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Infections and autoimmunity: role of human cytomegalovirus in autoimmune endothelial cell damage
M Dolcino1, A Puccetti2, A Barbieri3
1Institute Giannina Gaslini, Genova, Italy.
Abstract:
Molecular mimicry between infectious agents and normal human host cell proteins represents one of the possible mechanisms responsible for autoimmunity. Among infectious agents, human cytomegalovirus (HCMV) is an ideal candidate for involvement in autoimmune disorders because of its lifelong persistence through periods of reactivation and latency and because of the extensive manipulation of innate and adaptive immunity. HCMV has been implicated in the pathogenesis of vascular damage in systemic sclerosis (SSc) and atherosclerosis. Based on our data, which demonstrate a cause-and-effect relationship between HCMV and endothelial cell aggression in SSc and atherosclerosis, we propose that immune responses to particular HCMV proteins may result in autoaggression through a mechanism of molecular mimicry of normally expressed endothelial cell surface molecules.
Insights
Molecular mimicry by human cytomegalovirus (HCMV) may trigger autoimmunity. Our findings suggest HCMV proteins mimic host cell molecules, leading to endothelial cell damage in systemic sclerosis and atherosclerosis.
Area of Science:
- Immunology
- Infectious Diseases
- Vascular Biology
Background:
- Autoimmunity can arise from molecular mimicry between pathogens and host proteins.
- Human cytomegalovirus (HCMV) is a persistent virus with immune-modulating capabilities.
- HCMV has been linked to vascular pathologies like systemic sclerosis (SSc) and atherosclerosis.
Purpose of the Study:
- To investigate the role of human cytomegalovirus (HCMV) in the pathogenesis of autoimmune vascular diseases.
- To explore the mechanism of molecular mimicry in HCMV-associated endothelial cell aggression.
Main Methods:
- The study likely involved in vitro or in vivo models to assess HCMV's effect on endothelial cells.
- Analysis of immune responses targeting specific HCMV proteins and their cross-reactivity with host molecules.
Main Results:
- Demonstrated a cause-and-effect relationship between HCMV and endothelial cell aggression in SSc and atherosclerosis models.
- Identified potential HCMV proteins that mimic endothelial cell surface molecules.
Conclusions:
- Immune responses to specific HCMV proteins may drive autoimmune aggression via molecular mimicry.
- HCMV is proposed as a significant factor in the development of vascular damage in SSc and atherosclerosis.
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