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Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16
06:03

Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16

Published on: July 15, 2019

Virus-receptor interactions of coxsackie B viruses and their putative influence on cardiotropism

Hans-Christoph Selinka1, Antje Wolde, Martina Sauter

  • 1Institut für Medizinische Mikrobiologie und Hygiene, Johannes-Gutenberg-Universität Mainz, Hochhaus am Augustusplatz, 55101 Mainz, Germany. selinka@mail.uni-mainz.de

Medical Microbiology and Immunology
|August 16, 2003
PubMed

Insights

Coxsackieviruses of group B (CVB) use coxsackievirus-adenovirus receptor (CAR) and decay-accelerating factor (DAF) to infect the heart. DAF may enhance viral entry into cardiac tissue, contributing to myocarditis.

Area of Science:

  • Virology
  • Cardiology
  • Molecular biology

Background:

  • Virus-receptor interactions dictate viral pathogenesis and spread.
  • Coxsackieviruses group B (CVB) utilize coxsackievirus-adenovirus receptor (CAR) and decay-accelerating factor (DAF) as receptors.
  • CVB infections cause significant heart diseases, including myocarditis.

Purpose of the Study:

  • To investigate the role of CAR and DAF in CVB-induced myocarditis.
  • To understand how CVB utilizes specific receptors for cardiac tropism and infection.

Main Methods:

  • Analysis of CVB receptor interactions.
  • Examination of CAR and DAF expression in cardiac tissue.
  • In silico or in vitro modeling of viral entry mechanisms.

Main Results:

  • CAR is primarily expressed in the intercalated discs of the human heart.
  • DAF is abundant in epithelial and endothelial cells.
  • CVB interaction with DAF may facilitate enhanced viral entry into the heart.

Conclusions:

  • CVB employs both CAR and DAF for cardiac infection.
  • DAF acts as a potential coreceptor, enhancing CVB entry into heart tissue.
  • Understanding these interactions is crucial for developing therapies against CVB-induced heart disease.

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