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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
Induction of endothelial cell damage by hCMV molecular mimicry
Claudio Lunardi1, Caterina Bason, Roberto Corrocher
1Department of Clinical and Experimental Medicine, University of Verona, P.le L.A. Scuro 10, 37134 Verona, Italy. claudio.lunardi@univr.it
Abstract:
Molecular mimicry between infectious agents and normal human host cell components is one of the mechanisms responsible for autoimmunity. Among infectious agents, some viruses represent ideal candidates for their ability to infect human cells, where they are harbored for the duration of the life of the host in a latent state. Human cytomegalovirus (hCMV) infection has been implicated in the pathogenesis of vascular damage in systemic sclerosis (SSc) and atherosclerosis. Based on recent data describing a cause and effect relationship between hCMV and endothelial cell damage in SSc and atherosclerosis, we propose that the immune response to particular hCMV proteins might result in autoaggression through a mechanism of molecular mimicry of normally expressed endothelial cell surface molecules.
Insights
Molecular mimicry, where infectious agents resemble host cells, can trigger autoimmunity. Human cytomegalovirus (hCMV) infection may cause autoimmune responses against endothelial cells, contributing to systemic sclerosis and atherosclerosis.
Area of Science:
- Immunology
- Virology
- Pathogenesis of Autoimmune Diseases
Background:
- Autoimmunity can arise from molecular mimicry between pathogens and host tissues.
- Human cytomegalovirus (hCMV) establishes lifelong latent infections.
- hCMV infection is linked to vascular damage in systemic sclerosis (SSc) and atherosclerosis.
Purpose of the Study:
- To propose a mechanism for hCMV-induced autoimmunity.
- To investigate the role of molecular mimicry in hCMV-related endothelial cell damage.
Main Methods:
- Review of existing data on hCMV infection and autoimmune pathogenesis.
- Analysis of potential molecular mimicry between hCMV proteins and endothelial cell surface molecules.
Main Results:
- hCMV infection is associated with endothelial cell damage in SSc and atherosclerosis.
- A proposed mechanism involves immune responses to hCMV proteins mimicking host endothelial molecules.
Conclusions:
- Molecular mimicry of endothelial cell surface molecules by hCMV proteins may drive autoimmune responses.
- This mechanism could explain hCMV's role in the pathogenesis of SSc and atherosclerosis.

