{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE308nnn/GSE308157/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE308157"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptional reprogramming in immune cells of HTLV-1 asymptomatic carriers and HAM/TSP patients following antiretroviral therapy","description":"Human T-cell lymphotropic virus type 1 (HTLV-1) causes HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic, immune-mediated spinal cord disease in which peripheral immune activation is thought to fuel central neuroinflammation. To delineate cell type-specific programs linked to disease, we performed single-cell RNA sequencing on the peripheral blood mononuclear cells (PBMCs) of the HTLV-1 infected asymptomatic carrier (AC) and HAM/TSP patient. Differential expression and pathway analyses localized that the most pronounced transcriptional divergence to the monocyte compartment, revealing coordinated remodeling of macrophage classical (M1-like) activation, IL-10-regulatory signaling, leukocyte adhesion/diapedesis, and trans-endothelial migration pathway, and cytokine storm-related modules. Ingenuity Pathway Analysis highlighted overlap with multiple sclerosis-associated signaling, consistent with myeloid-driven neuroinflammation and potential blood-spinal cord barrier involvement. In an independent validation phase, we assayed the selected subsets of up- and down-regulated monocyte genes in AC and HAM/TSP participants enrolled in a randomized, open-label pilot trial in Brazil. Expression of several inflammatory markers was higher at baseline in HAM/TSP and decreased during dolutegravir (DTG) therapy, paralleling reductions in HTLV-1 proviral load (PVL) in the DTG arm. Collectively, these data suggest that antiviral strategies may modulate immune cell transcriptional programs that help reduce HTLV-1 PVL.","dates":{"publication":"2026/08/05"},"accession":"GSE308157","cross_references":{"GSM":["GSM9238853","GSM9238852","GSM9238851","GSM9238850","GSM9238857","GSM9238856","GSM9238855","GSM9238854"],"GPL":["24676"],"GSE":["308157"],"taxon":["Homo sapiens"],"PMID":["[42515031]"]}}