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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

Multiple viral determinants mediate myopathogenicity in coxsackievirus B1-induced chronic inflammatory myopathy

Patricia E Tam1, Melissa L Weber-Sanders, Ronald P Messner

  • 1Department of Medicine, Division of Rheumatic and Autoimmune Diseases, University of Minnesota, Minneapolis, Minnesota 55455, USA. tamxx001@umn.edu

Journal of Virology
|October 15, 2003
PubMed

Insights

Researchers identified specific viral genetic regions in coxsackievirus B1 Tucson (CVB1(T)) that cause chronic inflammatory myopathy (CIM) in mice. These determinants are crucial for understanding viral pathogenesis and developing targeted therapies.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Myopathic coxsackievirus B1 Tucson (CVB1(T)) infection in mice leads to chronic inflammatory myopathy (CIM), characterized by hind limb weakness and inflammation.
  • Amyopathic viral variants are infectious but do not cause CIM, suggesting specific viral factors are responsible for disease induction.

Purpose of the Study:

  • To identify the specific viral determinants responsible for inducing chronic inflammatory myopathy (CIM) and its associated symptoms, such as hind limb weakness and inflammation, in a mouse model.
  • To pinpoint the genetic regions and specific mutations within CVB1(T) that correlate with myopathic disease development.

Main Methods:

  • Utilized viral clones, chimeric viruses, and DNA sequencing to analyze genetic variations in CVB1(T) and their correlation with disease phenotypes.
  • Employed genetic mapping techniques to localize determinants of viral weakness and inflammation to specific regions of the viral genome, including the VP1 capsid and 5' untranslated region (UTR).

Main Results:

  • Identified several viral regions involved in CIM pathogenesis. A key determinant for hind limb weakness was localized to nucleotides 2493 to 3200 of the VP1 gene.
  • Sequencing revealed five conserved candidate determinants in myopathic CVB1(T) strains: one in the 5' UTR, three in the VP1 capsid, and one in the 3C protease.
  • Specific amino acid residues Tyr-87 and/or Val-136 in VP1 were implicated as potential determinants of weakness, alongside other factors for inflammation and weakness.

Conclusions:

  • The study implicates specific viral genetic determinants within CVB1(T), particularly in the VP1 capsid and 5' UTR, as critical for inducing chronic inflammatory myopathy and associated weakness in mice.
  • These findings provide crucial insights into the molecular mechanisms of CVB1(T) pathogenesis and highlight potential targets for therapeutic interventions against viral myopathy.

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