  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 a
fraction of infected individuals. These HTLV-1-infected cells typically have
phenotypes similar to that of CD4${^+}$ T cells, but the cell status is not
well understood. To extract the inherent information of HTLV-1-infected CD4$^+$
cells, we integratively analyzed the ATAC-seq and RNA-seq data of infected
cells. Compared to CD4${^+}$ T cells from healthy donors, we found anomalous
chromatin accessibility in HTLV-1-infected CD4${^+}$ cells derived from ATL
cases in terms of location and sample-to-sample fluctuations in open chromatin
regions. Further, by focusing on systematically selected genes near the open
chromatin regions, all the gene expressions in ATL cases were found to be
distinct from those of healthy CD4$^+$ T cells. Based on a further analysis of
chromatin accessibility, we detected TLL1 (Tolloid Like 1) as one of the key
genes that exhibit unique gene expressions in ATL cases. A luciferase assay
indicated that TLL1 has a strong regulatory effect on TGF-$\beta$. Overall,
this study provides results about the status of HTLV-1 infected cells, which
are qualitatively consistent across the different scales of chromatin
accessibility, transcription, and immunophenotype.
