1. Department of Modern Sciences and Technology, Mashhad University of Medical Sciences 2. Antimicrobial Resistance Research Center, Mashhad University of Medical Sciences 3. Department of Modern Sciences and Technology, Mashhad University of Medical Sciences 4. Department of Modern Sciences and Technology, Mashhad University of Medical Sciences
Abstract
Introduction
Human t cell lymphotropic virus-1 (htlv-1) is an oncogenic retrovirus which can cause adult t-cell leukemia lymphoma (atll). it is also the causative agent for a neurologic disease named htlv-i- associated myelopathy/tropical spastic paraparesis (ham/tsp). infection with this virus (htlv) is endemic in some parts of the world including khorasan razavi in iran. lipoproteins are molecules which carry triglycerides and cholesterol in the blood. their chemical composition is influenced by the action of different enzymes which overlap and interact with each other. considering the occurrence of different biochemical events during htlv-1 infection and the fact that chronic inflammatory diseases may disrupt lipid metabolism, we conducted this study to review the literature relevant with lipid disorders in htlv-1 infection.
Methods
The databases of pubmed, scopus, isi web of science, medlib and sid were searched using htlv-1, lipid and lipid disorders.
Results
It has been shown that virus infected cells release a vldl receptor fragment, which inhibits the viral infection by attaching to the virus. triglyceride and vldl levels are also showed to be higher in htlv-1-infected women than in non infected women. lipid disorders have been implicated in many neurodegenerative diseases such as ham/tsp. on the other hand, women with ham/tsp show faster progression of the disease when the disease starts before menopause, which suggests that sex hormones might be implicated in sex-specific infection by htlv-1.
the disruption of lipid metabolism in chronic inflammatory diseases may lead to lesions of the endothelium and higher levels of monocyte chemoattractant protein-1 (mcp-1) which itself increases the migration of monocytes towards the lesion.
Conclusion
While some lipid fragments are reported to be higher in some htlv-1 infected patients; the mechanisms underlying this relationship still needs to be studied.
