Abstract:
:HTLV-I infection is characterized by low viremia and restricted viral expression. While the mechanisms regulating viral latency are poorly understood, it is believed that interactions between viral and host cellular factor(s) are involved. Several lines of evidence indicate that HTLV-I provirus may be methylated in primary ATL leukemic cells. To determine whether methylation of the viral promoting sequences was sufficient to inhibit gene transcription, we methylated the HTLV-I LTR enzymatically at the HpaII (CCGG) sites. HTLV-I LTR contains several HpaII methylase-sensitive sites, and some involve one of the three 21-bp motifs, responsible for tax induction, as well as sequences that respond to phorbol 12-myristate 13-acetate (PMA). We found that CpG site-specific methylation of HTLV-I LTR sequences inhibits their transcriptional activation mediated by both tax product and PMA. This transcriptional block, however, was overcome when tax product and PMA were added together, thus indicating that tax and PMA act synergistically in bypassing the transcriptional block exerted by methylation.
journal_name
Virologyjournal_title
Virologyauthors
Saggioro D,Forino M,Chieco-Bianchi Ldoi
10.1016/0042-6822(91)90649-vsubject
Has Abstractpub_date
1991-05-01 00:00:00pages
68-75issue
1eissn
0042-6822issn
1096-0341pii
0042-6822(91)90649-Vjournal_volume
182pub_type
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