Development of a broad-spectrum antiviral with activity against Ebola virus

被引：74

作者：

Aman, M. Javad ^{[2
]}

Kinch, Michael S. ^{[1
]}

Warfield, Kelly ^{[2
]}

Warren, Travis ^{[2
]}

Yunus, Abdul ^{[1
]}

Enterlein, Sven ^{[3
]}

Stavale, Eric ^{[3
]}

Wang, Peifang ^{[4
]}

Chang, Shaojing ^{[1
]}

Tang, Qingsong ^{[1
]}

Porter, Kevin ^{[4
]}

Goldblatt, Michael ^{[1
]}

Bavari, Sina ^{[2
]}

机构：

[1] Funct Genet Inc, Gaithersburg, MD 20878 USA

[2] USA, Med Res Inst Infect Dis, Ft Detrick, MD 21702 USA

[3] Integrated BioTherapeut, Germantown, MD 20876 USA

[4] USN, Med Res Ctr, Silver Spring, MD 20910 USA

来源：

ANTIVIRAL RESEARCH | 2009年 / 83卷 / 03期

关键词：

Ebola virus; Antiviral; Dengue Fever; VESICULAR STOMATITIS-VIRUS; IMP DEHYDROGENASE; DENGUE VIRUS; PATHOGENESIS; RIBAVIRIN; FEVER; INFECTION; TOXICITY; THERAPY; INVITRO;

D O I：

10.1016/j.antiviral.2009.06.001

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

We report herein the identification of a small molecule therapeutic, FGI-106, which displays potent and broad-spectrum inhibition of lethal viral hemorrhagic fevers pathogens, including Ebola, Rift Valley and Dengue Fever viruses, in cell-based assays. Using mouse models of Ebola virus, we further demonstrate that FGI-106 can protect animals from an otherwise lethal infection when used either in a prophylactic or therapeutic setting. A single treatment, administered 1 day after infection, is sufficient to protect animals from lethal Ebola virus challenge. Cell-based assays also identified inhibitory activity against divergent virus families, which supports a hypothesis that FGI-106 interferes with a common pathway utilized by different viruses. These findings suggest FGI-106 may provide an opportunity for targeting viral diseases. (C) 2009 Elsevier B.V. All rights reserved.

引用

页码：245 / 251

页数：7

共 22 条

[21] Emergence of resistant human immunodeficiency virus type 1 in patients receiving fusion inhibitor (T-20) monotherapy [J].