INHIBITION OF VIRAL REPLICATION BY INTERFERON-GAMMA-INDUCED NITRIC-OXIDE SYNTHASE

被引：770

作者：

KARUPIAH, G ^{[1
]}

XIE, QW ^{[1
]}

BULLER, RML ^{[1
]}

NATHAN, C ^{[1
]}

DUARTE, C ^{[1
]}

MACMICKING, JD ^{[1
]}

机构：

[1] CORNELL UNIV, MED CTR,COLL MED,DEPT MED,DIV HEMATOL ONCOL, BEATRICE & SAMUEL A SEAVER LAB, NEW YORK, NY 10021 USA

来源：

SCIENCE | 1993年 / 261卷 / 5127期

关键词：

D O I：

10.1126/science.7690156

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Interferons (IFNs) induce antiviral activity in many cell types. The ability of IFN-gamma to inhibit replication of ectromelia, vaccinia, and herpes simplex-1 viruses in mouse macrophages correlated with the cells' production of nitric oxide (NO). Viral replication was restored in IFN-gamma-treated macrophages exposed to inhibitors of NO synthase. Conversely, epithelial cells with no detectable NO synthesis restricted viral replication when transfected with a complementary DNA encoding inducible NO synthase or treated with organic compounds that generate NO. In mice, an inhibitor of NO synthase converted resolving ectromelia virus infection into fulminant mousepox. Thus, induction of NO synthase can be necessary and sufficient for a substantial antiviral effect of IFN-gamma.

引用

页码：1445 / 1448

页数：4

共 40 条

[1] VACCINIA VIRUS-ENCODED EIF-2-ALPHA HOMOLOG ABROGATES THE ANTIVIRAL EFFECT OF INTERFERON [J].