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Updated: Jul 15, 2026

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
09:53

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus

Published on: August 25, 2017

Targeting the PI3K and MAPK pathways to treat Kaposi's-sarcoma-associated herpes virus infection and pathogenesis

Phelps J Lambert1, Aniqa Z Shahrier, Audy G Whitman

  • 1Brody School of Medicine at East Carolina University, Department of Microbiology & Immunology, Greenville, NC 27834, USA.

Expert Opinion on Therapeutic Targets
|May 1, 2007
PubMed

Insights

Kaposi

Area of Science:

  • Cellular biology
  • Virology
  • Molecular signaling

Background:

  • Cellular signaling pathways, including phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK), are crucial for regulating diverse cellular functions.
  • Viruses often exploit these signaling pathways to manipulate host cell processes for their own benefit.
  • Kaposi's sarcoma-associated herpes virus (KSHV) is a notable virus that targets PI3K and MAPK signaling.

Purpose of the Study:

  • To review how KSHV manipulates PI3K and MAPK signaling pathways.
  • To explore the role of these pathways in KSHV infection and pathogenesis.
  • To discuss the potential of targeting PI3K and MAPK pathways to inhibit KSHV.

Main Methods:

  • Literature review of existing research on KSHV, PI3K, and MAPK signaling.
  • Analysis of studies detailing viral manipulation of cellular pathways.
  • Synthesis of information on the role of these pathways in viral replication and disease.

Main Results:

  • KSHV manipulates PI3K and MAPK pathways to control cell survival, migration, and immune responses.
  • These pathways are critical for KSHV reactivation and lytic replication.
  • KSHV-induced manipulation of PI3K and MAPK signaling contributes to malignant transformation.

Conclusions:

  • Targeting PI3K and MAPK signaling pathways presents a potential therapeutic strategy against KSHV infection.
  • Understanding KSHV's manipulation of these pathways is key to developing novel antiviral treatments.
  • Inhibition of PI3K and MAPK could disrupt KSHV pathogenesis and viral replication.

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