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脊髓灰质炎病毒诱导的细胞质膜复合物被超感染的小鼠埃尔伯费尔德(ME)病毒的RNA聚合酶利用。

A poliovirus-induced cytoplasmic membrane complex is exploited by the RNA polymerase of superinfecting Mouse Elberfeld (ME) virus.

作者信息

Zeichhardt H, Habermehl K O, Wetz K

出版信息

J Gen Virol. 1983 Apr;64 (Pt 4):951-5. doi: 10.1099/0022-1317-64-4-951.

Abstract

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.

摘要

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。

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