Long noncoding RNA NRON contributes to HIV-1 latency by specifically inducing tat protein degradation

Jun Li, Cancan Chen, Xiancai Ma, Guannan Geng, Bingfeng Liu, Yijun Zhang, Shaoyang Zhang, Fudi Zhong, Chao Liu, Yue Yin, Weiping Cai and Hui Zhang ()
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Jun Li: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University
Cancan Chen: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University
Xiancai Ma: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University
Guannan Geng: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University
Bingfeng Liu: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University
Yijun Zhang: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University
Shaoyang Zhang: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University
Fudi Zhong: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University
Chao Liu: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University
Yue Yin: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University
Weiping Cai: Guangzhou 8th People’s Hospital
Hui Zhang: Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University

Nature Communications, 2016, vol. 7, issue 1, 1-10

Abstract: Abstract Long noncoding RNAs (lncRNAs) play multiple key regulatory roles in various cellular pathways. However, their functions in HIV-1 latent infection remain largely unknown. Here we show that a lncRNA named NRON, which is highly expressed in resting CD4+ T lymphocytes, could be involved in HIV-1 latency by specifically inducing Tat protein degradation. Our results suggest that NRON lncRNA potently suppresses the viral transcription by decreasing the cellular abundance of viral transactivator protein Tat. NRON directly links Tat to the ubiquitin/proteasome components including CUL4B and PSMD11, thus facilitating Tat degradation. Depletion of NRON, especially in combination with a histone deacetylase (HDAC) inhibitor, significantly reactivates the viral production from the HIV-1-latently infected primary CD4+ T lymphocytes. Our data indicate that lncRNAs play a role in HIV-1 latency and their manipulation could be a novel approach for developing latency-reversing agents.

Date: 2016
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DOI: 10.1038/ncomms11730

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