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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...
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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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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...
Infection01:20

Infection

When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
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Symbiosis00:58

Symbiosis

Symbiotic relationships are long-term, close interactions between individuals of different species that affect the distribution and abundance of those species. When a relationship is beneficial to both species, this is called mutualism. When the relationship is beneficial to one species but neither beneficial nor harmful to the other species, this is called commensalism. When one organism is harmed to benefit another, the relationship is known as parasitism. These types of relationships often...
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Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...

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Related Experiment Video

Updated: May 13, 2026

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

Published on: April 28, 2019

The pathogenesis of dengue.

Sophie Yacoub1, Juthathip Mongkolsapaya, Gavin Screaton

  • 1Department of Medicine, Imperial College, Hammersmith Campus, London, UK. s.yacoub@imperial.ac.uk

Current Opinion in Infectious Diseases
|March 2, 2013
PubMed
Summary

Dengue pathogenesis involves complex interactions between host immunity, genetics, and viral factors. Understanding these mechanisms is key to developing effective treatments and vaccines for this growing global health threat.

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Published on: November 1, 2018

Area of Science:

  • Virology
  • Immunology
  • Epidemiology

Background:

  • Dengue incidence has surged globally, with no current treatments or vaccines.
  • Severe dengue pathogenesis is increasingly understood as immune-mediated, particularly in secondary infections.

Purpose of the Study:

  • To review recent advances in understanding dengue pathogenesis.
  • To explore host and viral determinants contributing to disease severity.

Main Methods:

  • Review of recent immunological, genetic, and epidemiological studies.
  • Analysis of monoclonal antibody data and T-cell responses.
  • Examination of genome-wide association studies and viral virulence factors.

Main Results:

  • Evidence highlights neutralizing vs. enhancing monoclonal antibodies and their epitopes, impacting vaccine design.
  • T-cell immunopathology shows cross-reactive, pro-inflammatory T cells in severe dengue.
  • Genome-wide association studies identified susceptibility loci; epidemiological studies defined at-risk groups.

Conclusions:

  • Dengue pathogenesis is a complex interplay of host immunity, genetic predisposition, and viral factors.
  • Understanding these mechanisms is vital for developing prognostic markers, diagnostics, therapeutics, and a safe vaccine.