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Human kinome profiling identifies a requirement for AMP-activated protein kinase during human cytomegalovirus

Laura J Terry1, Livia Vastag, Joshua D Rabinowitz

  • 1Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.

Proceedings of the National Academy of Sciences of the United States of America
|February 9, 2012
PubMed

Insights

Human cytomegalovirus (HCMV) infection alters cellular signaling and metabolism. A new study reveals that AMP-activated protein kinase (AMPK) is crucial for viral replication and metabolic reprogramming during HCMV infection.

Area of Science:

  • Virology
  • Cellular Biology
  • Molecular Biology

Background:

  • Human cytomegalovirus (HCMV) infection significantly alters host cell signaling pathways, evidenced by widespread changes in protein phosphorylation and kinase activity.
  • Numerous cellular kinases are implicated in viral replication, yet many remain uncharacterized in the context of HCMV infection.

Purpose of the Study:

  • To conduct a comprehensive RNA interference (RNAi) screen to identify cellular kinases influencing HCMV replication.
  • To investigate the role of the AMP-activated protein kinase (AMPK) pathway in HCMV-induced cellular reprogramming and viral production.

Main Methods:

  • A genome-wide RNAi screen was performed to identify host kinases affecting HCMV growth.
  • The effects of an AMPK inhibitor (compound C) on HCMV-induced metabolic changes and viral protein accumulation were assessed.

Main Results:

  • The RNAi screen identified 106 cellular kinases that influence HCMV replication, with many not previously associated with HCMV.
  • Multiple components of the AMPK pathway were implicated in the screen.
  • Inhibition of AMPK with compound C reversed significant HCMV-induced metabolic alterations, reduced viral protein synthesis, and decreased infectious virus production.

Conclusions:

  • HCMV infection relies on host cell signaling, particularly the AMPK pathway, for efficient viral replication.
  • AMPK plays a critical role in regulating host cell metabolism to support HCMV replication and propagation.

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