Ghendon Y, Tucková E, Vonka V, Klimov A, Ginzburg V, Markushin S
J Gen Virol. 1979 Jul;44(1):179-86. doi: 10.1099/0022-1317-44-1-179.
The replication of influenza viruses A/NWS-D, A/WS-MK and their r12 recombinant in human embryo fibroblast (HEF) and human diploid fibroblast (LEP) cell lines was studied. In HEF cells virus NWS-D and recombinant r12 induced synthesis of virus-specific macromolecules and produced infectious virions; virus WS-MK induced synthesis of virus complementary RNA (cRNA), virion RNA (vRNA), protein, RNP and non-infectious virions, but haemagglutinin cleavage was impaired and the virions formed contained uncleaved haemagglutinin. In LEP cells, infectious virions were formed only by virus NWS-D; viruses WS-MK and r12 induced synthesis of virus cRNA, vRNA, proteins and RNP; virus r12 had the haemagglutinin cleaved, whereas in virus WS-MK this process was impaired; neither virus WS-MK nor r12 was capable of forming virions. Analysis of the recombinant r12 genome showed that it had only inherited a single gene from NWS-D, the one coding for neuraminidase, having inherited all others (P1, P2, P3, HA, NP, M, NS) from WS-MK. The data obtained suggested that the inability of virus WS-MK to form infectious virions in HEF cells is due to the character of its neuraminidase, which is incapable of participating in haemagglutinin cleavage. The deficient reproduction of this virus in the other host-cell system (LEP) is apparently associated with some characteristics of another protein (other proteins) of this virus.
对甲型流感病毒A/NWS-D、A/WS-MK及其r12重组体在人胚成纤维细胞(HEF)和人二倍体成纤维细胞(LEP)细胞系中的复制情况进行了研究。在HEF细胞中,病毒NWS-D和重组体r12诱导了病毒特异性大分子的合成并产生了感染性病毒粒子;病毒WS-MK诱导了病毒互补RNA(cRNA)、病毒粒子RNA(vRNA)、蛋白质、核糖核蛋白(RNP)和非感染性病毒粒子的合成,但血凝素裂解受损,形成的病毒粒子含有未裂解的血凝素。在LEP细胞中,仅病毒NWS-D形成了感染性病毒粒子;病毒WS-MK和r12诱导了病毒cRNA, vRNA、蛋白质和RNP的合成;病毒r12的血凝素被裂解,而在病毒WS-MK中此过程受损;病毒WS-MK和r12均不能形成病毒粒子。对重组体r12基因组的分析表明,它仅从NWS-D继承了一个基因,即编码神经氨酸酶的基因,而所有其他基因(P1、P2、P3、血凝素(HA)、核蛋白(NP)、基质蛋白(M)、非结构蛋白(NS))均从WS-MK继承。所获得的数据表明,病毒WS-MK在HEF细胞中无法形成感染性病毒粒子是由于其神经氨酸酶的特性,该神经氨酸酶无法参与血凝素裂解。该病毒在另一种宿主细胞系统(LEP)中的繁殖缺陷显然与该病毒的另一种蛋白质(其他蛋白质)的某些特性有关。