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Downregulation of Poly(ADP-Ribose) Polymerase 1 by a Viral Processivity Factor Facilitates Lytic Replication of

Woo-Chang Chung1, Joo-Hee Park1, Hye-Ri Kang1

  • 1Virus-Host Interactions Laboratory, Department of Biosystems and Biotechnology, Division of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.

Journal of Virology
|July 10, 2015
PubMed
Abstract

Insights

Kaposi's sarcoma-associated herpesvirus (KSHV) uses its PF-8 protein to degrade the host factor PARP-1, which normally inhibits viral replication. This viral strategy promotes KSHV lytic replication by overcoming host defenses.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Gammaherpesviruses are human pathogens linked to tumors, establishing latency in B lymphocytes.
  • Kaposi's sarcoma-associated herpesvirus (KSHV) replication and transcription activator (RTA) is key for lytic replication, regulated by host and viral factors.
  • Poly(ADP-ribose) polymerase 1 (PARP-1) inhibits KSHV lytic replication.

Purpose of the Study:

  • To investigate how KSHV overcomes the inhibitory effect of PARP-1 on RTA activity.
  • To elucidate the viral mechanism for promoting gammaherpesvirus lytic replication.

Main Methods:

  • Investigated the interaction between KSHV PF-8 and host PARP-1.
  • Assessed the degradation of PARP-1 via proteasome-dependent pathways.
  • Analyzed the impact of PF-8 on RTA activity and KSHV lytic replication.
  • Examined conservation in murine gammaherpesvirus 68.

Main Results:

  • KSHV downregulates PARP-1 during reactivation.
  • KSHV PF-8 interacts with and degrades PARP-1 in a proteasome-dependent manner.
  • PF-8 knockdown reduces lytic replication and increases PARP-1 levels.
  • PF-8 overexpression reduces PARylated RTA and enhances RTA transactivation.

Conclusions:

  • KSHV employs a novel mechanism involving PF-8 to degrade the host inhibitor PARP-1.
  • This viral strategy facilitates gammaherpesvirus lytic replication.
  • The mechanism is conserved in other gammaherpesviruses, suggesting a common viral strategy.

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