PCID2 dysregulates transcription and viral RNA processing to promote HIV-1 latency

Crespo, Raquel; Ne, Enrico; Reinders, Julian; Meier, Jenny I.J.; Li, Chengcheng; Jansen, Sanne; Górska, Alicja; Koçer, Selin; Kan, Tsung Wai; Doff, Wouter; Dekkers, Dick; Demmers, Jeroen; Palstra, Robert-Jan; Rao, Shringar; Mahmoudi, Tokameh

doi:10.1016/j.isci.2024.109152

Cited by 2 publications

(4 citation statements)

References 57 publications

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“…HIV-1 MS vRNAs are basically produced in the early stages of HIV transcription since they encode for Tat, which enhances HIV transcription initiation, and Rev, which will be responsible in part for the translocation of HIV-1 US vRNA from the nucleus to the cytoplasm [28]. It has been recently reported that PCID2 establishes blocks to alternative splicing during HIV-1 latency and misregulates alternative splicing in cells obtained from PWH [29]. However, there is limited knowledge of the specific cellular molecules and proteins involved in HIV splicing.…”

Section: Multiple Splicingmentioning

confidence: 99%

“…It has also been shown that ZBTB2 binds the HIV-1 promoter, recruiting histone deacetylases (HDACs) and repressing HIV-1 transcription [50]. Furthermore, it has been recently reported that PCI domaincontaining 2 (PCID2) protein, a subunit of the transcription and export complex 2 (TREX2) complex, binds to the latent HIV-1 LTR as a transcriptional repressor [29]. Moreover, PCF11, a protein involved in 3 ′ end processing of mRNA and transcription termination of proteinencoding genes [51,52], causes premature termination of HIV-1 transcription [53].…”

Section: Repressive Transcriptional Factorsmentioning

confidence: 99%

“…domain-containing 2 (PCID2) protein, a subunit of the transcription and export complex 2 (TREX2) complex, binds to the latent HIV-1 LTR as a transcriptional repressor [29]. Moreover, PCF11, a protein involved in 3′ end processing of mRNA and transcription termination of protein-encoding genes [51,52], causes premature termination of HIV-1 transcription [53].…”

Section: Repressive Transcriptional Factorsmentioning

confidence: 99%

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Targeting Viral Transcription for HIV Cure Strategies

Izquierdo-Pujol,

Puertas,

Martinez-Picado

et al. 2024

Microorganisms

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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.

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Section: Multiple Splicingmentioning

confidence: 99%

Section: Repressive Transcriptional Factorsmentioning

confidence: 99%

Section: Repressive Transcriptional Factorsmentioning

confidence: 99%

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Targeting Viral Transcription for HIV Cure Strategies

Izquierdo-Pujol,

Puertas,

Martinez-Picado

et al. 2024

Microorganisms

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“…Interacts with TREX2 complex, which is necessary for transcription initiation and alternative RNA splicing. The complex binds HIV-1 LTR to repress HIV-1 expression both at the transcriptional and post-transcriptional levels[76] -1…”

mentioning

confidence: 99%

Post-Transcriptional HIV-1 Latency: A Promising Target for Therapy?

Kobayashi-Ishihara,

Tsunetsugu-Yokota

2024

Viruses

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Human Immunodeficiency Virus type 1 (HIV-1) latency represents a significant hurdle in finding a cure for HIV-1 infections, despite tireless research efforts. This challenge is partly attributed to the intricate nature of HIV-1 latency, wherein various host and viral factors participate in multiple physiological processes. While substantial progress has been made in discovering therapeutic targets for HIV-1 transcription, targets for the post-transcriptional regulation of HIV-1 infections have received less attention. However, cumulative evidence now suggests the pivotal contribution of post-transcriptional regulation to the viral latency in both in vitro models and infected individuals. In this review, we explore recent insights on post-transcriptional latency in HIV-1 and discuss the potential of its therapeutic targets, illustrating some host factors that restrict HIV-1 at the post-transcriptional level.

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PCID2 dysregulates transcription and viral RNA processing to promote HIV-1 latency

Cited by 2 publications

References 57 publications

Targeting Viral Transcription for HIV Cure Strategies

Targeting Viral Transcription for HIV Cure Strategies

Post-Transcriptional HIV-1 Latency: A Promising Target for Therapy?

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