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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Suppression of HIV-1 infection in primary CD4 T cells transduced with a self-inactivating lentiviral vector encoding a membrane expressed gp41-derived fusion inhibitor.
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Suppression of HIV-1 infection in primary CD4 T cells transduced with a self-inactivating lentiviral vector encoding a membrane expressed gp41-derived fusion inhibitor.

机译：用编码膜表达的gp41衍生的融合抑制剂的自灭活慢病毒载体转导的原代CD4 T细胞中HIV-1感染的抑制。

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摘要

Peptidomimetics of HIV-1 gp41 sequences required for membrane fusion are potent inhibitors of HIV-1 entry. We hypothesize that expression of a membrane-bound gp41-derived fusion inhibitor will confer HIV-1 resistance to primary CD4 T cells. Efficient gene delivery and stable expression of a membrane-bound gp41-derived fusion inhibitor to primary CD4 T cells was accomplished using a self-inactivating lentiviral vector. A potent antiviral effect was observed when transduced CD4 T cells were challenged with a highly virulent CXCR4-tropic strain of HIV-1. Production of soluble p24 in the supernatant was inhibited 100-fold, and cytopathic effects were evident early in non-transduced cells and absent in transduced cells. Expression of the gp41 sequences was not detrimental to CD4 cells as transduced CD4 T cells exhibited a population doubling time that was equivalent to T cells transduced with a control vector. Results from this study support the rationale to use this lentiviral vector targeted at HIV entry as a potential gene therapy for HIV infection.
机译：膜融合所需的HIV-1 gp41序列的拟肽是HIV-1进入的有效抑制剂。我们假设膜结合的gp41衍生的融合抑制剂的表达将赋予HIV-1对原代CD4 T细胞的抵抗力。使用自灭活慢病毒载体可以有效地将基因结合的膜结合gp41衍生的融合抑制剂传递至原代CD4 T细胞，并使之稳定表达。当用高毒力的HIV-1 CXCR4嗜性菌株攻击转导的CD4 T细胞时，观察到有效的抗病毒作用。上清液中可溶性p24的产生被抑制了100倍，并且在非转导细胞中很早就出现了细胞病变作用，而在转导细胞中则没有这种现象。 gp41序列的表达对CD4细胞无害，因为转导的CD4 T细胞的群体倍增时间与对照载体转导的T细胞相当。这项研究的结果支持使用这种针对HIV进入的慢病毒载体作为HIV感染的潜在基因疗法的理由。

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