Zeichhardt H, Habermehl K O, Wetz K
J Gen Virol. 1983 Apr;64 (Pt 4):951-5. doi: 10.1099/0022-1317-64-4-951.
The preexistence of a cytoplasmic membrane complex in HEp-2 cells, induced by poliovirus when inhibited in its reproduction by guanidine, was a prerequisite for accelerated reproduction of superinfecting Mouse Elberfeld (ME) virus. Guanidine-inhibited poliovirus induced a membrane complex of 470S that was successively modified into a faster sedimenting membrane complex (up to 700S) by superinfecting ME virus and exploited for ME virus reproduction. The modified membrane complex was the site for ME virus-specific RNA polymerization characterized by the existence of in vivo and in vitro activity of ME virus RNA polymerase associated with the modified membrane complex. Proof of membrane-bound RNA polymerase and newly synthesized ME virus RNA including replicative intermediate led to the conclusion that superinfecting ME virus exploits the 'poliovirus/guanidine'-induced complex as the site of action of its replication complex.
当脊髓灰质炎病毒在繁殖过程中被胍抑制时,HEp-2细胞中会预先存在一种细胞质膜复合物,这是超级感染的小鼠埃尔伯费尔德(ME)病毒加速繁殖的前提条件。被胍抑制的脊髓灰质炎病毒诱导形成一种470S的膜复合物,该复合物会被超级感染的ME病毒相继修饰成沉降更快的膜复合物(高达700S),并被用于ME病毒的繁殖。修饰后的膜复合物是ME病毒特异性RNA聚合的场所,其特征是与修饰后的膜复合物相关的ME病毒RNA聚合酶在体内和体外均有活性。膜结合RNA聚合酶以及包括复制中间体在内的新合成的ME病毒RNA的证据得出结论,超级感染的ME病毒利用“脊髓灰质炎病毒/胍”诱导的复合物作为其复制复合物的作用位点。