期刊
ANTIVIRAL RESEARCH
卷 84, 期 1, 页码 67-75出版社
ELSEVIER
DOI: 10.1016/j.antiviral.2009.07.014
关键词
Cyanovirin-N; Microbicide; HSV-1; Viral entry
资金
- NIH [RO1, AI057860, EY001792]
- Glaucoma Foundation, New York
Herpes simplex virus type-1 (HSV-1) causes significant health problems from periodic skin and corneal lesions to encephalitis. It is also considered a cofactor in the development of age-related secondary glaucoma. Inhibition of HSV-1 at the stage of viral entrygenerates a unique opportunity for preventative and/or therapeutic intervention. Here we provide evidence that a sugar binding antiviral protein, cyanovirin-N (CV-N), can act as a potent inhibitor of HSV-1 entry into natural target cells. Inhibition of entry was independent of HSV-1 gD receptor usage and it was observed in transformed as well as primary cell cultures. Evidence presented herein suggests that CV-N can not only block virus entry to cells but also, it is capable of significantly inhibiting membrane fusion mediated by HSV glycoproteins. While CV-N treated virions were significantly deficient in entering into cells, HSV-1 glycoproteins-expressing cells pretreated with CV-N demonstrated reduced cell-to-cell fusion and polykaryocytes formation. The observation that CV-N can block both entry as well as membrane fusion suggests a stronger potential for this compound in antiviral therapy against HSV-1. (C) 2009 Elsevier B.V. All rights reserved.
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