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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
07:02

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)

Published on: September 14, 2010

The cell cycle and how it is steered by Kaposi's sarcoma-associated herpesvirus cyclin

Emmy W Verschuren1, Nic Jones2, Gerard I Evan3

  • 1Stanford University, Pathology Department, 300 Pasteur Drive, MC 5324, Stanford, CA 94305, USA.

The Journal of General Virology
|May 29, 2004
PubMed

Insights

Kaposi

Area of Science:

  • Molecular Biology
  • Virology
  • Cell Biology

Background:

  • Cell cycle progression relies on cyclin-dependent kinases (Cdks) and cyclins.
  • Gammaherpesviruses, including Kaposi's sarcoma-associated herpesvirus (KSHV), encode viral cyclins (v-cyclins).
  • KSHV's v-cyclin is found in malignant cells, suggesting a role as a viral oncogene.

Purpose of the Study:

  • To review the structural and functional properties of mammalian cyclin/Cdk complexes.
  • To explain the molecular events governing cell cycle progression through G1/S and G2/M phases.
  • To elucidate the specific functional properties of KSHV's v-cyclin.

Main Methods:

  • Review of existing literature on mammalian cyclin/Cdk complexes.
  • Analysis of molecular events in cell cycle regulation.
  • Examination of v-cyclin's structural and functional characteristics.

Main Results:

  • Mammalian cyclin/Cdk complexes regulate cell cycle progression.
  • v-Cyclin shares properties with cellular cyclin D, potentially deregulating host cell cycle.
  • v-Cyclin is expressed in KSHV-associated malignancies.

Conclusions:

  • v-Cyclin acts as a viral oncogene by mimicking cellular cyclins.
  • v-Cyclin's deregulation of the cell cycle may contribute to KSHV-associated neoplasms.
  • Further research is needed to understand the interplay between v-cyclin and KSHV pathogenesis.

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