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Effect of PLK3 inhibitors treatment on the global transcriptome of resting CD4+ T Cells [RNA-Seq]

GSE310288 Homo sapiens Expression profiling by high throughput sequencing 8 samples Submitted 2025/11/20 Platform GPL29480
Summary
The persistence of HIV-1 reservoirs in resting CD4⁺ T cells despite the administration of antiretroviral therapy (ART) remains a major barrier to achieving a cure. In this research, we identified polo-like kinase 3 (PLK3) as a host antiviral factor able to suppress HIV-1 translation by targeting rare host tRNAs—specifically, tRNA-Ile-TAT and tRNA-Leu-TAA—in resting CD4⁺ T cells.The inhibition of PLK3 increases the production of viral proteins, including gp120 and Gag, in active reservoirs without cellular stimulation, thereby rendering infected cells vulnerable to CAR-T–mediated clearance.Together, these findings provide evidence that PLK3 is a key host regulator of HIV-1 translation in resting CD4⁺ T cells as well as a potential therapeutic target for reservoir eradication that may lead to a functional cure.
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Also filed as BioProject PRJNA1365708 and SRA study SRP646051. Searching any of these in the dataset finder brings you back here.

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