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[人类免疫缺陷病毒gp160蛋白在感染细胞中的病理性裂解作为感染慢性化的一个可能因素]

[Pathological cleavage of human immunodeficiency virus gp160 protein in infected cells as a probable factor for infection becoming chronic].

作者信息

Veselovskaia T V, Rykova L A, Selimova L M, Zaĭdes V M

出版信息

Mol Biol (Mosk). 1993 Jan-Feb;27(1):211-21.

PMID:8483471
Abstract

The synthesis of HIV-1 (IIIb isolate) structural protein in chronically (CI) and acutely infected (AI) MT4 cells was studied. During long-term cultivation the CI system was characterized by high involvement of the cells into infection (up to 100%), high level of virus-specific protein synthesis, moderate virus yield, but absence of any virus-induced cytopathic effects and normal growth potential of infected cells. AI cells demonstrated a similar level of synthesis of virus specific proteins, higher virus yield, and rapid progression of cytopathicity followed by total cell death. Most of the HIV gp160 protein molecules undergo rapid cleavage in the region between the point of conventional cleavage and the transmembrane domain, being removed from the physiologically competent pool, but a small portion of gp160s undergo apparently normal intracellular development. According to our data, the two HIV variants (normal and defective) persist in CI system and pathological cleavage of defective virus gp160 protein results most probably in chronization of infection.

摘要

研究了HIV-1(IIIb分离株)结构蛋白在慢性感染(CI)和急性感染(AI)的MT4细胞中的合成情况。在长期培养过程中,CI系统的特点是细胞参与感染的程度高(高达100%),病毒特异性蛋白合成水平高,病毒产量中等,但没有任何病毒诱导的细胞病变效应,且感染细胞具有正常的生长潜力。AI细胞表现出相似水平的病毒特异性蛋白合成、更高的病毒产量,以及细胞病变迅速进展,随后细胞全部死亡。大多数HIV gp160蛋白分子在传统切割点与跨膜结构域之间的区域迅速裂解,从生理活性池中被去除,但一小部分gp160显然经历了正常的细胞内发育过程。根据我们的数据,两种HIV变体(正常和缺陷型)在CI系统中持续存在,缺陷型病毒gp160蛋白的病理性切割很可能导致感染的慢性化。

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