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Related Concept Videos

Herpes01:28

Herpes

Herpes simplex type 1 (HSV‑1) is a widespread pathogen responsible for orolabial lesions. It is an enveloped, double-stranded DNA (dsDNA) virus belonging to the family Herpesviridae. Once the virus infects a host cell, its double‑stranded DNA genome is delivered into the nucleus, where a coordinated cascade of immediate‑early, early, and late gene expression directs viral DNA replication, structural protein synthesis, and virion assembly. After primary infection of epithelial cells, HSV-1...

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Updated: Jun 19, 2026

Ex Vivo Organotypic Corneal Model of Acute Epithelial Herpes Simplex Virus Type I Infection
07:55

Ex Vivo Organotypic Corneal Model of Acute Epithelial Herpes Simplex Virus Type I Infection

Published on: November 3, 2012

Time-Course Transcriptomic Analysis Reveals PANoptosis-CCL2 Axis in Herpes Simplex Keratitis.

Changyu Wu1, Junwen Ouyang1, Yaoyao Liu1

  • 1Department of Ophthalmology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.

Investigative Ophthalmology & Visual Science
|June 18, 2026
PubMed
Summary
This summary is machine-generated.

Herpes simplex keratitis involves sequential immune responses and programmed cell death (PCD), with PANoptosis amplifying antiviral immunity. Targeting the PANoptosis-CCL2/CCR2 axis offers a potential therapeutic strategy for HSK.

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Last Updated: Jun 19, 2026

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Recurrent Herpetic Stromal Keratitis in Mice, a Model for Studying Human HSK
07:27

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Published on: December 18, 2012

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Herpes simplex virus type 1 (HSV-1) causes herpes simplex keratitis (HSK), a significant ocular infection.
  • Understanding the interplay between immune responses and programmed cell death (PCD) is crucial for HSK pathogenesis.
  • PANoptosis, an integrated form of PCD, has emerged as a key cellular process in various inflammatory conditions.

Purpose of the Study:

  • To characterize the temporal dynamics of corneal immune responses and PCD after HSV-1 infection.
  • To investigate the specific role of PANoptosis in modulating immune responses during HSK.
  • To identify potential therapeutic targets within the identified pathways.

Main Methods:

  • Established a murine model of HSK induced by HSV-1 infection.
  • Performed time-course RNA sequencing on infected murine corneas.
  • Utilized quantitative real-time PCR, western blotting, immunofluorescence, flow cytometry, and co-culture experiments for mechanistic analysis.
  • Assessed PCD pathways using antagonists targeting PANoptosis.

Main Results:

  • Identified sequential immune response phases: homeostasis disruption, immune amplification, and tissue reorganization.
  • Demonstrated that the immune amplification phase involves apoptosis, pyroptosis, and necroptosis, culminating in PANoptosis.
  • Confirmed Z-DNA-binding protein 1 (ZBP1) as a driver of PANoptosome formation in HSK.
  • Showed that PANoptosis promotes C-C motif chemokine ligand 2 (CCL2) release, enhancing macrophage activation and migration via the CCL2/CCR2 axis.
  • Found that the PANoptosis-CCL2/CCR2 axis is upregulated in infected corneas and can be suppressed by inhibitors.

Conclusions:

  • HSK pathogenesis involves a temporal coordination between immune activation and PANoptosis.
  • PANoptosis plays a critical role in amplifying antiviral immune responses during HSK.
  • The ZBP1-PANoptosome-mediated PANoptosis-CCL2/CCR2 axis represents a promising therapeutic target for HSK treatment.