Related Experiment Video

Updated: Oct 23, 2026

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
11:28

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

Published on: October 7, 2011

Inhibition of host cellular ribonucleic acid synthesis by glycoprotein of mumps virus

A Yamada, M Tsurudome, M Hishiyama

    Virology
    |June 1, 1984
    PubMed

    Insights

    Mumps virus infection depresses cellular RNA synthesis in EL4 cells. This inhibition is caused by viral envelope glycoproteins, not necessarily by virus replication, and can be enhanced by antibodies.

    Area of Science:

    • Virology
    • Molecular Biology
    • Immunology

    Background:

    • Mumps virus infection can impact host cell functions.
    • Cellular ribonucleic acid (RNA) synthesis is crucial for cell function and gene expression.

    Purpose of the Study:

    • To investigate the effect of mumps virus infection on cellular RNA synthesis in a murine lymphoma cell line (EL4).
    • To determine if active virus replication is necessary for the observed inhibition.
    • To identify the viral component responsible for inhibiting RNA synthesis.

    Main Methods:

    • Infection of EL4 cells with mumps virus.
    • Treatment of cells with ultraviolet-inactivated virus or mouse interferon.
    • Isolation and application of mumps virus envelope glycoproteins.
    • Addition of specific antibodies and cytochalasin D to assess effects on RNA synthesis.

    Main Results:

    • Mumps virus infection significantly depressed cellular RNA synthesis in EL4 cells.
    • Inhibition occurred even with inactivated virus or interferon, suggesting replication is not required.
    • Isolated mumps virus envelope glycoproteins inhibited RNA synthesis.
    • Antibodies enhanced the inhibitory effect of glycoproteins, likely via aggregate formation.
    • Glycoproteins did not inhibit RNA synthesis in the presence of cytochalasin D.

    Conclusions:

    • Mumps virus envelope glycoproteins are responsible for inhibiting cellular RNA synthesis in EL4 cells.
    • The inhibition mechanism does not solely depend on active viral replication.
    • Antibody-mediated aggregation of glycoproteins may potentiate the inhibitory effect.

    More Related Videos

    Using Click Chemistry to Measure the Effect of Viral Infection on Host-Cell RNA Synthesis09:35

    Using Click Chemistry to Measure the Effect of Viral Infection on Host-Cell RNA Synthesis

    Published on: August 9, 2013

    Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein09:39

    Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein

    Published on: April 21, 2015

    Related Concept Videos

    Inhibitors of Bacterial Protein Synthesis01:25

    Inhibitors of Bacterial Protein Synthesis

    Aminoglycosides constitute a highly potent class of bactericidal antibiotics that exert their antimicrobial effects by targeting the bacterial ribosome, specifically disrupting protein synthesis. These polycationic molecules consist of amino-modified sugars linked via glycosidic bonds to an aminocyclitol core such as 2-deoxystreptamine or streptamine. Their strong positive charges facilitate tight binding to the negatively charged phosphate backbone of ribosomal RNA (rRNA), primarily at the 16S...
    Inhibitors of Bacterial DNA Synthesis01:28

    Inhibitors of Bacterial DNA Synthesis

    Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...
    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...
    Antiviral Nucleoside Inhibitors01:22

    Antiviral Nucleoside Inhibitors

    Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...
    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...