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Emerging concepts in dengue pathogenesis: interplay between plasmablasts, platelets, and complement in triggering

Eduardo J M Nascimento1, Eugenio D Hottz2, Tatiana M Garcia-Bates3

  • 1Center for Vaccine Research and Departments of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

Critical Reviews in Immunology
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Summary
This summary is machine-generated.

Severe dengue disease involves plasmablasts, complement, and platelets. These factors form immune complexes, activate complement, and deplete platelets, leading to vasculopathy and potentially fatal plasma leakage.

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Area of Science:

  • Immunology
  • Virology
  • Pathology

Background:

  • Dengue virus (DENV) infection is a growing global health concern.
  • Severe dengue causes life-threatening vasculopathy and plasma leakage.
  • The exact causes of dengue-associated vasculopathy remain largely unknown.

Purpose of the Study:

  • To investigate the roles of plasmablasts, complement, and platelets in severe dengue disease.
  • To elucidate the mechanisms underlying dengue-associated vasculopathy.

Main Methods:

  • Observational study analyzing immune responses during the critical phase of DENV infection.
  • Measurement of plasmablast expansion, complement activation, and platelet levels.
  • Proposed a step-wise model of disease pathogenesis.

Main Results:

  • Virus-specific plasmablasts massively expand during the critical phase of DENV infection.
  • Complement activation and platelet depletion coincide with plasmablast expansion.
  • Evidence suggests immune complexes, complement activation, and platelet activation drive vasculopathy.

Conclusions:

  • Plasmablasts, complement, and platelets play a combined role in severe dengue pathogenesis.
  • A proposed model highlights immune complex formation, complement activation, and platelet sequestration as key triggers of vasculopathy.