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Published on: March 14, 2019
Viral infection and atherosclerosis
Nima Hemmat1,2, Amin Ebadi1,2, Reza Badalzadeh3,4
1Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Viral infections may contribute to atherosclerosis through direct or indirect pathways, impacting vascular and systemic inflammation. This review examines the role of DNA and RNA viruses in the development of atherosclerotic diseases.
Area of Science:
- Cardiovascular Science
- Infectious Disease Epidemiology
Background:
- Atherosclerosis pathogenesis involves multiple risk factors.
- The role of infectious agents, particularly viruses, in atherosclerosis is an area of ongoing research.
- Two primary hypotheses explain viral involvement: direct cellular infection and indirect systemic inflammation.
Purpose of the Study:
- To review and synthesize current data on the relationship between viral infections and atherosclerosis.
- To explore the mechanisms by which DNA and RNA viruses may contribute to atherogenesis.
Main Methods:
- Literature review of studies investigating viral infections and atherosclerosis.
- Analysis of proposed direct and indirect pathways of viral influence on the disease process.
Main Results:
- Viruses can directly infect vascular cells, leading to endothelial and smooth muscle cell inflammation.
- Viruses can indirectly promote atherosclerosis by inducing systemic inflammation through non-vascular cell infection.
- Both DNA and RNA viruses are considered in the context of their potential atherogenic effects.
Conclusions:
- Viral infections represent a potential contributing factor to atherosclerosis development.
- Understanding the direct and indirect mechanisms of viral pathogenesis is crucial for comprehending atherosclerosis.
- Further research into specific viral correlations with atherosclerotic diseases is warranted.
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