{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chakraborty S"],"funding":["HHS | National Institutes of Health","Department of Biotechnology, Ministry of Science and Technology, India"],"pagination":["e00503-20"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7495361"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["94(19)"],"pubmed_abstract":["The magnitude of transcription factor binding site variation emerging in HIV-1 subtype C (HIV-1C), especially the addition of NF-κB motifs by sequence duplication, makes the examination of transcriptional silence challenging. How can HIV-1 establish and maintain latency despite having a strong long terminal repeat (LTR)? We constructed panels of subgenomic reporter viral vectors with varying copy numbers of NF-κB motifs (0 to 4 copies) and examined the profile of latency establishment in Jurkat cells. Surprisingly, we found that the stronger the viral promoter, the faster the latency establishment. Importantly, at the time of commitment to latency and subsequent points, Tat levels in the cell were not limiting. Using highly sensitive strategies, we demonstrate the presence of Tat in the la"],"journal":["Journal of virology"],"pubmed_title":["A Stronger Transcription Regulatory Circuit of HIV-1C Drives the Rapid Establishment of Latency with Implications for the Direct Involvement of Tat."],"pmcid":["PMC7495361"],"funding_grant_id":["BT/PR7359/29/651/2012","NIDA 5RO1DA041751-02"],"pubmed_authors":["Kabi M","Chakraborty S","Ranga U"],"additional_accession":[]},"is_claimable":false,"name":"A Stronger Transcription Regulatory Circuit of HIV-1C Drives the Rapid Establishment of Latency with Implications for the Direct Involvement of Tat.","description":"The magnitude of transcription factor binding site variation emerging in HIV-1 subtype C (HIV-1C), especially the addition of NF-κB motifs by sequence duplication, makes the examination of transcriptional silence challenging. How can HIV-1 establish and maintain latency despite having a strong long terminal repeat (LTR)? We constructed panels of subgenomic reporter viral vectors with varying copy numbers of NF-κB motifs (0 to 4 copies) and examined the profile of latency establishment in Jurkat cells. Surprisingly, we found that the stronger the viral promoter, the faster the latency establishment. Importantly, at the time of commitment to latency and subsequent points, Tat levels in the cell were not limiting. Using highly sensitive strategies, we demonstrate the presence of Tat in the la","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Sep","modification":"2025-04-04T09:01:34.655Z","creation":"2021-03-18T08:39:02Z"},"accession":"S-EPMC7495361","cross_references":{"pubmed":["32669338"],"doi":["10.1128/JVI.00503-20","10.1128/jvi.00503-20"]}}