MECHANISM OF VACCINIA VIRUS RELEASE AND ITS SPECIFIC-INHIBITION BY N1-ISONICOTINOYL-N2-3-METHYL-4-CHLOROBENZOYLHYDRAZINE
MECHANISM OF VACCINIA VIRUS RELEASE AND ITS SPECIFIC-INHIBITION BY N1-ISONICOTINOYL-N2-3-METHYL-4-CHLOROBENZOYLHYDRAZINE
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DOI：
10.1128/jvi.32.2.614-622.1979
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发表时间：
1979-01-01
影响因子：
5.4
通讯作者：
KRISTENSON, K
中科院分区：
文献类型：
--
作者：
PAYNE, LG;KRISTENSON, K
研究了牛痘病毒在RK-13（兔肾）细胞中的释放及其被n1 -异烟碱- n2 -3-甲基-4-氯苯甲酰肼（IMCBH）特异性抑制的情况。细胞内裸痘苗病毒（INV）被胞质内膜包裹，形成细胞内双膜病毒粒子。包裹的病毒粒子迁移到细胞表面，在那里外病毒粒子膜可能与质膜融合，释放出被内膜包围的病毒，称为细胞外包膜痘苗病毒（EEV）。在任何时候都没有证据表明牛痘病毒是通过细胞质膜上的裸病毒出芽而获得包膜的。感染后8和12 h，裸膜病毒和双膜病毒各占细胞内病毒的1/3左右。从16 h开始，细胞内病毒以双膜病毒形式出现的比例稳步下降至24 h的1%，而裸膜病毒的比例上升至87%。IMCBH抑制了双膜病毒粒子的形成和EEV的出现，但不影响INV的产生。IMCBH对INV的感染性、多肽组成、痘苗病毒特异性膜相关蛋白或糖蛋白以及血液吸附没有影响。IMCBH的存在直到4小时，并没有减少48小时的EEV量，而如果药物在前16小时存在，则获得不到正常48小时EEV产量的10%。在没有药物的情况下，以非常低的增殖率感染的细胞培养显示出病毒的快速传播，而IMCBH的存在非常有效地抑制了这种传播。显然，牛痘病毒通过双膜中间体作为包膜病毒粒子被释放，正是这种细胞外包膜病毒负责感染的传播。
The release of vaccinia virus from RK-13 [rabbit kidney] cells and its specific inhibition by N1-isonicotinoyl-N2-3-methyl-4-chlorobenzoylhydrazine (IMCBH) was studied. Intracellular naked vaccinia virus (INV) was wrapped by intracytoplasmic membranes, forming an intracellular double-membraned virion. Wrapped virions migrated to the cell surface where the outer virion membrane presumably fused with the plasma membrane, releasing virus surrounded by the inner membrane, referred to as extracellular enveloped vaccinia virus (EEV). At no time was there any evidence that vaccinia virus acquired an envelope by budding of naked virus from the cytoplasmic membrane. Naked virus and double-membraned virus each constituted about 1/3 of intracellular virus at 8 and 12 h postinfection (p.i.). Beginning at 16 h p.i., the proportion of intracellular virus occurring as double-membraned virus steadily decreased to 1% at 24 h while the proportion of naked virus rose to 87%. IMCBH inhibited the formation of the double-membraned virion and the appearance of EEV while not affecting the production of INV. IMCBH had no effect on INV infectivity or polypeptide composition, on vaccinia virus-specified membrane-associated proteins or glycoproteins or on hemadsorption. The presence of IMCBH until 4 h p.i. did not decrease the amount of EEV at 48 h p.i., whereas less than 10% of the normal 48-h EEV yield was obtained if the drug was present during the first 16 h p.i. Cell cultures infected at very low multiplicities showed a rapid virus dissemination in the absence of the drug, whereas the presence of IMCBH very effectively inhibited this spread. Apparently, vaccinia virus is liberated via a double-membraned intermediate as an enveloped virion and it is this extracellular enveloped virus that is responsible for dissemination of infection.