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Human Pirh2 is a novel inhibitor of prototype foamy virus replication

Lanlan Dong1,2, Qingqing Cheng3, Zhihao Wang4

  • 1Pathogenic Organism and Infectious Diseases Research Institute, School of Basic Medical Sciences, Wuhan University, Donghu Road No. 185, Wuchang, Wuhan 430071, China. donglanlan.2006@163.com.

Viruses
|April 8, 2015
PubMed

Insights

Human Pirh2 protein inhibits prototype foamy virus (PFV) replication by targeting its transactivator Tas. This discovery offers insights into controlling chronic retroviral infections and PFV latency.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Prototype foamy virus (PFV) is a nonpathogenic retrovirus causing chronic infections.
  • Host cell factors play a role in restricting PFV replication.
  • Understanding host-viral interactions is crucial for managing persistent infections.

Purpose of the Study:

  • To identify novel host factors that inhibit prototype foamy virus (PFV) replication.
  • To elucidate the mechanism by which Pirh2 suppresses PFV.
  • To explore the role of Pirh2 in the latency of PFV infection.

Main Methods:

  • Overexpression and siRNA-mediated knockdown of human p53-induced RING-H2 protein (Pirh2).
  • Assessment of PFV replication levels.
  • Dual-luciferase assays and coimmunoprecipitation to study protein interactions and transcriptional activity.

Main Results:

  • Pirh2 was identified as a novel inhibitor of PFV replication.
  • Pirh2 overexpression decreased PFV replication, while Pirh2 knockdown increased it.
  • Pirh2 interacts with the PFV transactivator Tas, down-regulating its expression and activity, thereby suppressing viral transcription from PFV LTR and IP promoters.

Conclusions:

  • Pirh2 suppresses PFV replication by inhibiting the Tas transactivator and viral promoter transcription.
  • The inhibitory function of Pirh2 depends on its N-terminal and RING domains.
  • Pirh2's role in suppressing PFV replication may contribute to the establishment and maintenance of PFV latency.

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