identification of hub genes and molecular pathways in human t-lymphotropic virus type 1 associated diseases using protein-protein interactions networks

background and objectives: human t-lymphotropic virus type 1 (htlv-1) is the cause of adult t-cell leukemia (atl) and htlv-1-associated myelopathy/tropical spastic paraparesis (ham/tsp). the present study aims to analyze gene expression patterns in atl and ham/tsp. materials and methods: microarray gene expression profiling of t-lymphocytes from htlv-1 associated disease and healthy control were obtained from gene expression omnibus (geo). several bioinformatics tools were used to identify dif- ferentially expressed genes (degs). among the generated degs, we constructed protein-protein interaction (ppi) between ham/tsm and atl in comparison to asymptomatic carriers (acs). subsequently, gene ontology (go) and topological analysis were performed. results: we found that the majority of degs in atl and ham/tsp were importantly implicated in immune response cat- egories. the nodes and edges number of normal-ac, ac-atl and atl-ham/tsp ppis were 168 and 145, 116 and 97, and 275 and 327, respectively. based on the topological analyses of protein-protein interaction networks, app (amyloid beta precursor protein) was detected as a critical player in progression of htlv-1 disease. conclusion: dysregulation of immune response associated transcripts play a critical role in htlv-1 disease progression. immune response associated genes may be biomarker for prognosis in cancer development and therapeutic targets.