Ebola virus (EBOV) infection: Therapeutic strategies

被引:61
作者
De Clercq, Erik [1 ]
机构
[1] Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Louvain, Belgium
关键词
Ebola; VSV (vesicular stomatitis virus); BCX4430; 3-Deazaneplanocin A; Favipiravir; Filoviridae; HUMAN-IMMUNODEFICIENCY-VIRUS; PROTECTS NONHUMAN-PRIMATES; VESICULAR STOMATITIS VIRUS; SMALL-MOLECULE INHIBITORS; RESPIRATORY SYNDROME CORONAVIRUS; CHRONIC HEPATITIS-C; NIEMANN-PICK C1; ANTIVIRAL ACTIVITY; HEMORRHAGIC-FEVER; POSTEXPOSURE PROTECTION;
D O I
10.1016/j.bcp.2014.11.008
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Within less than a year after its epidemic started (in December 2013) in Guinea, Ebola virus (EBOV), a member of the filoviridae, has spread over a number of West-African countries (Guinea, Sierra Leone and Liberia) and gained allures that have been unprecedented except by human immunodeficiency virus (HIV). Although EBOV is highly contagious and transmitted by direct contact with body fluids, it could be counteracted by the adequate chemoprophylactic and -therapeutic interventions: vaccines, antibodies, siRNAs (small interfering RNAs), interferons and chemical substances, i.e. neplanocin A derivatives (i.e. 3-deazaneplanocin A), BCX4430, favipiravir (T-705), endoplasmic reticulum (ER) alpha-glucosidase inhibitors and a variety of compounds that have been found to inhibit EBOV infection blocking viral entry or by a mode of action that still has to be resolved. Much has to be learned from the mechanism of action of the compounds active against VSV (vesicular stomatitis virus), a virus belonging to the rhabdoviridae, that in its mode of replication could be exemplary for the replication of filoviridae. (C) 2014 Elsevier Inc. All rights reserved.
引用
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页码:1 / 10
页数:10
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