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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’...
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...
Viral Replication: Lytic Cycle01:20

Viral Replication: Lytic Cycle

Bacteriophages, or phages, are viruses that specifically infect bacteria. Among them, T-even bacteriophages, such as T4, exhibit a well-characterized lytic replication cycle in Escherichia coli (E. coli). This process ensures the rapid proliferation of the virus while ultimately leading to the destruction of the bacterial host.Attachment and DNA InjectionThe infection process begins with the recognition and binding of the T4 phage to the E. coli cell surface. Tail fibers of the phage...
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...

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Related Experiment Video

Updated: Jun 26, 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

Simian virus 40-host cell interaction during lytic infection.

E L Gershey

    Journal of Virology
    |April 1, 1979
    PubMed
    Summary

    Simian virus 40 (SV40) infection halts cell division in permissive cells, causing them to accumulate in G2 phase. Viral DNA synthesis proceeds, but cellular DNA replication initiation is blocked despite T-antigen presence.

    Area of Science:

    • Virology
    • Cell Biology
    • Molecular Biology

    Background:

    • Simian virus 40 (SV40) is a DNA tumor virus that infects permissive cells.
    • SV40 T-antigen plays a crucial role in viral replication and cellular processes.
    • Understanding SV40's impact on the host cell cycle is vital for comprehending viral pathogenesis.

    Purpose of the Study:

    • To investigate the effects of SV40 infection on the cell cycle progression of permissive CV-1 cells.
    • To determine the relationship between SV40 DNA replication and host cell division.
    • To elucidate the role of SV40 T-antigen in cell cycle regulation.

    Main Methods:

    • Infection of exponentially growing and serum-arrested CV-1 cells with SV40.
    • Analysis of SV40 T-antigen expression using immunofluorescence.

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    Published on: September 25, 2018

    Electrophoretic Analysis of Replication Through Structure-Prone DNA Repeats Within the SV40-Based Human Episome
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    Electrophoretic Analysis of Replication Through Structure-Prone DNA Repeats Within the SV40-Based Human Episome

    Published on: September 13, 2024

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    Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
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    Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques
    13:13

    Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques

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    Electrophoretic Analysis of Replication Through Structure-Prone DNA Repeats Within the SV40-Based Human Episome
    05:22

    Electrophoretic Analysis of Replication Through Structure-Prone DNA Repeats Within the SV40-Based Human Episome

    Published on: September 13, 2024

  • Quantification of cellular DNA content via flow cytometry.
  • Assessment of cell cycle distribution and mitotic index.
  • Main Results:

    • SV40 infection led to the accumulation of >90% of cells in the G2 phase by 24-48 hours post-infection.
    • Viral DNA synthesis occurred, but cellular DNA replication initiation was blocked.
    • A significant decrease in mitotic cells was observed, linked to an event at the G1-S phase border.
    • Cytopathic effects were first observed at 60 hours post-infection.

    Conclusions:

    • SV40 infection induces stationary cells to cycle and halts cell division after one round of DNA synthesis.
    • Sufficient T-antigen and DNA replication enzymes do not enable reinitiation of cellular DNA synthesis.
    • SV40 effectively disrupts host cell cycle regulation to favor viral replication.