Mohadeseh Zarei-Ghobadi1, Mohsen Sheikhi1, Majid Teymoori-Rad1, Sahar Yaslianifard2, Mehdi Norouzi1,3, Somayeh Yaslianifard4,5, Reza Faraji4, Mohammad Farahmand1, Shiva Bayat6, Mohieddin Jafari7, Sayed-Hamidreza Mozhgani8,9. 1. Institute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran. 2. Department of Biochemistry, Faculty of Life Sciences of Islamic, Azad University, Tehran north branch, Tehran, Iran. 3. Research Center for Clinical Virology, Tehran University of Medical Sciences, Tehran, Iran. 4. Department of Microbiology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. 5. Dietary Supplements and Probiotic Research Center, Alborz University of Medical Sciences, Karaj, Iran. 6. Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. 7. Research Program in Systems Oncology, Faculty of Medicine, University of Helsinki, Helsinki, Finland. 8. Department of Microbiology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran. hamidrezamozhgani@gmail.com. 9. Non-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran. hamidrezamozhgani@gmail.com.
Abstract
OBJECTIVES: Human T cell leukemia virus-1 (HTLV-1) infection may lead to one or both diseases including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) or adult T cell leukemia lymphoma (ATLL). The complete interactions of the virus with host cells in both diseases is yet to be determined. This study aims to construct an interaction network for distinct signaling pathways in these diseases based on finding differentially expressed genes (DEGs) between HAM/TSP and ATLL. RESULTS: We identified 57 hub genes with higher criteria scores in the primary protein-protein interaction network (PPIN). The ontology-based enrichment analysis revealed following important terms: positive regulation of transcription from RNA polymerase II promoter, positive regulation of transcription from RNA polymerase II promoter involved in meiotic cell cycle and positive regulation of transcription from RNA polymerase II promoter by histone modification. The upregulated genes TNF, PIK3R1, HGF, NFKBIA, CTNNB1, ESR1, SMAD2, PPARG and downregulated genes VEGFA, TLR2, STAT3, TLR4, TP53, CHUK, SERPINE1, CREB1 and BRCA1 were commonly observed in all the three enriched terms in HAM/TSP vs. ATLL. The constructed interaction network was then visualized inside a mirrored map of signaling pathways for ATLL and HAM/TSP, so that the functions of hub genes were specified in both diseases.
OBJECTIVES:Human T cell leukemia virus-1 (HTLV-1) infection may lead to one or both diseases including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) or adult T cell leukemia lymphoma (ATLL). The complete interactions of the virus with host cells in both diseases is yet to be determined. This study aims to construct an interaction network for distinct signaling pathways in these diseases based on finding differentially expressed genes (DEGs) between HAM/TSP and ATLL. RESULTS: We identified 57 hub genes with higher criteria scores in the primary protein-protein interaction network (PPIN). The ontology-based enrichment analysis revealed following important terms: positive regulation of transcription from RNA polymerase II promoter, positive regulation of transcription from RNA polymerase II promoter involved in meiotic cell cycle and positive regulation of transcription from RNA polymerase II promoter by histone modification. The upregulated genes TNF, PIK3R1, HGF, NFKBIA, CTNNB1, ESR1, SMAD2, PPARG and downregulated genes VEGFA, TLR2, STAT3, TLR4, TP53, CHUK, SERPINE1, CREB1 and BRCA1 were commonly observed in all the three enriched terms in HAM/TSP vs. ATLL. The constructed interaction network was then visualized inside a mirrored map of signaling pathways for ATLL and HAM/TSP, so that the functions of hub genes were specified in both diseases.
Entities:
Keywords:
Adult T-cell leukemia/lymphoma; HTLV-1 associated myelopathy/tropical spastic paraparesis; Human T-lymphotropic virus type 1; Pathogenesis; Systems virology
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