Related Experiment Video

Updated: Sep 7, 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

Interferon induction by viruses. XI. Early events in the induction process

C Svitlik, P I Marcus

    Journal of Interferon Research
    |January 1, 1984
    PubMed

    Insights

    Researchers used NH4Cl to study how Newcastle disease virus (NDV), Sindbis virus, and vesicular stomatitis virus (VSV) enter aged cells to induce interferon (IFN). They found distinct entry mechanisms, with Sindbis and VSV entry dependent on acidic conditions for RNA release into the cytosol.

    Area of Science:

    • Virology
    • Cell Biology
    • Immunology

    Background:

    • Understanding virus entry mechanisms is crucial for controlling viral infections and modulating immune responses.
    • Interferon (IFN) induction is a key antiviral defense pathway initiated by the detection of viral components.
    • Previous studies suggested that low pH-dependent fusion is involved in the entry of some viruses into cells.

    Purpose of the Study:

    • To elucidate the entry mechanisms of Newcastle disease virus (NDV), Sindbis virus, and vesicular stomatitis virus (VSV) into aged primary chick embryo cells.
    • To investigate the role of low pH-dependent processes in viral entry and subsequent IFN induction.
    • To differentiate the entry pathways of Sindbis virus and VSV using specific inhibitors.

    Main Methods:

    • Utilized NH4Cl, a lysosomotropic weak base, to disrupt low pH-dependent membrane fusion during virus entry.
    • Monitored three key parameters: dose-response curves for IFN yield, activity of IFN-inducing particles (IFP), and quantum yield of IFN.
    • Employed cytochalasin B to further distinguish between the entry mechanisms of Sindbis virus and VSV.

    Main Results:

    • NDV entry and IFN induction were unaffected by NH4Cl, indicating an acidic-independent fusion mechanism at the plasma membrane.
    • Sindbis virus infectivity and IFP activity were inhibited by NH4Cl in a dose-dependent manner, consistent with acidic-fusion entry.
    • VSV infectivity was highly sensitive to NH4Cl, while IFP activity remained largely functional, but IFN quantum yield was reduced, suggesting acidic-endocytosis and a critical step of RNA transfer from endosomes.

    Conclusions:

    • NDV, Sindbis virus, and VSV exhibit distinct entry mechanisms into aged chick embryo cells, influencing IFN induction.
    • Sindbis virus and VSV share a common, rate-limiting step involving the transfer of viral RNA from acidic vacuoles to the cytosol.
    • The study differentiates Sindbis virus (acidic-fusion) and VSV (acidic-endocytosis) entry pathways, highlighting the importance of endosomal pH for viral RNA release and subsequent IFN stimulation.

    More Related Videos

    Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production08:32

    Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

    Published on: March 2, 2014

    High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes10:00

    High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

    Published on: March 24, 2015

    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...
    Immune Response Against Viral Pathogens01:29

    Immune Response Against Viral Pathogens

    The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
    NK Cells
    NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
    Size and Structure of Viral Genomes01:26

    Size and Structure of Viral Genomes

    Viral genomes exhibit remarkable diversity in size, structure, and composition, influencing their replication strategies and interactions with host cells. These genomes consist of either DNA or RNA and may be linear or circular. Additionally, they can be single-stranded or double-stranded, with each configuration affecting how the virus propagates within a host. RNA viruses, for instance, generally have smaller genomes than DNA viruses, a factor that contributes to their high mutation rates and...
    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...