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Porcine Corneal Tissue Explant to Study the Efficacy of Herpes Simplex Virus-1 Antivirals
Published on: September 20, 2021
Herpes simplex virus as a determinant risk factor for coronary artery atherosclerosis and myocardial infarction
Dimosthenis Kotronias1, Nikiforos Kapranos
1MITERA Maternity and Surgical Center, 6 Erythrou Stavrou Str., 151 23 Athens, Greece.
Insights
Herpes simplex virus (HSV) is detected in coronary arteries, suggesting a role in the initiation and progression of atherosclerosis. Antiviral treatments may offer new ways to prevent vascular damage.
Area of Science:
- Cardiovascular Research
- Virology
- Pathogenesis of Atherosclerosis
Background:
- Viruses are implicated in atherogenesis, appearing in vascular tissues.
- Herpes simplex virus (HSV) role in coronary artery atherosclerosis stages requires investigation.
Purpose of the Study:
- Investigate the role of herpes simplex virus (HSV) in early and late stages of coronary artery atherosclerosis.
Main Methods:
- Nested polymerase chain reaction (nPCR) and in situ hybridization with tyramide signal amplification (ISH-TSA) were used.
- Coronary artery samples from 42 myocardial infarction (MI) cases and 28 young individuals were analyzed.
Main Results:
- HSV was detected in 43% of MI cases and 25% of young individuals by nPCR.
- HSV DNA was found in 38% of MI cases and 25% of young individuals by ISH-TSA.
- HSV DNA localized in endothelial cells, smooth muscle cells, macrophages, and lymphocytes in MI cases.
Conclusions:
- HSV appears to significantly contribute to the initiation and progression of coronary atherosclerosis.
- Findings suggest potential for antiviral therapies in preventing vascular damage.
Background:
Viruses have been detected in atherosclerotic and non-atherosclerotic vascular tissues and may be involved in the mechanisms of atherogenesis. In the present study, we investigated the role of herpes simplex virus (HSV) in the early and late stages of coronary artery atherosclerosis.
Methods And Results:
HSV prevalence was investigated in coronary artery samples from 42 autopsy cases, in which death was related to myocardial infarction (MI), and 28 young age autopsy cases without heart disease, who had died from fatal injuries (young victim group), using nested polymerase chain reaction (nPCR) and the highly sensitive in situ hybridization with tyramide signal amplification (ISH-TSA). HSV was detected by nPCR in 18 out of 42 (43%) myocardial infarction cases and in 7 out of 28 (25%) young victim group cases, respectively. Using ISH-TSA, HSV DNA was detected in the coronary arteries of the MI group in 16 out of 42 (38%) of the cases; the hybridization signal was localized in the nuclei of endothelial cells, the nuclei of smooth muscle cells, the macrophages around the atheroma, and in the lymphocytes infiltrating the vascular wall. In the young victim group, HSV DNA was detected by ISH-TSA in 7 out of 28 (25%) autopsy cases; the signal was localized in the endothelial and the intimal spindle cells of the coronary arteries.
Conclusion:
The findings of this study suggest that HSV seems to play a significant role in the initiation and progression of coronary atherosclerosis, and may open new perspectives in preventing the development of vascular damage via an appropriate antiviral treatment.
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