Abstract

Dengue disease includes from mild dengue fever to severe dengue hemorrhagic fever (DHF), which is an important health problem in tropical or sub‐tropical areas. The immunopathogenesis of DHF is initiated by aberrant immune activation and autoantibody production caused by virus infection. There is a molecular mimicry between dengue antigens and self‐proteins. The anti‐dengue antibody cross‐react with platelet and endothelial cell, and would trigger the subsequent dysfunction of endothelial cells and hemorrhage during the acute infection. The antibody‐dependent enhancement theory plays a central role in the dengue disease. The enhancing antibody is dependent on the types of the target cells and the specificity of the enhancing antibody. The enhancing antibody can be either anti‐prM or anti‐E antibody. For anti‐E Ab‐mediated enhancement on monocytic cells, it can be concentration‐dependent: enhancing at sub‐neutralization level or enhance regardless of concentration by Fc and FcR interaction. For anti‐prM Ab‐mediated enhancement, it enhanced the dengue virion binding on both FcR or non‐FcR bearing cells with dual specificity. The anti‐dengue antibodies seem to be either enhancing antibody or the pathogenic antibody, and play a major role in the DHF pathogenesis.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.