High proviral load of human T cell lymphotropic virus type-1 facilitates coronary artery diseases
محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 23، شماره: 4
سال انتشار: 1398
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 469
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شناسه ملی سند علمی:
JR_IJBMS-23-4_011
تاریخ نمایه سازی: 27 مرداد 1399
چکیده مقاله:
Objective(s): Coronary artery disease (CAD) is known as a life threatening disease, worldwide. In this study the role of HTLV-1 infection was evaluated on cardiac involvement in an endemic region of northeastern Iran.Materials and Methods: Serologic and molecular tests for HTLV-1 infection were carried out in subjects who had coronary angiography. A real-time PCR, TaqMan method, to quantify HTLV-1 proviral load (PVL), and routine hematological and biochemical tests were performed for study subjects. Results: Twenty nine patients were HTLV-1+CAD+ and 13 cases were HTLV-1+CAD-. Although, there were no significant differences for risk factors like FBS, HDL, triglyceride, systolic and diastolic blood pressure (Cbp, Dbp), waist circumference (WC), hip circumference (WL), cholesterol (P=0.003), and LDL (P=0.007) levels, and monocyte count (P=0.05) had meaningful differences. The mean HTLV-1 PVL in HTLV-1+CAD+ subjects was 992.62±120 which was higher compared with HTLV-1+CAD- group (406.54±302 copies/104 PBMCs). Moreover, HTLV-1 PVL in males (833±108) was lower compared with females (1218±141 copies/104 PBMCs) (P=0.05). Patients with HTLV-1-PVL of more than 500 copies/104 had more diffused atherosclerosis plaque than patients with less than 500 (OR=6.87, 95% CI=1.34-35.05; P=0.016). Furthermore, patients with diffused coronary atherosclerosis had significantly higher levels of HTLV-1 PVL than patients with middle, proximal, and normal location of coronary sclerotic lesions (P<0.05). Conclusion: Taken together, in endemic area, HTLV-1 infection, more likely is a facilitating factor for heart complications and the high HTLV-1 PVL might affect CAD manifestations.
کلیدواژه ها:
نویسندگان
Farnaz Mozayeni
Allergy Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Seyed Abdolrahim Rezaee
Immunology Research Center, Inflammation and Inflammatory Disease Division, Mashhad University of Medical Sciences, Mashhad, Iran
Farahnaz Jabbari Azad
Allergy Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Mahmoud Shabestari
Department of Cardiology, Emam Reza Hospital, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
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