Bosch J V, Tlusty A, McDowell W, Legler G, Schwarz R T
Virology. 1985 May;143(1):342-6. doi: 10.1016/0042-6822(85)90122-9.
The effects of inhibitors, which interfere with oligosaccharide trimming by blocking mannosidases, on the processing and export of the viral glycoproteins of Rous sarcoma virus (RSV), have been studied. 1-Deoxymannojirimycin (DIM) prevents removal of mannose residues from the Man9 (GlcNAc)2 oligosaccharide whereas swainsonine (SW) blocks at a later stage resulting in the formation of so-called hybrid oligosaccharides. Under a regime of these inhibitors, proteolytic cleavage of the viral glycoprotein precursor can still occur to yield aberrant glycoprotein products, gp75DIM/gp30DIM and gp80SW/gp30SW. Virus particles carrying these aberrant viral glycoproteins are released from inhibitor-treated cultures in normal amounts and these virions are fully infectious. Thus blocking oligosaccharide trimming at the stages described here or, using different inhibitors, at different stages as described previously (J. V. Bosch and R. T. Schwarz, Virology 132, 95-109 (1984)), does not have any influence on the infectivity of Rous sarcoma virus.
已经研究了通过阻断甘露糖苷酶来干扰寡糖修剪的抑制剂对劳氏肉瘤病毒（RSV）病毒糖蛋白加工和输出的影响。1-脱氧甘露基野尻霉素（DIM）可防止从Man9（GlcNAc）2寡糖中去除甘露糖残基，而苦马豆素（SW）则在后期阻断，导致形成所谓的杂合寡糖。在这些抑制剂的作用下，病毒糖蛋白前体的蛋白水解切割仍可发生，产生异常的糖蛋白产物，即gp75DIM/gp30DIM和gp80SW/gp30SW。携带这些异常病毒糖蛋白的病毒颗粒以正常数量从经抑制剂处理的培养物中释放出来，并且这些病毒粒子具有完全的感染性。因此，在此处所述阶段阻断寡糖修剪，或者如先前所述（J. V. Bosch和R. T. Schwarz，《病毒学》132，95 - 109（1984））使用不同抑制剂在不同阶段阻断寡糖修剪，对劳氏肉瘤病毒的感染性没有任何影响。
