Bach C, Cramer A, Scholtissek C
Institut für Virologie, Justus-Liebig-Universität Giessen, Germany.
J Gen Virol. 1995 Apr;76 ( Pt 4):1025-32. doi: 10.1099/0022-1317-76-4-1025.
In the presence of the methyltransferase inhibitor 3-deazaadenosine (3DA-Ado) the production of infectious Autographa californica nuclear polyhedrosis virus (AcMNPV) in tissue culture was only slightly affected, while the synthesis of very late proteins (polyhedrin and p10) was abolished. The synthesis of the influenza virus proteins NS1 and HA, expressed under the polyhedrin promoter, was also abolished by 3DA-Ado. Furthermore, 3DA-Ado interfered with the shut-off of early and late AcMNPV proteins. Most of these results were also obtained with 5-azadeoxycytidine (5A-dCyt). In cells in which NS1 was produced abundantly, at least one specific AcMNPV protein was not synthesized. However, if the production of NS1 was inhibited by 3DA-Ado, or if HA was synthesized instead, this AcMNPV protein showed up normally.
在甲基转移酶抑制剂3 - 脱氮腺苷(3DA - Ado)存在的情况下,苜蓿银纹夜蛾核型多角体病毒(AcMNPV)在组织培养中的感染性产生仅受到轻微影响,而极晚期蛋白(多角体蛋白和p10)的合成则被消除。在多角体蛋白启动子控制下表达的流感病毒蛋白NS1和HA的合成也被3DA - Ado消除。此外,3DA - Ado干扰了AcMNPV早期和晚期蛋白的关闭。使用5 - 氮杂脱氧胞苷(5A - dCyt)也获得了大多数这些结果。在大量产生NS1的细胞中,至少有一种特定的AcMNPV蛋白没有合成。然而,如果3DA - Ado抑制了NS1的产生,或者如果改为合成HA,这种AcMNPV蛋白会正常出现。