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Updated: Nov 22, 2025

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
Published on: September 14, 2010
Interplay Between KSHV and the Host DNA Damage Response
1Division of Virology, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, Suita, Japan.
Abstract:
Interactions between viruses and cellular factors are essential for viral replication or host defense. The DNA damage response (DDR) orchestrates a molecular network of cellular mechanisms that integrates cell cycle regulation and DNA repair or apoptosis. Numerous studies have revealed that the DDR is activated by virus infection, aberrant DNA structures generated by viral DNA replication, or the integration of retroviruses. Although the DDR is an essential function for maintaining the genomic integrity of cells, viruses may utilize this mechanism to build a convenient environment for themselves, and the resulting perturbation of the DDR has been shown to increase the risk of tumorigenesis. There have been many studies investigating the roles of the DDR in oncogenic viruses such as Epstein-Barr virus (EBV), human papillomavirus (HPV), hepatitis B virus (HBV), human T-cell leukemia virus type 1 (HTLV-1), and Kaposi's sarcoma-associated herpesvirus (KSHV). This review summarizes current knowledge on the roles of DDR in the KSHV lifecycle.
Insights
Viruses hijack the DNA damage response (DDR) to aid replication, potentially increasing cancer risk. This review explores the DDR
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.
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