Mariner J M, McMahon J B, O'Keefe B R, Nagashima K, Boyd M R
Laboratory of Drug Discovery Research and Development, National Cancer Institute, Frederick Cancer Research & Development Center, Maryland 21702-1201, USA.
Biochem Biophys Res Commun. 1998 Jul 30;248(3):841-5. doi: 10.1006/bbrc.1998.9060.
Concentrations of the potent, HIV(human immunodeficiency virus) inactivating protein, cyanovirin-N (CV-N), which completely inhibit HIV-1 infectivity, do not block the binding of soluble CD4-receptor (sCD4) to HIV-1 lysates nor the attachment of intact HIV-1 virions to several target T-cell lines. Furthermore, in contrast to the known disassociative effects of sCD4 on viral envelope glycoproteins, treatment of HIVRF with high concentrations of CV-N results in complete viral inactivation but without apparent shedding of gp120 or other ultrastructural changes. These results are consistent with the view that the virucidal effects of CV-N result from interference with step(s) in the fusion process subsequent to the initial binding of the virus to target cells.
强效的HIV(人类免疫缺陷病毒)灭活蛋白蓝绿菌素-N(CV-N)的浓度能完全抑制HIV-1的感染性,却不会阻断可溶性CD4受体(sCD4)与HIV-1裂解物的结合,也不会阻止完整的HIV-1病毒体与几种靶T细胞系的附着。此外,与sCD4对病毒包膜糖蛋白已知的解离作用相反,用高浓度的CV-N处理HIVRF会导致病毒完全失活,但不会明显脱落gp120或出现其他超微结构变化。这些结果与以下观点一致,即CV-N的杀病毒作用是由于干扰了病毒与靶细胞初始结合后融合过程中的某个(些)步骤。