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Immune Response Against Viral Pathogens01:29

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The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
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Updated: Nov 22, 2025

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
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Interplay Between KSHV and the Host DNA Damage Response.

Eriko Ohsaki1, Keiji Ueda1

  • 1Division of Virology, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, Suita, Japan.

Frontiers in Cellular and Infection Microbiology
|January 11, 2021
PubMed
Summary
This summary is machine-generated.

Viruses hijack the DNA damage response (DDR) to aid replication, potentially increasing cancer risk. This review explores the DDR

Keywords:
DDRDNA damage responseDNA repairKSHVKaposi’s sarcoma-associated herpesviruscell cyclelatencylytic replication

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Area of Science:

  • Molecular Biology
  • Virology
  • Cellular Biology
  • Oncology

Background:

  • Viral infections trigger cellular responses, including the DNA damage response (DDR).
  • The DDR is crucial for maintaining genomic integrity through DNA repair, cell cycle regulation, and apoptosis.
  • Viruses can exploit the DDR to facilitate their replication and survival.

Purpose of the Study:

  • To review the current understanding of the DNA damage response (DDR) in the context of viral infections.
  • To specifically summarize the roles of the DDR in the lifecycle of Kaposi's sarcoma-associated herpesvirus (KSHV).
  • To highlight how viral manipulation of the DDR may contribute to oncogenesis.

Main Methods:

  • Literature review of existing studies on viral-DDR interactions.
  • Analysis of research focusing on oncogenic viruses, including KSHV, EBV, HPV, HBV, and HTLV-1.
  • Synthesis of current knowledge regarding DDR activation and modulation during viral infection.

Main Results:

  • The DDR is frequently activated during infection by various viruses, including oncogenic types.
  • Viruses can manipulate DDR pathways to create a favorable environment for replication.
  • Perturbation of the DDR by viral factors is linked to an increased risk of tumorigenesis.

Conclusions:

  • The interplay between viruses and the DDR is a critical aspect of viral pathogenesis.
  • Understanding the DDR's role in KSHV lifecycle is essential for developing therapeutic strategies.
  • Targeting viral manipulation of the DDR may offer novel approaches for cancer prevention and treatment.