Investigation of the Relationship between HTLV-1 Infection and MMP-3 Gene Expression in HTLV-1 Positive Cardiac Patients
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Mina Mohammadhosayni , Fatemeh Hajighasemi , Abdolrahim Rezaee , Farnaz Mozayani , Fatemeh Sadat Mohammadi , Nastaran Tarban , Navid Momenifar , Mehdi Norouzi * |
Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran |
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Abstract: (3260 Views) |
Background and Aims: Human T-lymphotropic virus type 1 (HTLV-1) is a member of retroviridae family that causes ATL and HAM/TSP. Many inflammatory diseases are associated with this virus, such as Sjögren's syndrome, Hashimoto's thyroiditis, Uveitis and also Atherosclerosis. HTLV-1 performs in long latency period and can activate the immune responses in coronary vessels. Activated immune system produces inflammatory factors such as TNF-α cytokine that can increase Matrix Metalloproteinases as a main factor in patients with coronary artery diseases (CAD). We aimed to determine the relation between this virus infection and MMP-3 expression in Atherosclerosis patients.
Materials and Methods: 44 patients (13 individuals CAD+ HTLV-1+, 8 individuals CAD- HTLV-1+, 13 individuals CAD+ HTLV-1- and 10 individuals CAD- HTLV-1-) were selected and MMP-3 gene expression was measured by Real-time polymerase chain reaction. Results: There was no significant correlation between MMP-3 gene expression and HTLV-1 expression level in HTLV-1-positive cardiac and Atherosclerosis patients.
Conclusions: Although the main risk factor in Atherosclerosis patients is MMP-3, despite our expectation, no significant correlation was observed in our statistical analysis within four examined groups (p≥0.05). This evaluation showed higher MMP-3gene expression but not significant in CAD+ HTLV-1+ group compared to CAD+ HTLV-1- group. The larger sample sizes may help to improve the outcome to reach a significant level. |
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Keywords: HTLV-1, MMP-3, TNF-α, Atherosclerosis, Real-time PCR |
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Full-Text [PDF 537 kb]
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Type of Study: Original article |
Subject:
Special Received: 2018/06/14 | Accepted: 2018/09/7 | Published: 2018/09/7
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