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KSHV-Mediated Angiogenesis in Tumor Progression.

Pravinkumar Purushothaman1, Timsy Uppal2, Roni Sarkar3

  • 1Department of Microbiology and Immunology, University of Nevada, Reno, School of Medicine, 1664 N Virginia Street, MS 320, Reno, NV 89557, USA. pravinp@medicine.nevada.edu.

Viruses
|July 23, 2016
PubMed
Summary

Human herpesvirus 8 (HHV-8) drives Kaposi's sarcoma (KS) by inducing blood vessel growth. Understanding HHV-8's role in angiogenesis is key to developing new therapies for KS and related diseases.

Keywords:
KSHVKaposi’s sarcomaKaposi’s sarcoma-associated herpesvirusangiogenesislymphangiogenesisoncogenesisoncoproteins

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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
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Area of Science:

  • Oncology
  • Virology
  • Immunology

Background:

  • Human herpesvirus 8 (HHV-8), or Kaposi's sarcoma-associated herpesvirus (KSHV), is a gamma herpesvirus linked to Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman's disease (MCD).
  • KS is an endothelial cell tumor often seen in immunocompromised individuals, characterized by abnormal angiogenesis, inflammation, and proliferation.
  • KSHV infection triggers angiogenesis via viral and cellular factors, contributing to KS pathogenesis alongside immune evasion strategies and pro-inflammatory stimuli.

Purpose of the Study:

  • To review current knowledge on KSHV-mediated angiogenesis regulation.
  • To integrate findings on host and viral genes in KSHV-driven oncogenesis.
  • To discuss recent advancements in KSHV research models and anti-angiogenic therapies.

Main Methods:

  • Literature review integrating findings on host and viral genes.
  • Analysis of cell-culture and animal models of KSHV infection.
  • Examination of anti-angiogenic therapeutic strategies.

Main Results:

  • KSHV directly induces angiogenesis through autocrine and paracrine signaling.
  • Viral oncoproteins produced by KSHV infection transform endothelial cells by regulating host signaling pathways.
  • Angiogenesis and lymph-angiogenesis pathways likely modulate KSHV-induced tumorigenesis rates.

Conclusions:

  • KSHV employs sophisticated mechanisms to promote angiogenesis, crucial for KS development.
  • Understanding these mechanisms is vital for developing targeted anti-angiogenic therapies.
  • Further research integrating genetic, cellular, and therapeutic insights is needed for effective KSHV-related disease management.