Effects of prM antibody on dengue virus infection

• Main Authors: Ting-yu Chien, 簡廷宇
• Other Authors: Trai-ming Yeh
• Format: Others
• Language: zh-TW
• Published: 2009
• Online Access: http://ndltd.ncl.edu.tw/handle/44909099575258138581

碩士 === 國立成功大學 === 醫學檢驗生物技術學系碩博士班 === 97 === Dengue virus (DV) is an important re-emerging infectious pathogen in tropical and sub-tropical region worldwide that pose a threat to public health. DV can induce mild dengue fever or severe dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). The major two symptoms of DHF/DSS are thrombocytopenia and plasma leakage. Even though the main target cells of DV in vivo is macrophage or monocyte, many different cell lines such as endothelium (HMEC-1) are susceptible to DV infection in vitro. The antibody dependent enhancement (ADE) has been proposed to explain why DHF/DSS occur mostly in secondary DV infection with different serotypes of DV. However the molecular mechanism of ADE is still unclear. In this study, we used an anti-prM monoclonal antibody (70-21) to study this question. We found anti-prM Ab, but not anti-E Ab (50-2), can cross-react to different cells such as BHK, HMEC-1, and Huh-7 as demonstrated by flow cytometery and immunofluorescent antibody analysis. Although anti-prM Ab could bind to these cells, we didn’t find any damage or other effects to them. However, DV infection rate and the secretion of chemokine MCP-1, MIF and IL-8 of monocytic cell line THP-1 was enhanced by anti-prM antibody. On the contrary, in the presence of anti-E antibody, DV-induced IL-8 production in THP1 cell was inhibited. These results indicated that anti-prM antibody not only can enhance DV infection of monocytes but also increase chemokines secretion, which may contribute to the immunopathogenesis in DHF/DSS by recruiting more immune cells to be infected.