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Related Concept Videos

Arboviral Encephalitis01:25

Arboviral Encephalitis

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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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Encephalitis ll: Pathophysiology01:26

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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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Related Experiment Video

Updated: May 6, 2026

Protocol for Dengue Infections in Mosquitoes A. aegypti and Infection Phenotype Determination
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How dengue defies dogma: An extrafollicular tale.

Jordan Polster1, David R Martinez1,2

  • 1Department of Microbial Pathogenesis, Yale School of Medicine, New Haven, CT, USA.

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Severe dengue triggers an unusual immune response outside lymph nodes. This response is orchestrated by a specialized group of CD4-positive (CD4+) T cells, revealing new insights into dengue pathogenesis.

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Area of Science:

  • Immunology
  • Virology
  • Pathogenesis

Background:

  • Dengue is a significant global health concern, causing severe illness through complex immune mechanisms.
  • The typical humoral immune response involves germinal centers within lymphoid tissues.

Purpose of the Study:

  • To investigate the cellular and spatial characteristics of the acute humoral immune response in severe dengue.
  • To identify the specific T cell subsets involved in driving this response.

Main Methods:

  • Analysis of immune cell populations in patient samples.
  • Characterization of T cell subsets and their interactions with B cells.
  • Assessment of the location of immune responses within affected tissues.

Main Results:

  • The acute humoral immune response in severe dengue occurs predominantly in an extrafollicular pattern.
  • A distinct subset of CD4-positive (CD4+) T cells was identified as the primary driver of this extrafollicular response.
  • These CD4+ T cells exhibit unique functional properties contributing to antibody production.

Conclusions:

  • The findings challenge the traditional view of humoral immunity in severe dengue.
  • This extrafollicular response, mediated by specific CD4+ T cells, represents a key pathogenic mechanism in severe dengue.
  • Targeting these unique CD4+ T cells could offer novel therapeutic strategies for severe dengue.