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Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia(ATL) and HTLV-1-associated myelopathy (HAM) after a long latent period in afraction of infected individuals. These HTLV-1-infected cells typically havephenotypes similar to that of CD4${^+}$ T cells, but the cell status is notwell understood. To extract the inherent information of HTLV-1-infected CD4$^+$cells, we integratively analyzed the ATAC-seq and RNA-seq data of infectedcells. Compared to CD4${^+}$ T cells from healthy donors, we found anomalouschromatin accessibility in HTLV-1-infected CD4${^+}$ cells derived from ATLcases in terms of location and sample-to-sample fluctuations in open chromatinregions. Further, by focusing on systematically selected genes near the openchromatin regions, all the gene expressions in ATL cases were found to bedistinct from those of healthy CD4$^+$ T cells. Based on a further analysis ofchromatin accessibility, we detected TLL1 (Tolloid Like 1) as one of the keygenes that exhibit unique gene expressions in ATL cases. A luciferase assayindicated that TLL1 has a strong regulatory effect on TGF-$\beta$. Overall,this study provides results about the status of HTLV-1 infected cells, whichare qualitatively consistent across the different scales of chromatinaccessibility, transcription, and immunophenotype.

Integrative analysis of ATAC-seq and RNA-seq for cells infected by human T-cell leukemia virus type 1