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Updated: Mar 30, 2026

Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus
07:10

Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus

Published on: August 15, 2025

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Kaposi's sarcoma-associated herpesvirus: the role of lytic replication in targeted therapy

Graciela Andrei1, Robert Snoeck

  • 1Laboratory of Virology, Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium.

Current Opinion in Infectious Diseases
|November 3, 2015
PubMed
Abstract

Insights

Targeting Kaposi's sarcoma-associated herpesvirus (KSHV) lytic replication is crucial for preventing KSHV-related cancers. New therapies aim to inhibit viral replication or induce lytic replication for tumor cell death.

Area of Science:

  • Virology
  • Oncology
  • Infectious Diseases

Background:

  • Kaposi's sarcoma-associated herpesvirus (KSHV) is linked to Kaposi sarcoma, primary effusion lymphoma, and multicentric Castleman disease.
  • Current treatments for KSHV-associated malignancies are suboptimal and toxic, with no established therapeutic guidelines.
  • Antiherpesvirus drugs show inconsistent efficacy against KSHV in its latent state.

Purpose of the Study:

  • To review the role of KSHV lytic replication in disease pathogenesis.
  • To assess advancements in targeting KSHV lytic replication for preventing KSHV-related malignancies.

Main Methods:

  • Review of current research on KSHV pathobiology and therapeutic strategies.
  • Investigation of novel antiviral agents and cellular process targets.
  • Exploration of lytic induction therapy for tumor cell death.

Main Results:

  • New inhibitors of KSHV lytic replication are under development.
  • Novel therapeutic modalities targeting virus-hijacked cellular processes are being explored.
  • Lytic induction therapy aims to promote tumor cell death by reactivating latent KSHV.

Conclusions:

  • KSHV lytic replication is critical in KSHV-associated tumorigenesis.
  • Targeting viral replication and cellular processes is a promising strategy.
  • Combination therapies, including antivirals and lytic inducers, are being investigated.

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