<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13</volume><submitter>Schnell AP</submitter><pubmed_abstract>The viral transactivator Tax plays a key role in HTLV-1 reactivation and &lt;i>de novo&lt;/i> infection. Previous approaches focused on the histone deacetylase inhibitor (HDACi) Valproate as a latency-reversing agent to boost Tax expression and expose infected cells to the host's immune response. However, following treatment with Valproate proviral load decreases in patients with HAM/TSP were only transient. Here, we hypothesize that other compounds, including more potent and selective HDACi, might prove superior to Valproate in manipulating Tax expression. Thus, a panel of HDACi (Vorinostat/SAHA/Zolinza, Panobinostat/LBH589/Farydak, Belinostat/PXD101/Beleodaq, Valproate, Entinostat/MS-275, Romidepsin/FK228/Istodax, and MC1568) was selected and tested for toxicity and potency in enhancing Tax ex</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>978800</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9424546</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>HDAC inhibitors Panobinostat and Romidepsin enhance &lt;i>tax&lt;/i> transcription in HTLV-1-infected cell lines and freshly isolated patients' T-cells.</pubmed_title><pmcid>PMC9424546</pmcid><pubmed_authors>Aristodemou A</pubmed_authors><pubmed_authors>Taylor GP</pubmed_authors><pubmed_authors>Bangham CRM</pubmed_authors><pubmed_authors>Kohrt S</pubmed_authors><pubmed_authors>Schnell AP</pubmed_authors><pubmed_authors>Thoma-Kress AK</pubmed_authors></additional><is_claimable>false</is_claimable><name>HDAC inhibitors Panobinostat and Romidepsin enhance &lt;i>tax&lt;/i> transcription in HTLV-1-infected cell lines and freshly isolated patients' T-cells.</name><description>The viral transactivator Tax plays a key role in HTLV-1 reactivation and &lt;i>de novo&lt;/i> infection. Previous approaches focused on the histone deacetylase inhibitor (HDACi) Valproate as a latency-reversing agent to boost Tax expression and expose infected cells to the host's immune response. However, following treatment with Valproate proviral load decreases in patients with HAM/TSP were only transient. Here, we hypothesize that other compounds, including more potent and selective HDACi, might prove superior to Valproate in manipulating Tax expression. Thus, a panel of HDACi (Vorinostat/SAHA/Zolinza, Panobinostat/LBH589/Farydak, Belinostat/PXD101/Beleodaq, Valproate, Entinostat/MS-275, Romidepsin/FK228/Istodax, and MC1568) was selected and tested for toxicity and potency in enhancing Tax ex</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-04T21:51:31.044Z</modification><creation>2025-04-04T21:51:31.044Z</creation></dates><accession>S-EPMC9424546</accession><cross_references><pubmed>36052071</pubmed><doi>10.3389/fimmu.2022.978800</doi></cross_references></HashMap>