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Updated: Feb 16, 2026

Extended Time-lapse Intravital Imaging of Real-time Multicellular Dynamics in the Tumor Microenvironment
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Timing Is Everything.

Luis M Schang1

  • 1Baker Institute for Animal Health, Cornell University, Ithaca, New York, USA lms428@cornell.edu.

Mbio
|January 4, 2018
PubMed
Summary

Herpes simplex virus 1 (HSV-1) infection success depends on the host cell cycle stage. Cells in early G1 and S phases are most permissive, while those in G2/mitosis are less permissive for HSV-1 gene expression.

Area of Science:

  • Virology
  • Cell Biology
  • Proteomics

Background:

  • Herpes simplex virus 1 (HSV-1) establishes lifelong infections.
  • Understanding factors influencing HSV-1 replication and reactivation is crucial for therapeutic strategies.

Purpose of the Study:

  • To investigate the impact of host cell cycle state on HSV-1 infection outcomes.
  • To identify specific cell cycle phases that are most permissive for HSV-1 gene expression and replication.

Main Methods:

  • Dynamic proteomics was employed to analyze protein expression changes during infection.
  • Machine learning algorithms were utilized to correlate cell cycle states with infection success.
  • HSV-1 gene expression was monitored across different host cell cycle phases.
Keywords:
cell cycledynamic proteomicsgene expressionherpes simplex virussingle-cell analyses

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Main Results:

  • Cell cycle stage significantly influences HSV-1 infection, accounting for 60% of infection success.
  • Cells infected during early G1 through S phases showed the highest permissivity for HSV-1 gene expression.
  • Infection of cells in late G2 to mitosis resulted in significantly reduced HSV-1 gene expression, with many cells becoming permanently nonpermissive after mitosis.

Conclusions:

  • The host cell cycle is a critical determinant of HSV-1 productive infection and reactivation efficiency.
  • Neurons and specific epidermal cells, which remain in permissive cell cycle stages and do not re-enter mitosis, are ideal for HSV-1 reactivation.
  • This cellular permissivity optimizes HSV-1 reactivation before the adaptive immune response can be mounted effectively.