Immunopathogenesis of dengue hemorrhagic fever

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Dengue virus infection causes Dengue Fever (DF), Dengue Hemorrhagic Fever (DHF) and Dengue Shock Syndrome (DSS) whose pathogeneses were not clearly understood. A new hypothesis of immunopathogenesis is proposed for the development of the DHF/DSS. An aberrant immune over-activation after dengue virus infection not only impair the immune response to clear the virus, but also result in overproduction of cytokines that affect monocytes, endothelial cells, and hepatocytes, as well as the abnormal production of autoantibodies to platelet and endothelial cells. A molecular mimicry occurs between platelets/endothelial cells and dengue virus antigens. Platelets and endothelial cells are bound by the cross-reactive anti-dengue virus antibodies such as anti-NS1 or anti-prM antibodies. The IFN-γ activated macrophage would phagocytosize the osponized targets. Dengue virus-induced vasculopathy and coagulopathy are involved in the pathogenesis of hemorrhage, and the imbalance between coagulation and fibrinolysis activation increases the likelihood of severe hemorrhage in DHF/DSS. This theory of transient hemophagocytic activity in immunopathogenesis of DHF/DSS can account for specific characteristics of clinical, pathologic, and epidemiological observations in dengue virus infection.

Original languageEnglish
Pages (from-to)1-9
Number of pages9
JournalAmerican Journal of Infectious Diseases
Volume4
Issue number1
DOIs
Publication statusPublished - 2008 Jan 1

Fingerprint

Severe Dengue
Dengue Virus
Virus Diseases
Endothelial Cells
Blood Platelets
Hemorrhage
Molecular Mimicry
Dengue
Fibrinolysis
Autoantibodies
Monocytes
Anti-Idiotypic Antibodies
Hepatocytes

All Science Journal Classification (ASJC) codes

  • Infectious Diseases

Cite this

@article{47bd0f61c16e4bd48f44489503d32826,
title = "Immunopathogenesis of dengue hemorrhagic fever",
abstract = "Dengue virus infection causes Dengue Fever (DF), Dengue Hemorrhagic Fever (DHF) and Dengue Shock Syndrome (DSS) whose pathogeneses were not clearly understood. A new hypothesis of immunopathogenesis is proposed for the development of the DHF/DSS. An aberrant immune over-activation after dengue virus infection not only impair the immune response to clear the virus, but also result in overproduction of cytokines that affect monocytes, endothelial cells, and hepatocytes, as well as the abnormal production of autoantibodies to platelet and endothelial cells. A molecular mimicry occurs between platelets/endothelial cells and dengue virus antigens. Platelets and endothelial cells are bound by the cross-reactive anti-dengue virus antibodies such as anti-NS1 or anti-prM antibodies. The IFN-γ activated macrophage would phagocytosize the osponized targets. Dengue virus-induced vasculopathy and coagulopathy are involved in the pathogenesis of hemorrhage, and the imbalance between coagulation and fibrinolysis activation increases the likelihood of severe hemorrhage in DHF/DSS. This theory of transient hemophagocytic activity in immunopathogenesis of DHF/DSS can account for specific characteristics of clinical, pathologic, and epidemiological observations in dengue virus infection.",
author = "Lei, {Huan Yao} and Huang, {Kao Jean} and Yee-Shin Lin and Trai-Ming Yeh and Hsiao-Sheng Liu and Ching-Chuan Liu",
year = "2008",
month = "1",
day = "1",
doi = "10.3844/ajidsp.2008.1.9",
language = "English",
volume = "4",
pages = "1--9",
journal = "American Journal of Infectious Diseases",
issn = "1553-6203",
publisher = "Science Publications",
number = "1",

}

Immunopathogenesis of dengue hemorrhagic fever. / Lei, Huan Yao; Huang, Kao Jean; Lin, Yee-Shin; Yeh, Trai-Ming; Liu, Hsiao-Sheng; Liu, Ching-Chuan.

In: American Journal of Infectious Diseases, Vol. 4, No. 1, 01.01.2008, p. 1-9.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Immunopathogenesis of dengue hemorrhagic fever

AU - Lei, Huan Yao

AU - Huang, Kao Jean

AU - Lin, Yee-Shin

AU - Yeh, Trai-Ming

AU - Liu, Hsiao-Sheng

AU - Liu, Ching-Chuan

PY - 2008/1/1

Y1 - 2008/1/1

N2 - Dengue virus infection causes Dengue Fever (DF), Dengue Hemorrhagic Fever (DHF) and Dengue Shock Syndrome (DSS) whose pathogeneses were not clearly understood. A new hypothesis of immunopathogenesis is proposed for the development of the DHF/DSS. An aberrant immune over-activation after dengue virus infection not only impair the immune response to clear the virus, but also result in overproduction of cytokines that affect monocytes, endothelial cells, and hepatocytes, as well as the abnormal production of autoantibodies to platelet and endothelial cells. A molecular mimicry occurs between platelets/endothelial cells and dengue virus antigens. Platelets and endothelial cells are bound by the cross-reactive anti-dengue virus antibodies such as anti-NS1 or anti-prM antibodies. The IFN-γ activated macrophage would phagocytosize the osponized targets. Dengue virus-induced vasculopathy and coagulopathy are involved in the pathogenesis of hemorrhage, and the imbalance between coagulation and fibrinolysis activation increases the likelihood of severe hemorrhage in DHF/DSS. This theory of transient hemophagocytic activity in immunopathogenesis of DHF/DSS can account for specific characteristics of clinical, pathologic, and epidemiological observations in dengue virus infection.

AB - Dengue virus infection causes Dengue Fever (DF), Dengue Hemorrhagic Fever (DHF) and Dengue Shock Syndrome (DSS) whose pathogeneses were not clearly understood. A new hypothesis of immunopathogenesis is proposed for the development of the DHF/DSS. An aberrant immune over-activation after dengue virus infection not only impair the immune response to clear the virus, but also result in overproduction of cytokines that affect monocytes, endothelial cells, and hepatocytes, as well as the abnormal production of autoantibodies to platelet and endothelial cells. A molecular mimicry occurs between platelets/endothelial cells and dengue virus antigens. Platelets and endothelial cells are bound by the cross-reactive anti-dengue virus antibodies such as anti-NS1 or anti-prM antibodies. The IFN-γ activated macrophage would phagocytosize the osponized targets. Dengue virus-induced vasculopathy and coagulopathy are involved in the pathogenesis of hemorrhage, and the imbalance between coagulation and fibrinolysis activation increases the likelihood of severe hemorrhage in DHF/DSS. This theory of transient hemophagocytic activity in immunopathogenesis of DHF/DSS can account for specific characteristics of clinical, pathologic, and epidemiological observations in dengue virus infection.

UR - http://www.scopus.com/inward/record.url?scp=58449118019&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=58449118019&partnerID=8YFLogxK

U2 - 10.3844/ajidsp.2008.1.9

DO - 10.3844/ajidsp.2008.1.9

M3 - Article

VL - 4

SP - 1

EP - 9

JO - American Journal of Infectious Diseases

JF - American Journal of Infectious Diseases

SN - 1553-6203

IS - 1

ER -