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Related Concept Videos

Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
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Mechanisms of Retrovirus-induced Cancers01:51

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Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
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Retroviruses02:33

Retroviruses

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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’...
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Viral Recombination00:57

Viral Recombination

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Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.
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Viruses with RNA Genomes01:29

Viruses with RNA Genomes

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RNA viruses are categorized into positive-strand, negative-strand, or double-stranded groups based on their genomic structure and replication mechanisms. This classification dictates how they exploit host cellular machinery for protein synthesis and replication. Some RNA viruses also utilize reverse transcription as part of their life cycle, further diversifying their replication strategies.Positive-Strand RNA VirusesPositive-strand RNA viruses have genomes that function directly as messenger...
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DNA Damage can Stall the Cell Cycle02:37

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Related Experiment Video

Updated: Sep 26, 2025

Visualization of SARS-CoV-2 using Immuno RNA-Fluorescence In Situ Hybridization
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SARS-CoV-2 hijacks host cell genome instability pathways.

Joshua Victor1, Tristan Jordan2, Erica Lamkin1

  • 1University of Vermont.

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|April 20, 2022
PubMed
Summary
This summary is machine-generated.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes genome instability and genetic alterations in host cells. A novel inhibitor, JH-RE-06, suppresses viral proliferation and DNA damage, offering therapeutic potential.

Keywords:
REV1SARS-CoV-2autophagymicrosatellite-instabilitymutagenesistelomeres

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Area of Science:

  • Molecular Biology
  • Genetics
  • Virology

Background:

  • The molecular mechanisms underlying COVID-19's adverse health outcomes, including long-COVID, remain unclear.
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection's impact on host cell genome integrity is poorly understood.

Approach:

  • Investigated SARS-CoV-2's effect on host cell DNA repair and translesion synthesis pathways.
  • Analyzed genetic alterations such as mutagenesis, telomere dysregulation, and microsatellite instability (MSI) in infected cells.
  • Examined the impact of a REV1 inhibitor (JH-RE-06) on viral proliferation and genome instability.

Key Points:

  • SARS-CoV-2 infection induces host cell genome instability by altering DNA repair and translesion synthesis.
  • Infection leads to increased mutagenesis, telomere dysregulation, and MSI, linked to reduced DNA repair proteins (MLH1, MSH6, MSH2).
  • JH-RE-06, a translesion DNA synthesis inhibitor, suppressed SARS-CoV-2 proliferation and genome instability, potentially via autophagy induction.

Conclusions:

  • SARS-CoV-2 infection compromises host cell genome stability, contributing to COVID-19's pathology.
  • Targeting translesion DNA synthesis with inhibitors like JH-RE-06 may offer a therapeutic strategy against SARS-CoV-2 and its associated genomic consequences.