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Related Experiment Video

Updated: May 5, 2026

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

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

Published on: December 18, 2012

Herpes simplex virus and atherosclerosis

M R Visser¹, G M Vercellotti

¹Department of Clinical Microbiology, University Hospital Utrecht, The Netherlands.

European Heart Journal

|December 1, 1993

Summary

This summary is machine-generated.

Herpes simplex virus (HSV) may contribute to atherosclerosis through various mechanisms, including lipid accumulation and inflammation in vascular cells. Further research is needed to confirm HSV

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Area of Science:

Cardiovascular Science
Virology
Immunology

Background:

Atherosclerosis is a complex disease with multifactorial causes.
The role of viral infections, specifically herpes simplex virus (HSV), as a potential trigger for atherosclerosis is under investigation.
Previous studies have detected HSV in some atherosclerotic lesions, but its prevalence in the general population complicates interpretation.

Purpose of the Study:

To provide an overview of the current understanding of the relationship between herpes simplex virus (HSV) and atherogenesis.
To explore potential mechanisms by which HSV may contribute to the development of atherosclerosis.

Main Methods:

Review of existing literature on HSV detection in atherosclerotic lesions.
Discussion of proposed biological mechanisms linking HSV infection to cardiovascular pathology.

Main Results:

Herpes simplex virus (HSV) has been detected in a subset of atherosclerotic lesions.
HSV infection in vascular cells can induce lipid accumulation.
HSV infection promotes endothelial inflammation, procoagulant activity, and altered cell-matrix interactions.

Conclusions:

Herpes simplex virus (HSV) infection presents several plausible mechanisms that could contribute to atherogenesis.
Further research is required to establish the definitive role of HSV in the pathogenesis of atherosclerosis and to determine if these mechanisms are clinically relevant.