<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE308nnn/GSE308157/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE308157</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcriptional reprogramming in immune cells of HTLV-1 asymptomatic carriers and HAM/TSP patients following antiretroviral therapy</name><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.</description><dates><publication>2026/08/05</publication></dates><accession>GSE308157</accession><cross_references><GSM>GSM9238853</GSM><GSM>GSM9238852</GSM><GSM>GSM9238851</GSM><GSM>GSM9238850</GSM><GSM>GSM9238857</GSM><GSM>GSM9238856</GSM><GSM>GSM9238855</GSM><GSM>GSM9238854</GSM><GPL>24676</GPL><GSE>308157</GSE><taxon>Homo sapiens</taxon><PMID>[42515031]</PMID></cross_references></HashMap>