：1型人类免疫缺陷病毒进入允许细胞的参与因素：缺乏CD26作用的证据。

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It has been proposed recently that the cell surface peptidase CD26 acts in concert with CD4, the human immunodeficiency virus (HIV) primary receptor molecule, to mediate HIV entry into permissive cells. We have failed to detect significant levels of CD26 cell surface expression and enzymatic activity in a number of commonly propagated human CD4+ cell lines, although CD26 mRNA was present at very low levels, as detected by reverse transcription PCR. No relationship existed between the expression of CD26 and the ability of these cells to be infected with HIV or to fuse to form syncytia. We have tested two inhibitors of CD26 enzymatic activity and several anti-CD26 monoclonal antibodies and found that they inhibit neither HIV infection nor HIV-induced syncytium formation. NIH 3T3 cells stably transfected with the cDNAs for human CD4 and CD26 expressed these molecules at the cell surface and had CD26 enzymatic activity. Inoculation of the double transfectants with HIV did not result in virus entry above the background level, as verified by PCR amplification of viral DNA. We were unable to recover infectious virus from the HIV-inoculated NIH 3T3 double transfectants either by transfer of supernatants or by cocultivation with human CD4+ indicator cells. Moreover, the transfectants did not fuse with HIV-infected cells to form syncytia, nor were syncytia observed in HIV-inoculated cultures. These results are inconsistent with the CD26 molecule being a cofactor for entry of HIV in CD4+ cells.
机译：最近已经提出，细胞表面肽酶CD26与人免疫缺陷病毒（HIV）主要受体分子CD4协同作用，以介导HIV进入允许细胞。尽管通过反转录PCR检测到CD26 mRNA的含量非常低，但我们仍未在许多通常繁殖的人CD4 +细胞系中检测到显着水平的CD26细胞表面表达和酶活性。 CD26的表达与这些细胞感染HIV或融合形成合胞体的能力之间没有关系。我们测试了两种CD26酶促活性抑制剂和几种抗CD26单克隆抗体，发现它们既不抑制HIV感染，也不抑制HIV诱导的合胞体形成。用人CD4和CD26的cDNA稳定转染的NIH 3T3细胞在细胞表面表达了这些分子，并具有CD26的酶促活性。如通过病毒DNA的PCR扩增所证实的，用HIV接种双重转染子不会导致病毒进入本底水平以上。我们无法通过转移上清液或与人CD4 +指标细胞共培养而从HIV感染的NIH 3T3双转染子中恢复感染性病毒。此外，转染子没有与HIV感染的细胞融合形成合胞体，在HIV感染的培养物中也没有观察到合胞体。这些结果与CD26分子是HIV进入CD4 +细胞的辅助因子不一致。

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