Kropotkina E A, Rudneva I A, Rusanova O S, Varich N L, Kadoshnikov Iu P, Gambarian A S, Kaverin N V
Vopr Virusol. 1998 Jan-Feb;43(1):17-20.
The mechanism of decrease in the level of virus accumulation in reassortants with hemagglutinin (HA) and neuraminidase (NA) genes from different parents is studied. The reassortant viruses and their passage variants do not differ by the rate of virus protein production or their stability in infected cells. Electron microscopy and titration of infectious virus in culture fluid and cell-associated virus showed that the variants selected by serial passages accumulated mainly in the culture fluid, whereas the initial reassortant virions were predominantly cell-associated. These data suggest that incomplete removal of sialic acid residues by viral neuraminidase N1 in some reassortants results in re-attachment of virions to the infected cells and thus impairs the virus dissemination, which may be regarded as a reassortant-limiting factor probably significant for virus evolution.
研究了具有来自不同亲本的血凝素(HA)和神经氨酸酶(NA)基因的重配体中病毒积累水平降低的机制。重配病毒及其传代变体在病毒蛋白产生速率或其在感染细胞中的稳定性方面没有差异。电子显微镜检查以及对培养液中感染性病毒和细胞相关病毒的滴定表明,通过连续传代选择的变体主要积累在培养液中,而初始重配病毒粒子主要与细胞相关。这些数据表明,在一些重配体中,病毒神经氨酸酶N1对唾液酸残基的不完全去除导致病毒粒子重新附着于感染细胞,从而损害病毒传播,这可能被视为一个可能对病毒进化具有重要意义的重配限制因素。