Abstract
Human T cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia-lymphoma (ATL) and inflammatory diseases. The HTLV-1 bZIP factor (HBZ) gene is constantly expressed in HTLV-1 infected cells and ATL cells. HBZ protein suppresses transcription of the tax gene through blocking the LTR recruitment of not only ATF/CREB factors but also CBP/p300. HBZ promotes transcription of Foxp3, CCR4, and T-cell immunoreceptor with Ig and ITIM domains (TIGIT). Thus, HBZ is critical for the immunophenotype of infected cells and ATL cells. HBZ also functions in its RNA form. HBZ RNA suppresses apoptosis and promotes proliferation of T cells. Since HBZ RNA is not recognized by cytotoxic T cells, HTLV-1 has a clever strategy for avoiding immune detection. HBZ plays central roles in maintaining infected T cells in vivo and determining their immunophenotype.
Highlights
Complex retroviruses like Human T-cell leukemia virus type 1 (HTLV-1) harbor all three common retroviral genes in addition to both regulatory genes directly involved in regulation of viral expression and accessory genes
A crucial study published in 2002 demonstrated undeniably the existence of a negative-strand-encoded protein termed HBZ (HTLV-1 bZIP factor) [1] synthesized from antisense transcripts produced from the 3′ Long Terminal Repeat (LTR) [2–5]
We summarize what is known about HBZ and discuss its significance in pathogenesis by HTLV-1
Summary
Complex retroviruses like Human T-cell leukemia virus type 1 (HTLV-1) harbor all three common retroviral genes (gag, pol, and env) in addition to both regulatory genes directly involved in regulation of viral expression and accessory genes All these genes are expressed through transcripts initiating from the enhancer/promoter in 5′ Long Terminal Repeat (LTR) region. Analysis of viral protein expression in HTLV-1-infected T-cell lines confirmed very low HBZ levels in cells expressing elevated amounts of Gag [16, 17] Taken together, all these observations suggest that Tax could indirectly keep antisense transcription to low levels through its stimulation of sense transcription and viral production. The HTLV-1 LTR contains three viral cyclic AMP response elements (vCREs) allowing for transcription transactivation by Tax; the viral transactivator does not bind to vCRE sites but instead interacts with cellular ATF/ CREB factors like CREB and CREB-2 (Fig. 1) [21–26]. Both CBP and p300 possess a histone acetyltransferase (HAT) domain that plays an essential role in transcriptional activation by
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