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Related Experiment Videos

Myocarditis as systemic disease: new perspectives on pathogenesis

C M Carthy1, D Yang, D R Anderson

  • 1Department of Pathology and Laboratory Medicine, University of British Columbia, St Paul's Hospital, Vancouver, Canada.

Clinical and Experimental Pharmacology & Physiology
|December 24, 1997
PubMed
Summary

Coxsackie B viruses (CVB) can cause myocarditis and potentially lead to dilated cardiomyopathy. This study explores how CVB3 infects heart and immune cells, potentially hindering the immune response and viral clearance.

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Area of Science:

  • Virology
  • Immunology
  • Cardiology

Background:

  • Myocarditis, an inflammation of the heart muscle, can be an early sign of or lead to dilated cardiomyopathy.
  • Coxsackie B viruses (CVB), particularly CVB3, are common viral agents implicated in myocarditis.
  • The pathogenesis of CVB3-induced myocarditis involves direct myocyte damage and immunopathological mechanisms.

Purpose of the Study:

  • To investigate the pathogenesis of CVB3-induced myocarditis.
  • To explore the interaction between CVB3 and immune cells.
  • To understand the role of viral translation mechanisms in disease progression.

Main Methods:

  • In situ hybridization and gene amplification to detect viral RNA persistence.
  • Terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) to assess cell death.

Related Experiment Videos

  • Analysis of viral internal ribosome entry site (IRES) function.

    • Main Results:

    • CVB3 infection leads to non-apoptotic injury in cardiac tissue, with apoptotic bodies primarily from immune cells.
    • CVB3 infects and persists in immune cells, localizing to splenic and lymph node follicles.
    • CVB3 may perturb the immune response, potentially delaying viral clearance and influencing disease severity.
    • CVB3 utilizes an internal ribosome entry site (IRES) for translation, arresting host cell translation to favor viral replication.

    Conclusions:

    • CVB3 infection of heart and immune cells contributes to myocarditis and potentially dilated cardiomyopathy.
    • The virus-host-immune cell interaction is complex and influences disease outcome.
    • Viral translation mechanisms, such as IRES, play a role in viral replication and pathogenesis.