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Betaherpesvirus-conserved cytomegalovirus tegument protein ppUL32 (pp150) controls cytoplasmic events during virion

David P AuCoin1, Geoffrey B Smith, Christopher D Meiering

  • 1Department of Microbiology and Immunology, Fairchild Science Building, 299 Campus Drive, Stanford University School of Medicine, Stanford, CA 94305-5124, USA.

Journal of Virology
|July 29, 2006
PubMed

Insights

Human cytomegalovirus (CMV) pp150 protein is essential for virion maturation and egress. Deletion mutants show impaired viral spread, highlighting pp150

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Human cytomegalovirus (CMV) is a significant pathogen, particularly in immunocompromised individuals.
  • The UL32 gene product, pp150, is a conserved tegument protein crucial for betaherpesvirus replication.
  • pp150 accumulates in cytoplasmic inclusions during late-stage CMV infection.

Purpose of the Study:

  • To investigate the role of the pp150 protein in human cytomegalovirus (CMV) virion maturation and replication.
  • To identify critical domains within pp150 essential for its function.
  • To explore the evolutionary conservation of UL32 homologs in CMV replication.

Main Methods:

  • Construction and analysis of a UL32 deletion mutant of CMV (DeltaUL32-BAC).
  • Complementation studies using pp150 expression plasmids and heterologous UL32 homologs.
  • Analysis of viral gene expression, DNA replication, and particle assembly in infected cells.
  • Assessment of viral spread and infectivity in cell culture.

Main Results:

  • pp150 is critical for virion maturation within the cytoplasm.
  • The amino terminus and conserved regions (CR1, CR2) of pp150 are essential for replication.
  • Deletion of the carboxyl terminus or disruption of glycosylation sites had minimal impact on maturation.
  • African green monkey CMV UL32 complemented replication, but murine CMV M32 did not.
  • DeltaUL32-BAC exhibited normal viral gene expression and DNA replication but failed to spread, indicating a block in virion egress.

Conclusions:

  • pp150 plays a vital role in CMV virion egress, potentially during final envelopment.
  • Specific domains of pp150 are crucial for its function in viral replication and spread.
  • Evolutionary divergence exists between primate and rodent CMV UL32 proteins.
  • The absence of pp150 blocks secondary viral spread without affecting dense body release.

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