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Home
Intranasal Hsv-1 Infection Drives Region-specific Interferon-dominant Microglial Remodeling.

Home
Intranasal Hsv-1 Infection Drives Region-specific Interferon-dominant Microglial Remodeling.

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Published on: October 28, 2019

Intranasal HSV-1 Infection Drives Region-Specific Interferon-Dominant Microglial Remodeling.

Seth Frietze, Cameron Lunn, Dean Oldham

Biorxiv : the Preprint Server for Biology

|April 3, 2026

View abstract on PubMed

Summary

This summary is machine-generated.

Herpes simplex virus type 1 (HSV-1) infection alters brain immune cells, promoting neuroinflammation. This study reveals how HSV-1 reshapes microglial responses, contributing to neurological vulnerability.

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Detection of the Genome and Transcripts of a Persistent DNA Virus in Neuronal Tissues by Fluorescent In situ Hybridization Combined with Immunostaining

Detection of the Genome and Transcripts of a Persistent DNA Virus in Neuronal Tissues by Fluorescent In situ Hybridization Combined with Immunostaining

Published on: January 23, 2014

Area of Science:

Neuroimmunology
Virology
Genomics

Background:

Herpes simplex virus type 1 (HSV-1) is a neurotropic virus impacting the central nervous system (CNS).
HSV-1 is linked to chronic neuroinflammation, cognitive decline, and neurodegenerative diseases.
Microglial roles in sustained HSV-1 neuroinflammation are not fully understood.

Purpose of the Study:

To define transcriptional and epigenetic mechanisms of microglial responses during HSV-1 infection.
To investigate how HSV-1 shapes microglial activity in vivo.
To understand the molecular basis of HSV-1-induced neuroinflammation.

Main Methods:

Integrated single-nucleus RNA sequencing, chromatin accessibility, and spatial transcriptomics.
Utilized a physiologically relevant intranasal HSV-1 infection model.

Analyzed CD11b+ nuclei to identify distinct microglial and macrophage populations.

Main Results:

HSV-1 infection induced distinct interferon (IFN)-responsive microglial and macrophage populations.
Identified amplification of STAT1/2, IRF1, and CEBPB regulons in IFN-responsive states.
Observed reduced homeostatic microglial gene signatures (e.g., ApoE, Cst3) and localized HSV-1 to brainstem regions.

Conclusions:

HSV-1 drives significant transcriptional and epigenetic remodeling of microglia.
Characterized by IFN-responsive states and loss of homeostatic signatures.
Provides mechanistic insight into persistent neuroinflammation and neurological disease risk.