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Related Concept Videos

Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
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Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...
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Diphtheria

Diphtheria is an acute, toxin-mediated infectious disease that primarily affects the upper respiratory tract. It is caused by Corynebacterium diphtheriae, a Gram-positive, pleomorphic rod that lacks spore-forming capability and exhibits a characteristic club-shaped morphology under microscopic examination. While C. diphtheriae can asymptomatically colonize mucosal surfaces, clinical disease manifests only when the bacterial strain is lysogenized by a specific β-corynephage. This phage...
Arboviral Encephalitis01:25

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...

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Updated: May 15, 2026

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
04:23

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease

Published on: April 28, 2019

Autoimmunity in dengue pathogenesis.

Shu-Wen Wan1, Chiou-Feng Lin, Trai-Ming Yeh

  • 1Department of Microbiology and Immunology, National Cheng Kung University Medical College, 1 University Road,Tainan, Taiwan.

Journal of the Formosan Medical Association = Taiwan Yi Zhi
|January 22, 2013
PubMed
Summary
This summary is machine-generated.

Dengue virus (DENV) infection causes severe illness through complex immunopathogenesis, including antibody-dependent enhancement and autoantibody production. Understanding these mechanisms is crucial for developing effective dengue vaccines.

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Area of Science:

  • * Virology
  • * Immunology
  • * Tropical Medicine

Background:

  • * Dengue virus (DENV) is a significant vector-borne disease with expanding geographical reach due to climate change and travel.
  • * DENV infection presents a spectrum of illness, from mild dengue fever to severe dengue hemorrhagic fever and shock syndrome.
  • * Key clinical features of severe dengue include vascular leakage, low platelet counts (thrombocytopenia), and bleeding, with underlying mechanisms not fully elucidated.

Purpose of the Study:

  • * To explore the immunopathogenesis of severe dengue disease.
  • * To investigate the role of antibody-dependent enhancement (ADE) in DENV infection.
  • * To understand the contribution of T-cell activation and autoantibody production to dengue's severe manifestations.

Main Methods:

  • * Review of existing literature on dengue virus (DENV) infection and its immunopathogenesis.
  • * Analysis of mechanisms including antibody-dependent enhancement (ADE), T-cell responses, and autoantibody generation.
  • * Examination of molecular mimicry as a potential cause for autoantibody cross-reactivity.

Main Results:

  • * Immunopathogenesis, beyond direct viral effects, significantly contributes to severe dengue.
  • * Antibody-dependent enhancement (ADE) enhances DENV infection and can impair antiviral responses.
  • * Aberrant T-cell activation and autoantibodies against host components (endothelial cells, platelets) promote vascular leakage and dysfunction.

Conclusions:

  • * Severe dengue pathogenesis involves complex immune responses, including ADE and autoantibody formation.
  • * Molecular mimicry may explain cross-reactivity in DENV-induced autoantibodies.
  • * Consideration of these immunopathogenic complications is essential for the development of safe and effective dengue vaccines.