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Human T-Lymphotropic Virus 1 (Htlv-1) Pathogenesis: A Systems Virology Study Publisher Pubmed



Mozhgani SH1, 2 ; Zareighobadi M1, 3 ; Teymoorirad M1 ; Mokhtariazad T1 ; Mirzaie M4 ; Sheikhi M1 ; Jazayeri SM1, 2 ; Shahbahrami R1 ; Ghourchian H3 ; Jafari M5 ; Rezaee SA6 ; Norouzi M1, 2
Authors
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Authors Affiliations
  1. 1. Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Research Center for Clinical Virology, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Institute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran
  4. 4. Department of Applied Mathematics, Faculty of Mathematical Sciences, Tarbiat Modares University, Tehran, Iran
  5. 5. Drug Design and Bioinformatics Unit, Medical Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran
  6. 6. Immunology Research Center, Inflammation and Inflammatory Diseases Division, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

Source: Journal of Cellular Biochemistry Published:2018


Abstract

The main mechanisms of interaction between Human T-lymphotropic virus type 1 (HTLV-1) and its hosts in the manifestation of the related disease including HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) and Adult T-cell leukemia/lymphoma (ATLL) are yet to be determined. It is pivotal to find out the changes in the genes expression toward an asymptomatic or symptomatic states. To this end, the systems virology analysis was performed. Firstly, the differentially expressed genes (DEGs) were taken pairwise among the four sample sets of Normal, Asymptomatic Carriers (ACs), ATLL, and HAM/TSP. Afterwards, the protein-protein interaction networks were reconstructed utilizing the hub genes. In conclusion, the pathways of cells proliferation and transformation were identified in the ACs state. In addition to immune pathways in ATLL, the inflammation and cancer pathways were discened in both diseases of ATLL and HAM/TSP. The outcomes can specify the genes involved in the pathogenesis and help to design the drugs in the future. © 2017 Wiley Periodicals, Inc.
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