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Updated: Oct 29, 2025

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
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Infectious disease-associated encephalopathies.

Maria C Barbosa-Silva1, Maiara N Lima1, Denise Battaglini2

  • 1Laboratory of Immunopharmacology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Fiocruz, Av. Brasil, 4365, Pavilhão 108, sala 45, Manguinhos, Rio de Janeiro, RJ, 21040-360, Brazil.

Critical Care (London, England)
|July 7, 2021
PubMed
Summary
This summary is machine-generated.

Peripheral infections can cause brain dysfunction (encephalopathy) through systemic inflammation and neuroinflammation, leading to cognitive deficits. Understanding these mechanisms is crucial for developing new treatments for infectious disease-associated encephalopathy.

Keywords:
COVID-19CognitionEncephalopathyInfectionInfluenzaMalariaMicroglial primingNeuroinflammationSARS-CoV-2Sepsis

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Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Immunology

Background:

  • Infectious diseases can cause encephalopathy without direct central nervous system invasion.
  • Systemic inflammation triggers neuroinflammation, impacting brain function and cognition.

Purpose of the Study:

  • To review the pathophysiology of infectious disease-associated encephalopathy.
  • To explore emerging therapeutic strategies.
  • To highlight the role of neuroinflammation in these conditions.

Main Methods:

  • Literature review focusing on mechanisms of encephalopathy linked to peripheral infections.
  • Analysis of studies on sepsis, malaria, influenza, and COVID-19 associated encephalopathies.
  • Examination of neuroinflammatory pathways and their consequences.

Main Results:

  • Systemic inflammation leads to glial activation, cytokine release, BBB dysfunction, and neurotransmitter imbalances.
  • Neuroinflammation contributes to neurotoxicity and cognitive/behavioral impairments.
  • Mechanisms may differ from non-infectious encephalopathies and are under-investigated.

Conclusions:

  • Infectious disease-associated encephalopathy is a significant clinical issue with complex pathophysiology.
  • Neuroinflammation plays a central role, necessitating targeted therapeutic approaches.
  • Further research into underlying mechanisms is vital for effective treatment development.