HERPES-SIMPLEX VIRUS TYPE-1 IMMEDIATE-EARLY GENE-EXPRESSION AND SHUT OFF OF HOST PROTEIN-SYNTHESIS ARE INHIBITED IN NEOMYCIN-TREATED HUMAN EPIDERMOID CARCINOMA-2 CELLS

被引：18

作者：

GARCIN, D

MASSE, T

MADJAR, JJ

JACQUEMONT, B

机构：

[1] ECOLE NORMALE SUPER LYON,INSERM,CONTRAT JEUNE FORMAT 88-11,46 ALLEE ITALIE,F-69364 LYONS 07,FRANCE

[2] UNIV LYON 1,FAC MED ALEXIS CARREL,CNRS,UMR 30,F-69365 LYONS 2,FRANCE

来源：

EUROPEAN JOURNAL OF BIOCHEMISTRY | 1990年 / 194卷 / 01期

关键词：

D O I：

10.1111/j.1432-1033.1990.tb19454.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Infection of human epidermoid carcinoma‐2 (HEp‐2) cells by Herpes simplex virus type 1 (HSV‐1) leads to significant activation of inositol phospholipid turnover after 15 min. The effect of neomycin, an inhibitor of inositol phospholipid turnover, has been investigated for its effect on HSV‐1 multiplication in HEp‐2 cells. HSV‐1 multiplication is inhibited by neomycin. This inhibition is not due to a block of virus adsorption or penetration. Neomycin inhibits the expression of virus immediate‐early genes, as well as expression of early genes and viral DNA synthesis. In neomycin‐treated cells, the usual virion‐associated shut off of host protein synthesis does not occur. These results indicate that the inositol phospholipid pathway is involved in immediate‐early gene expression and shut off of host protein synthesis in HEp‐2 cells. Copyright © 1990, Wiley Blackwell. All rights reserved

引用

页码：279 / 286

页数：8

共 56 条

[11] HEAT-STRESS STIMULATES INOSITOL TRISPHOSPHATE RELEASE AND PHOSPHORYLATION OF PHOSPHOINOSITIDES IN CHO AND BALB C-3T3 CELLS [J].