Immunopathologic mechanisms of dengue hemorrhagic fever and dengue shock syndrome
Biochemistry & Molecular Pharmacology
Graduate School of Biomedical Sciences; Department of Medicine, Division of Infectious Diseases and Immunology; Center for Infectious Disease and Vaccine Research
Life Sciences | Medicine and Health Sciences
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.
DOI of Published Version
Arch Virol Suppl. 1994;9:59-64.
Archives of virology. Supplementum
Kurane I, Rothman AL, Livingston PG, Green S, Gagnon SJ, Janus J, Innis BL, Nimmannitya S, Nisalak A, Ennis FA. (1994). Immunopathologic mechanisms of dengue hemorrhagic fever and dengue shock syndrome. GSBS Student Publications. https://doi.org/10.1007/978-3-7091-9326-6_7. Retrieved from https://escholarship.umassmed.edu/gsbs_sp/629