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Related Experiment Video

Updated: Apr 7, 2026

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

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

Published on: July 15, 2019

Recent progress in understanding coxsackievirus replication, dissemination, and pathogenesis.

Jon Sin¹, Vrushali Mangale², Wdee Thienphrapa²

¹Cedars-Sinai Heart Institute, 8700 Beverly Blvd., Los Angeles, CA 90048, USA.

|July 6, 2015

Summary

Coxsackieviruses (CVs) can cause severe diseases by evading immune responses and using host membranes for spread. Understanding their replication and tropism is key to combating these persistent viral infections.

Keywords:

Autophagy Cardiac progenitor cells Coxsackievirus Enterovirus Meningoencephalitis Microvesicles Myocarditis Neural progenitor cells Picornavirus Virus dissemination

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

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Published on: July 15, 2019

Isolation of Viral Replication Compartment-enriched Sub-nuclear Fractions from Adenovirus-infected Normal Human Cells

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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Published on: October 7, 2011

Area of Science:

Virology
Immunology
Cell Biology

Background:

Coxsackieviruses (CVs) are common picornaviruses linked to serious diseases like myocarditis.
Historically viewed as non-enveloped, CVs may acquire host membranes for enhanced survival.
CVs exhibit unique tropism for progenitor cells, affecting young hosts and causing chronic adult infections.

Purpose of the Study:

To review recent advancements in understanding CV replication and dissemination.
To identify factors determining CV tropism and host cell interactions.
To define viral strategies for evading host immune responses and discuss future research directions.

Main Methods:

Literature review of recent studies on Coxsackievirus pathogenesis.
Analysis of viral replication mechanisms, including membrane hijacking and autophagy exploitation.
Examination of viral tropism determinants and immune evasion strategies.

Main Results:

CVs can persist by reducing replication and evading immune surveillance.
Evidence suggests CVs acquire an envelope from host membranes, aiding antibody resistance and nonlytic spread.
CVs exploit host cell machinery, including autophagy, for replication and release.

Conclusions:

CVs employ sophisticated strategies, including membrane hijacking and autophagy, for replication and dissemination.
Understanding CV tropism and immune evasion is crucial for developing therapeutic interventions.
Further research is needed to fully elucidate CV pathogenesis and identify novel treatment targets.