C. R. M. Bangham

The paper investigates how HTLV-1 proviral transcription affects host chromatin structure and finds that it induces aberrant transcription but suppresses chromatin loop formation.

This study uses bulk RNA-seq to analyze host gene expression changes during HTLV-1 reactivation in primary CD4+ T cells, identifying Polycomb gene expression shifts and deubiquitinases that promote proviral transcription.

This study uses live-cell imaging and mathematical modeling to analyze Tax expression dynamics in HTLV-1 infected T-cells, revealing heterogeneous patterns and impacts on cell behavior.

This study examines how HTLV-1 transcriptional bursts affect host transcription over time in infected T-cells, finding transient activation of pathways like NF-κB and clone-specific differences in cell cycle regulation.

The paper identifies genomic features that determine the survival of HTLV-1 and HIV-1 clones in vivo, showing that radial chromatin organization, integration site, and host transcription influence clonal persistence.

This study shows HTLV-1 disrupts host chromatin structure and causes abnormal transcription patterns in cis.