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HTLV-1-host interactions facilitate the manifestations of cardiovascular disease

Fatemeh Sadat Mohammadi1, Arman Mosavat2, Mohammad Shabestari3

  • 1Immunology Research Center, Inflammation and Inflammatory Diseases Division, Mashhad University of Medical Sciences, Mashhad, Iran.

Microbial Pathogenesis
|June 9, 2019
PubMed

Insights

Human T-lymphotropic virus type 1 (HTLV-1) infection is linked to atherosclerosis. This study found HTLV-1 alters chemokine receptor 2 (CCR2) expression and correlates with lipid profiles in patients with coronary artery disease.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Cardiovascular Research

Background:

  • Atherosclerosis is a complex disease with multifactorial origins.
  • Previous studies suggest a potential association between Human T-lymphotropic virus type 1 (HTLV-1) infection and atherosclerosis.
  • Understanding the molecular mechanisms linking HTLV-1 to cardiovascular disease is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of HTLV-1 virulence factors, specifically Tax and proviral load (PVL), in the development of atherosclerosis.
  • To examine the expression levels of chemokine receptors CCR1 and CCR2 in patients with coronary artery disease (CAD) and HTLV-1 infection.
  • To assess the correlation between HTLV-1 markers, chemokine receptor expression, and traditional cardiovascular risk factors, including lipid profiles.

Main Methods:

  • A cross-sectional study involving 39 newly diagnosed subjects undergoing angiography, categorized into four groups: CAD+/HTLV-1+, CAD-/HTLV-1+, CAD+/HTLV-1-, and healthy controls (CAD-/HTLV-1-).
  • Real-time PCR (TaqMan method) was employed to quantify HTLV-1 proviral load (PVL), HTLV-1-Tax expression, and CCR1/CCR2 expression in peripheral blood mononuclear cells (PBMCs).
  • Standard clinical assessments including lipid profiles and complete blood counts (CBC) were performed.

Main Results:

  • CCR2 expression was significantly higher in the CAD+/HTLV-1+ group compared to both CAD-/HTLV-1+ and CAD+/HTLV-1- groups (P < 0.001, P < 0.005, respectively).
  • CCR1 expression was elevated in the CAD+/HTLV-1+ group compared to CAD-/HTLV-1+ (P=0.01) and healthy subjects (P=0.02).
  • A higher mean PVL was observed in the CAD+/HTLV-1+ group compared to the CAD-/HTLV-1+ group (P=0.041).
  • In HTLV-1+ patients, Tax showed a positive correlation with cholesterol and LDL, and a negative correlation with HDL, with stronger correlations observed in the CAD+/HTLV-1+ subgroup.

Conclusions:

  • HTLV-1 infection significantly alters the expression of CCR2 and, to a lesser extent, CCR1.
  • The HTLV-1 Tax protein may play a role in deregulating cytokine pathways, indirectly affecting lipid metabolism (cholesterol, LDL, HDL levels).
  • These findings highlight a potential link between HTLV-1 infection, chemokine receptor dysregulation, and the pathogenesis of atherosclerosis.

Keywords:
AtherosclerosisCoronary artery disease (CAD)HTLV-1IranReal-time PCRTax

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