Targeting Viral Transcription for HIV Cure Strategies
Izquierdo-Pujol, Jon (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa)
Puertas, Maria C. (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa)
Martínez Picado, Francisco Javier (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa)
Moron-Lopez, Sara (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa)

Data:	2024
Resum:	Combination antiretroviral therapy (ART) suppresses viral replication to undetectable levels, reduces mortality and morbidity, and improves the quality of life of people living with HIV (PWH). However, ART cannot cure HIV infection because it is unable to eliminate latently infected cells. HIV latency may be regulated by different HIV transcription mechanisms, such as blocks to initiation, elongation, and post-transcriptional processes. Several latency-reversing (LRA) and -promoting agents (LPA) have been investigated in clinical trials aiming to eliminate or reduce the HIV reservoir. However, none of these trials has shown a conclusive impact on the HIV reservoir. Here, we review the cellular and viral factors that regulate HIV-1 transcription, the potential pharmacological targets and genetic and epigenetic editing techniques that have been or might be evaluated to disrupt HIV-1 latency, the role of miRNA in post-transcriptional regulation of HIV-1, and the differences between the mechanisms regulating HIV-1 and HIV-2 expression.
Ajuts:	Agència de Gestió d'Ajuts Universitaris i de Recerca 2023FI-100207 Agència de Gestió d'Ajuts Universitaris i de Recerca 2020BP00046 Agencia Estatal de Investigación PID2022-139271OB-I00 European Commission 101057100 European Commission 101095606 Fundació la Marató de TV3 02130-30-31-3 Agència de Gestió d'Ajuts Universitaris i de Recerca CB21/13/00063
Nota:	J.M.-P. has received institutional grants and educational/consultancy fees from AbiVax, AstraZeneca, Gilead Sciences, Grifols, Janssen, Merck Sharp & Dohme, and ViiV Healthcare, all outside the submitted work. M.C.P. and S.M.-L. have received institutional grants from Gilead Sciences outside the submitted work. The remaining authors declare no conflicts of interest.
Nota:	J.I.-P. is supported by a PhD Joan Or\u00F3 fellowship (2023 FI-1 00207) from the Catalan Agency for Management of University and Research Grants. S.M.-L. is supported by the EU Gilead Research Scholars Program in HIV award 2021 and the 2020 BP 00046 grant from the Catalan Agency for Management of University and Research Grants. Research in the J.M.-P. laboratory is supported by the Spanish Ministry of Science and Innovation (grants PID2022-139271OB-I00 and CB21/13/00063, Spain), NIH/NIAID (1 UM1 AI164561-01 and 1P01AI178376-01, United States of America), EU HORIZON-HLTH-2021-DISEASE-04-07 (grants 101057100 and 101095606, European Union), Fundaci\u00F3 La Marat\u00F3 de TV3 (grant 202130-30-31-32, Spain), and Generalitat de Valencia (grant PROMETEO/2021/036, Spain).
Drets:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Llengua:	Anglès
Document:	Ressenya ; recerca ; Versió publicada
Matèria:	Viral persistence ; HIV ; HIV transcription ; HIV nuclear export ; HIV latency ; Latency-reversing ; Agents ; Latency-promoting agents
Publicat a:	Microorganisms, Vol. 12 Núm. 4 (april 2024) , p. 752, ISSN 2076-2607

DOI: 10.3390/microorganisms12040752
PMID: 38674696

16 p, 1.3 MB

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