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The Journal of Immunology, 2006, 176: 2825-2832.
Copyright © 2006 by The American Association of Immunologists

The Dual-Specific Binding of Dengue Virus and Target Cells for the Antibody-Dependent Enhancement of Dengue Virus Infection1

Kao-Jean Huang*, Yu-Ching Yang{dagger}, Yee-Shin Lin{dagger}, Jyh-Hsiung Huang, Hsiao-Sheng Liu{dagger}, Trai-Ming Yeh{ddagger}, Shun-Hua Chen{dagger}, Ching-Chuan Liu§ and Huan-Yao Lei2,*,{dagger}

* Department of Basic Medical Sciences, {dagger} Department of Microbiology and Immunology, {ddagger} Department of Medical Technology, and § Department of Pediatrics, College of Medicine, National Cheng Kung University, Tainan, Taiwan; and Center for Disease Control, Department of Health, Taipei, Taiwan, Republic of China

Using flow cytometric assay and monoclonal anti-dengue Ab, we observed that both anti-E and anti-prM Abs could enhance dengue virus infection in a concentration-dependent but serotype-independent manner. Increases were found in both the percentage of dengue-infected cells and the expression of dengue E and NS1 protein per cell. Dengue virion binding and infection were enhanced on FcR-bearing cells via the Fc-Fc{gamma}RII pathway. Furthermore, anti-prM Ab also enhanced dengue virion binding and infection on cells lacking FcR, such as BHK-21 or A549 cells, by the mechanism of peptide (CPFLKQNEPEDIDCW)-specific binding. Anti-prM Ab cross-reacted with BHK-21 or A549 cells and recognized self-Ags such as heat shock protein 60. In summary, a novel mechanism of anti-prM Ab-mediated enhancement on dengue virus infection was found to be mediated by dual specific binding to dengue virion and to target cells, in addition to the traditional enhancement on FcR-bearing cells.




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