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Molecular piracy of Kaposi's sarcoma associated herpesvirus
1Department of Microbiology and Molecular Genetics, Tumor Virology Division, New England Regional Primate Research Center, Harvard Medical School, 1 Pine Hill Drive, Southborough, MA 01772, USA.
Abstract:
Kaposi's Sarcoma associated Herpesvirus (KSHV) is the most recently discovered human tumor virus and is associated with the pathogenesis of Kaposi's sarcoma, primary effusion lymphoma, and Multicentric Casttleman's disease. KSHV contains numerous open reading frames with striking homology to cellular genes. These viral gene products play a variety of roles in KSHV-associated pathogenesis by disrupting cellular signal transduction pathways, which include interferon-mediated anti-viral responses, cytokine-regulated cell growth, apoptosis, and cell cycle control. In this review, we will attempt to cover our understanding of how viral proteins deregulate cellular signaling pathways, which ultimately contribute to the conversion of normal cells to cancerous cells.
Insights
Kaposi's Sarcoma-associated Herpesvirus (KSHV) disrupts cellular signaling pathways, leading to diseases like Kaposi's sarcoma. This review explores how KSHV proteins contribute to cancer development by deregulating cell functions.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Kaposi's Sarcoma-associated Herpesvirus (KSHV) is a human tumor virus linked to Kaposi's sarcoma, primary effusion lymphoma, and Multicentric Castleman's disease.
- KSHV possesses open reading frames homologous to cellular genes, suggesting viral protein involvement in pathogenesis.
Purpose of the Study:
- To review the mechanisms by which KSHV viral proteins deregulate cellular signaling pathways.
- To elucidate the role of these deregulated pathways in the transformation of normal cells into cancerous cells.
Main Methods:
- This is a review article, synthesizing existing research on KSHV and cellular signaling.
- Analysis of viral gene products and their homology to cellular proteins.
- Examination of KSHV's impact on cellular processes like signal transduction, apoptosis, and cell cycle control.
Main Results:
- KSHV viral proteins disrupt critical cellular signal transduction pathways.
- These disruptions affect interferon-mediated antiviral responses, cytokine-regulated cell growth, apoptosis, and cell cycle control.
- Viral proteins play a significant role in KSHV-associated pathogenesis.
Conclusions:
- KSHV proteins are key players in disrupting cellular functions, contributing to oncogenesis.
- Understanding these viral-host interactions is crucial for developing therapeutic strategies against KSHV-associated malignancies.