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Distinct and separate roles for herpesvirus-conserved UL97 kinase in cytomegalovirus DNA synthesis and encapsidation

D G Wolf1, C T Courcelle, M N Prichard

  • 1Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305-5124, USA.

Proceedings of the National Academy of Sciences of the United States of America
|February 15, 2001
PubMed

Insights

Human cytomegalovirus UL97 kinase is crucial for viral replication, impacting both DNA synthesis and capsid assembly. Its absence causes significant defects in viral DNA accumulation and maturation.

Area of Science:

  • Virology
  • Molecular Biology
  • Antiviral Therapy

Background:

  • Human cytomegalovirus (HCMV) UL97 kinase is a key target for antiviral drugs.
  • UL97 plays a role in multiple stages of viral replication.

Purpose of the Study:

  • To investigate the specific roles of the UL97 kinase in HCMV replication.
  • To elucidate the impact of UL97 on viral DNA synthesis and capsid maturation.

Main Methods:

  • Comparison of wild-type HCMV with a UL97 deletion mutant.
  • Block-release experiments using the antiviral 2-bromo-5,6-dichloro-1-(beta-D-ribofuranosyl)-benzimidazole.
  • Transmission electron microscopy (TEM) to analyze capsid structure.

Main Results:

  • UL97 deletion mutant showed a 4- to 6-fold reduction in DNA accumulation (early defect).
  • A significant late defect in capsid maturation was observed, reducing replication 100- to 1000-fold.
  • TEM revealed accumulation of empty A-like capsids lacking DNA and scaffold in UL97-deficient cells.

Conclusions:

  • UL97 kinase is essential for efficient viral DNA synthesis and proper capsid assembly.
  • Phosphorylation by UL97 enhances DNA packaging and maturation, critical for HCMV replication.
  • Understanding UL97 function is vital for developing effective antiviral strategies against HCMV.

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