Extended Data Fig. 10: A scheme illustrating the molecular mechanisms underlying HTLV-1 latency.
From: Intragenic viral silencer element regulates HTLV-1 latency via RUNX complex recruitment

At steady state, HTLV-1 sense expression is silenced, while antisense expression persists. Upon extracellular stimulation, promoter activity overrides silencing, triggering a transcriptional burst. Most cells are eliminated, but some revert to latency, sustaining viral persistence. Upregulation of Sin3A and GATA-3, or downregulation of EST-1, may reinforce silencing and promote latency re-establishment.