Related Experiment Video

Updated: Oct 12, 2026

Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency
18:10

Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency

Published on: June 16, 2011

Coxsackie B3 virus can replicate in cultured human foetal heart cells and is inhibited by interferon

R Kandolf, A Canu, P H Hofschneider

    Journal of Molecular and Cellular Cardiology
    |February 1, 1985
    PubMed

    Insights

    Coxsackie B3 virus causes acute viral myocarditis by infecting heart cells. Interferon-beta (IFN-beta) effectively inhibits viral replication, showing potential as an antiviral treatment for Coxsackie myocarditis.

    Area of Science:

    • Virology
    • Cardiology
    • Immunology

    Background:

    • Coxsackie B viruses (types 1-5) are primary causes of acute viral myocarditis.
    • Understanding the cellular pathogenesis of Coxsackie B3 (CB3) viral myocarditis is crucial for developing effective treatments.

    Purpose of the Study:

    • To investigate the cellular mechanisms of CB3 viral myocarditis.
    • To evaluate the potential of human fibroblast interferon-beta (IFN-beta) as an antiviral agent against CB3 infection.

    Main Methods:

    • Infection of cultured human foetal heart cells with CB3 virus.
    • Quantification of viral replication using plaque-forming units (PFU).
    • Assessment of CB3 virus inhibition by IFN-beta pre-incubation.

    Main Results:

    • CB3 virus successfully replicated in human foetal heart cells, leading to myocyte dysfunction and fibroblast overgrowth within 9 hours.
    • Infected human myocardial fibroblasts exhibited a carrier state, continuously producing CB3 virus for months.
    • IFN-beta significantly reduced CB3 virus yields by 1.2 x 1.8 x 10(5) PFU/ml when cells were pre-treated, demonstrating its potent antiviral activity.

    Conclusions:

    • CB3 infection leads to myocyte damage and persistent fibroblast infection in the heart.
    • IFN-beta demonstrates significant potential as a protective antiviral agent against CB3 viral myocarditis.
    • IFN-beta may be a viable therapeutic option for treating Coxsackie myocarditis.

    More Related Videos

    Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons09:11

    Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons

    Published on: August 23, 2016

    Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A1606:03

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

    Published on: July 15, 2019

    Related Concept Videos

    Retrovirus Life Cycles01:10

    Retrovirus Life Cycles

    Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...
    Retroviruses02:33

    Retroviruses

    Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...
    Cytomegalovirus Disease01:27

    Cytomegalovirus Disease

    Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...
    Inhibitors of Viral Protein Synthesis01:30

    Inhibitors of Viral Protein Synthesis

    Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
    Inhibitors Of Virion Release01:25

    Inhibitors Of Virion Release

    Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
    Inhibitors of Virion Maturation and Assembly01:19

    Inhibitors of Virion Maturation and Assembly

    As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...