Comparison amount of human herpes viruses DNA in vessels from different group of patients

Aim: It is generally thought, that myocardial infarction (MI) is the one of the main causes of death in developed countries. Vulnerable atherosclerotic plaque more likely can rupture and lead to myocardial infarction. The causes of plaques' maturation and rupture may be associated with inflammation and local and/or systemic immune activation. But it's still unknown, if there any infectious agent in plaques that may lead to such an activation. We have investigated if the presence of human herpes viruses DNA in vessels of different group of patients is associated with plaque instability. Methods: We included 30 patients hospitalized with MI and who died from MI or it's complications. Coronary arteries samples were taken during autopsy. Macroscopic observations of the tissues allowed their classification in 3 groups: 1) clean samples, without macroscopic signs on atherosclerosis, 2) non-ruptured plaques; 3) ruptured plaques, usually MI-causative vulnerable plaques with thrombus or ulceration. Also we analyzed samples obtained from 10 patients who dyed from coronary-artery–disease unrelated causes. In these samples there was no significant evidence of atherosclerosis. Tissue's DNA was extracted and HHVs DNA were measured by quantitative real-time-PCR (Q-PCR). HHVs genome copy numbers were normalized by cellular genomes and are reported as HHVs copies of per million cells. Results: Q-PCR results showed that in MI patients, more than 93% of samples contained at least one HHVs. HHV-1&2, HHV-3, HHV-5, and HHV-8 were found in more than 80% of the samples. HHV-4, HHV-6 and HHV-7 were the less frequent and were found in 49% to 55% of the samples. Analysis of the distribution of HHV-s between the three sample groups did not reveal any significant difference. However, in samples from patients with non MI-related cause of death, DNA of HHV1&2, HHV5, HHV8 was found in all samples, HHV6 in 90%, HHV3 and HHV7 in 80% and HHV4 in 70% of samples. Conclusion: We found that all HHVs are present in artery samples of people, who either died from MI or other causes. The higher viral DNA load in arterial tissues did not correlate with the presence of plaque or the stability thereof. Interestingly, HHV-8, the virus associated with Kaposi's sarcoma, a disease usually developed by immunosuppressed patients, was abundant in this cohort of non-immunosuppressed patients.