Clotet-Codina Imma, Bosch Berta, Senserrich Jordi, Fernández-Figueras María Teresa, Peña Ruth, Ballana Ester, Bofill Margarita, Clotet Bonaventura, Esté José A
Retrovirology Laboratory IrsiCaixa, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Badalona, Spain.
Antiviral Res. 2009 Jul;83(1):94-8. doi: 10.1016/j.antiviral.2009.03.009. Epub 2009 Apr 5.
Contacts between HIV-producing T cells and primary CD4+ T cells may induce the uptake of HIV by target cells that are endocytosed into trypsin-resistant compartments. We have now compared the mechanism of virus transmission from T cell-to-T cell versus infected dendritic cells (DCs)-to-T cell. In cocultures of HIV-1-infected DCs with primary CD4+ T cells, virus transmission to the target cells was resistant to trypsin treatment and could only be prevented by the anti-SUgp120 antibody IgGb12 but not by TAK-779, C34 or AZT. Importantly, upon stimulation of purified HIV-1-loaded CD4+ T cells with PHA/IL-2, cells became productively infected as measured by intracellular CAp24 staining and antigen determination in the cell supernatant. These results suggest that the viral endocytic transfer may represent a escape mechanism in the presence of drugs targeting HIV-1 entry or the host immune system.
产生HIV的T细胞与原代CD4+ T细胞之间的接触可能会诱导靶细胞摄取HIV，这些靶细胞会被内吞到对胰蛋白酶有抗性的区室中。我们现在比较了病毒从T细胞到T细胞与从感染的树突状细胞（DC）到T细胞的传播机制。在HIV-1感染的DC与原代CD4+ T细胞的共培养中，病毒向靶细胞的传播对胰蛋白酶处理有抗性，并且只能通过抗SUgp120抗体IgGb12阻止，而不能通过TAK-779、C34或AZT阻止。重要的是，在用PHA/IL-2刺激纯化的负载HIV-1的CD4+ T细胞后，通过细胞内CAp24染色和细胞上清液中的抗原测定发现细胞被有效感染。这些结果表明，在存在针对HIV-1进入或宿主免疫系统的药物的情况下，病毒的内吞转移可能代表一种逃逸机制。
