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Herpes

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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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Related Experiment Video

Updated: Jun 2, 2026

Live Cell Imaging of Alphaherpes Virus Anterograde Transport and Spread

Live Cell Imaging of Alphaherpes Virus Anterograde Transport and Spread

Published on: August 16, 2013

Herpes simplex virus dances with amyloid precursor protein while exiting the cell.

Shi-Bin Cheng¹, Paulette Ferland, Paul Webster

¹Department of Pathology and Laboratory Medicine, Alpert Medical School of Brown University, Providence, Rhode Island, United States of America.

|April 13, 2011

Summary

Herpes simplex type 1 (HSV1) hijacks amyloid precursor protein (APP) for transport within epithelial cells, impacting both viral movement and APP distribution. This interaction may explain the link between HSV1 infection and Alzheimer's disease risk.

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Published on: October 28, 2019

Area of Science:

Cell biology
Virology
Neuroscience

Background:

Herpes simplex type 1 (HSV1) causes cold sores by replicating in epithelial cells and traveling to neuronal nuclei for latency.
Amyloid precursor protein (APP) is involved in cellular transport and its breakdown product, A-beta, forms senile plaques in Alzheimer's disease.
A potential link exists between HSV1 infection and increased Alzheimer's disease risk.

Purpose of the Study:

To investigate the hypothesis that HSV1 recruits cellular APP during intracellular transport within epithelial cells.
To elucidate the functional consequences of HSV1-APP interactions on viral and cellular protein movement.

Main Methods:

Quantitative immuno-fluorescence and immuno-gold electron microscopy were used to visualize HSV1 and APP.
Live cell confocal imaging tracked the dynamics of viral particles and APP in infected epithelial cells.
siRNA-mediated knockdown of APP confirmed the specificity of observed interactions.

Main Results:

Nascent HSV1 particles co-localized with APP in the cytoplasm (72.8%) and traveled together (81.1%).
HSV1 infection decreased APP particle velocity and caused APP mal-distribution.
APP interaction enhanced HSV1 particle motility and velocity, while HSV1 lacking gE showed altered dual-label particle dynamics.

Conclusions:

Intracellular HSV1 particles dynamically interact with APP, facilitating viral transport and disrupting normal APP distribution.
These interactions provide a potential mechanistic link between HSV1 infection and Alzheimer's disease pathogenesis.