Conti C, Mastromarino P, Orsi N
Istituto di Microbiologia, Facoltà di Medicina, Università di Roma La Sapienza, Italia.
Comp Immunol Microbiol Infect Dis. 1991;14(4):303-13. doi: 10.1016/0147-9571(91)90136-2.
To identify membrane components of CER cells interacting with vesicular stomatitis virus (VSV) during fusion at acidic pH (fusion from without, FFWO) two different approaches have been used, i.e. (i) treating the whole cells with enzymes and (ii) testing the ability of isolated membrane molecules to interfere with FFWO. Phospholipase A2 and C digestion of cells greatly reduced syncytia formation, pointing towards the involvement of lipid structures as target sites for VSV. Cell susceptibility to FFWO was also reduced after neuraminidase, beta-galactosidase or periodate treatment, suggesting that carbohydrate residues may participate in a complex receptor structure required for virus fusion. When membrane molecules were examined separately for their ability to inhibit viral FFWO, phosphatidylserine, phosphatidylinositol, sphingomyelin, cholesterol and GM3 ganglioside were found to be active, confirming the role of membrane lipid moiety in the cell surface structures involved in the early phases of VSV infection.
为了确定在酸性pH条件下(胞外融合,FFWO)与水疱性口炎病毒(VSV)融合过程中与CER细胞相互作用的膜成分,采用了两种不同的方法,即:(i)用酶处理整个细胞,以及(ii)测试分离的膜分子干扰FFWO的能力。用磷脂酶A2和C消化细胞可大大减少合胞体的形成,这表明脂质结构作为VSV的靶位点参与其中。用神经氨酸酶、β-半乳糖苷酶或高碘酸盐处理后,细胞对FFWO的敏感性也降低,这表明碳水化合物残基可能参与病毒融合所需的复杂受体结构。当分别检测膜分子抑制病毒FFWO的能力时,发现磷脂酰丝氨酸、磷脂酰肌醇、鞘磷脂、胆固醇和GM3神经节苷脂具有活性,这证实了膜脂质部分在VSV感染早期阶段所涉及的细胞表面结构中的作用。