脊髓灰质炎病毒感染的HeLa细胞对胍敏感的钠离子积累
Guanidine-sensitive Na+ accumulation by poliovirus-infected HeLa cells.
作者信息
Nair C N, Stowers J W, Singfield B
出版信息
J Virol. 1979 Jul;31(1):184-9. doi: 10.1128/JVI.31.1.184-189.1979.
Abstract
The Na+ content of poliovirus-infected HeLa S3 cells increased during the late phase of virus replication, after virus inhibition of host cell protein synthesis and in coincidence with late viral functions. Guanidine hydrochloride blocked the rise in Na+ content, whereas the antiguanidine agent choline fully reversed the guanidine block. Expression of one or more late viral functions was essential for Na+ accumulation to occur because accumulation was inhibited by cycloheximide or guanidine added to the infected culture during the late phase. Increased adenosine triphosphatase activity appears to be primarily responsible for Na+ accumulation by virus-infected cells.
摘要
脊髓灰质炎病毒感染的HeLa S3细胞的Na⁺含量在病毒复制后期、病毒抑制宿主细胞蛋白质合成后以及与病毒晚期功能同时出现时增加。盐酸胍阻止了Na⁺含量的升高，而抗胍剂胆碱完全逆转了胍的阻断作用。一种或多种病毒晚期功能的表达对于Na⁺积累的发生至关重要，因为在后期向感染培养物中添加环己酰亚胺或胍会抑制积累。腺苷三磷酸酶活性的增加似乎是病毒感染细胞积累Na⁺的主要原因。
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