2026-06-14T03:29:10Zhttps://repisalud.isciii.es/rest/oai/request
oai:repisalud.isciii.es:20.500.12105/48462025-03-06T09:14:27Zcom_20.500.12105_2052com_20.500.12105_2051com_20.500.12105_15322com_20.500.12105_19604col_20.500.12105_19609col_20.500.12105_16938col_20.500.12105_19607col_20.500.12105_25179
Repisalud author Mateos, Elena author Lopez, Juan Antonio author Calvo, Enrique author Terrón-Orellana, Maria Carmen author Luque, Daniel author Alcamí, José author Coiras, Mayte author Lopez-Huertas, Maria Rosa author Rodriguez‑Mora, Sara author Moran, María author Martín, Miguel Ángel author Muriaux, Delphine funder Instituto de Salud Carlos III funder Ministerio de Sanidad, Servicios Sociales e Igualdad (España) funder Ministerio de Economía y Competitividad (España) funder Instituto de Salud Carlos III funder Ministerio de Sanidad, Servicios Sociales e Igualdad (España) 2017-09-04T16:33:50Z 2017-09-04T16:33:50Z 2015-09-16 Retrovirology. 2015 Sep 16;12:78. 10.1186/s12977-015-0203-3 1742-4690 Retrovirology http://hdl.handle.net/20.500.12105/4846 HIV-1 replication results in mitochondrial damage that is enhanced during antiretroviral therapy (ART). The onset of HIV-1 replication is regulated by viral protein Tat, a 101-residue protein codified by two exons that elongates viral transcripts. Although the first exon of Tat (aa 1–72) forms itself an active protein, the presence of the second exon (aa 73–101) results in a more competent transcriptional protein with additional functions. Results: Mitochondrial overall functions were analyzed in Jurkat cells stably expressing full-length Tat (Tat101) or one-exon Tat (Tat72). Representative results were confirmed in PBLs transiently expressing Tat101 and in HIV-infected Jurkat cells. The intracellular expression of Tat101 induced the deregulation of metabolism and cytoskeletal proteins which remodeled the function and distribution of mitochondria. Tat101 reduced the transcription of the mtDNA, resulting in low ATP production. The total amount of mitochondria increased likely to counteract their functional impairment. These effects were enhanced when Tat second exon was expressed. Conclusions: Intracellular Tat altered mtDNA transcription, mitochondrial content and distribution in CD4+ T cells. The importance of Tat second exon in non-transcriptional functions was confirmed. Tat101 may be responsible for mitochondrial dysfunctions found in HIV-1 infected patients. eng HIV-1 Tat Mitochondria Cytoskeletal rearrangements Aerobic glycolysis mtDNA transcription Intracellular expression of Tat alters mitochondrial functions in T cells: a potential mechanism to understand mitochondrial damage during HIV-1 replication research article URL https://repisalud.isciii.es/bitstreams/a3b2d590-aeef-4ae6-822f-edaac9e12389/download File MD5 3a14095416eebb096160b9b30806ebab 2510107 application/pdf IntracellularExpressionOfTat_2015 URL https://repisalud.isciii.es/bitstreams/d0296513-35a0-447e-b16d-09a23057228f/download File MD5 bb3177a908bb8c47cb2399769dd94b52 99209 text/plain 12977_2015_Article_203.pdf.txt URL https://repisalud.isciii.es/bitstreams/85f09449-3573-494d-94bf-2cb2b851c3b4/download File MD5 bb3177a908bb8c47cb2399769dd94b52 99209 text/plain IntracellularExpressionOfTat_2015.txt