HTLV-1 transactivator induces interleukin-2 receptor expression through an NF-κB-like factor

Abstract

Like other viruses that infect primate cells, the human T lym-photropic virus-I (HTLV-I) stimulates production of some host cell proteins. In particular, HTLV-I infected T cells synthesize interleukin-2 receptor α (IL-2Rα) chain, which is probably induced through the mediation of the tat-I gene product of the virus^1–5. Activated T cells contain a transcription factor called NF-κB⁶, which stimulates the expression of human immunodeficiency virus-1 (HIV-1) by binding to an 11-base-pair enhancer sequence called κB. We have now found evidence that a similar transcription factor is involved in the induction of IL-2Rα expression by tat-I. We have identified a sequence upstream of IL-2Rα which is the same as the κB site at 9 of 11 base pairs, competes for binding to the κB sequence, and serves as a tat-I responsive element when multiple copies are inserted upstream of a heterologous promoter. The tat-I product also induces κB and the IL-2Rα κB binding activity in transfected Jurkat T lymphoid leukaemia cells. Both HTLV-I and HIV-1 thus interact with NF-κB-like transcription factors which might normally regulate expression of a growth factor receptor gene.