Effect of dengue virus II core protein on the nitric oxide activity and cell apoptosis in human aortic endothelial cells

• Main Authors: Yu-Chiu Lin, 林余秋
• Other Authors: Kuang-tse Huang
• Format: Others
• Language: zh-TW
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/70565144383065842904

碩士 === 國立中正大學 === 化學工程所 === 96 === Dengue fever caused by flavivirus forms a wide range of syndromes from classical dengue fever (DF) to severe dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). It becomes an important mosquito-borne disease affecting humans after malaria. In this study, we investigated the effect of dengue type 2 virus core protein on nitric oxide (NO) release and cell apoptosis in human aortic endothelial cells in the presence and absence of CD55 antibody. We found that the NO release from the core protein transfected cells is increased as compared to the vector-only control, which results from the protein expression of inducible NO synthase (iNOS). CD55 antibody increases the NO release through the activation of endothelial NO synthase (eNOS) but causes reduction of iNOS and eNOS protein expression after 24 h treatment. Cell apoptosis is enhanced by 24 h treatment of CD55 antibody in the untransfected and vector-only cells but not the core protein-transfected cells. In summary, the cause of the early increased permeability of blood vessels in the secondary infection of dengue virus may be due mostly to the activation of eNOS by NS1 antibody