Immunopathologic mechanisms of dengue hemorrhagic fever and dengue shock syndrome
Authors
Kurane, IchiroRothman, Alan L.
Livingston, Peter G.
Green, Sharone
Gagnon, Susan J.
Janus, Jurand
Innis, Bruce L.
Nimmannitya, Suchitra
Nisalak, Ananda
Ennis, Francis A.
UMass Chan Affiliations
Center for Infectious Disease and Vaccine ResearchDepartment of Medicine, Division of Infectious Diseases and Immunology
Graduate School of Biomedical Sciences
Document Type
Journal ArticlePublication Date
1994-01-01Keywords
Cross Reactions; Dengue; Humans; Immunity, Cellular; Immunologic Memory; Lymphocyte Activation; Models, Biological; Shock, Septic; Syndrome; T-Lymphocytes, CytotoxicLife Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
Dengue virus infections are a major cause of morbidity and mortality in tropical and subtropical areas of the world. The immunopathological mechanisms that result in severe complications of dengue virus infection, i.e. dengue hemorrhagic fever (DHF), are important to determine. Primary dengue virus infections induce serotype-specific and serotype-cross-reactive, CD4+ and CD8+ memory cytotoxic T lymphocytes (CTL). In secondary infections with a virus of a different serotype from that which caused primary infections, the presence of cross-reactive non-neutralizing antibodies results in an increased number of infected monocytes by dengue virus--antibody complexes. This in turn results in marked activation of serotype cross-reactive CD4+ and CD8+ memory CTL. We hypothesize that the rapid release of cytokines and chemical mediators caused by T cell activation and by CTL-mediated lysis of dengue virus-infected monocytes triggers the plasma leakage and hemorrhage that occurs in DHF.Source
Arch Virol Suppl. 1994;9:59-64.
DOI
10.1007/978-3-7091-9326-6_7Permanent Link to this Item
http://hdl.handle.net/20.500.14038/33975PubMed ID
8032282Related Resources
ae974a485f413a2113503eed53cd6c53
10.1007/978-3-7091-9326-6_7