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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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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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DNA Damage Can Stall the Cell Cycle02:36

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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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Nucleotide Excision Repair01:38

Nucleotide Excision Repair

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DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Nucleotide Excision Repair01:08

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Overview
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Overview of DNA Repair02:25

Overview of DNA Repair

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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Overview of DNA Repair02:25

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Visualization of DNA Repair Proteins Interaction by Immunofluorescence
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HSV-I and the cellular DNA damage response.

Samantha Smith1, Sandra K Weller1

  • 1Department of Molecular Biology & Biophysics, University of Connecticut Health Center, Farmington, CT 06030, USA.

Future Virology
|July 28, 2015
PubMed
Summary

Herpes simplex virus (HSV) infection hijacks cellular DNA damage response (DDR) pathways. This review highlights recent findings on how HSV manipulates DDR to replicate its genome.

Keywords:
C-NHEJDDRDNA damage responseHRHSV-1Herpes simplex virus 1MMEJSSAclassic nonhomologous end-joininghomologous recombinationintrinsic antiviral defensemicrohomology-mediated end joiningsingle-strand annealingvirally encoded recombinasevirus–host interactions

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Area of Science:

  • Virology
  • Molecular Biology
  • Genetics

Background:

  • Genetic recombination in Herpes simplex virus (HSV) was first observed in 1955.
  • Understanding of DNA repair mechanisms and their interaction with viral infections has advanced significantly.
  • Cellular DNA damage response (DDR) pathways are increasingly recognized for their role in viral pathogenesis.

Purpose of the Study:

  • To review recent observations on the interaction between HSV and cellular DDR pathways.
  • To elucidate how HSV navigates the host cell's DDR machinery for its own replication.
  • To provide insights into the molecular mechanisms governing viral genome replication in the context of host defense.

Main Methods:

  • Literature review focusing on recent publications.
  • Analysis of studies investigating the interplay between HSV proteins and cellular DDR components.
  • Examination of experimental evidence detailing the manipulation of DDR pathways by HSV.

Main Results:

  • HSV-1 infection leads to the depletion of key DDR proteins, such as DNA-dependent protein kinase catalytic subunit, in an ICP0-dependent manner.
  • Numerous interactions between HSV and cellular DDR pathways have been reported.
  • Recent findings reveal specific strategies employed by HSV to exploit DDR for its genomic replication.

Conclusions:

  • HSV actively interacts with and manipulates host cell DDR pathways.
  • These interactions are crucial for successful viral genome replication.
  • Further research into these mechanisms can reveal novel therapeutic targets for HSV infections.