Puri A, Hug P, Muñoz-Barroso I, Blumenthal R
Section on Membrane Structure and Function, NCI-FCRDC, Frederick, Maryland 21702-1201, USA.
Biochem Biophys Res Commun. 1998 Jan 6;242(1):219-25. doi: 10.1006/bbrc.1997.7941.
We examined the role of target membrane glycolipids in CD4-mediated HIV-1 fusion by altering the glycolipid levels in CD4+ cells. CD4+ human cells exhibited 50% reduction in extent of fusion with gp120-gp41 expressing cells (TF228) when grown in the presence of a glycolipid synthesis inhibitor PPMP. We added erythrocyte glycolipids (GL) to fusion-incompetent CD4+ non-human cells by influenza-hemagglutinin-mediated fusion between GL-containing liposomes and target cells. Human erythrocyte GL (HuGL)-modified CD4+ non-human cells became susceptible to fusion with TF228 cells. Transfer of bovine erythrocyte glycolipids (BoGL) to CD4+ non-human cells under similar conditions did not complement HIV-1 fusion. Furthermore, addition of HuGL, but not BoGL, to PPMP-inhibited cells rescued fusion to the original levels. Our observations demonstrate that human erythrocyte glycolipids promote CD4-mediated HIV-1 fusion and certain glycolipid(s) from human erythrocytes may serve as alternative and/or additional cofactors in HIV-1 entry.
我们通过改变CD4⁺细胞中的糖脂水平，研究了靶膜糖脂在CD4介导的HIV-1融合中的作用。当在糖脂合成抑制剂PPMP存在的情况下生长时，CD4⁺人类细胞与表达gp120-gp41的细胞（TF228）的融合程度降低了50%。我们通过流感血凝素介导的含GL脂质体与靶细胞之间的融合，将红细胞糖脂（GL）添加到无融合能力的CD4⁺非人类细胞中。人红细胞GL（HuGL）修饰的CD4⁺非人类细胞变得易于与TF228细胞融合。在类似条件下，将牛红细胞糖脂（BoGL）转移到CD4⁺非人类细胞中并不能补充HIV-1融合。此外，向PPMP抑制的细胞中添加HuGL而非BoGL可将融合恢复到原始水平。我们的观察结果表明，人红细胞糖脂促进CD4介导的HIV-1融合，人红细胞中的某些糖脂可能作为HIV-1进入的替代和/或额外辅助因子。
