@article{Wang01022022,
author = {Wang, Yanqun and Li, Jie and Zhang, Lu and Sun, Hai-Xi and Zhang, Zhaoyong and Xu, Jinjin and Xu, Yonghao and Lin, Yu and Zhu, Airu and Luo, Yuxue and Zhou, Haibo and Wu, Yan and Lin, Shanwen and Sun, Yuzhe and Xiao, Fei and Chen, Ruiying and Wen, Liyan and Chen, Wei and Li, Fang and Ou, Rijing and Zhang, Yanjun and Kuo, Tingyou and Li, Yuming and Li, Lingguo and Sun, Jing and Sun, Kun and Zhuang, Zhen and Lu, Haorong and Chen, Zhao and Mai, Guoqiang and Zhuo, Jianfen and Qian, Puyi and Chen, Jiayu and Yang, Huanming and Wang, Jian and Xu, Xun and Zhong, Nanshan and Zhao, Jingxian and Li, Junhua and Zhao, Jincun and Jin, Xin}, 
title = {Plasma cell-free RNA characteristics in COVID-19 patients},
volume = {32}, 
number = {2}, 
pages = {228-241}, 
year = {2022}, 
doi = {10.1101/gr.276175.121}, 
abstract ={The pathogenesis of COVID-19 is still elusive, which impedes disease progression prediction, differential diagnosis, and targeted therapy. Plasma cell-free RNAs (cfRNAs) carry unique information from human tissue and thus could point to resourceful solutions for pathogenesis and host-pathogen interactions. Here, we performed a comparative analysis of cfRNA profiles between COVID-19 patients and healthy donors using serial plasma. Analyses of the cfRNA landscape, potential gene regulatory mechanisms, dynamic changes in tRNA pools upon infection, and microbial communities were performed. A total of 380 cfRNA molecules were up-regulated in all COVID-19 patients, of which seven could serve as potential biomarkers (AUC > 0.85) with great sensitivity and specificity. Antiviral (NFKB1A, IFITM3, and IFI27) and neutrophil activation (S100A8, CD68, and CD63)–related genes exhibited decreased expression levels during treatment in COVID-19 patients, which is in accordance with the dynamically enhanced inflammatory response in COVID-19 patients. Noncoding RNAs, including some microRNAs (let 7 family) and long noncoding RNAs (GJA9-MYCBP) targeting interleukin (IL6/IL6R), were differentially expressed between COVID-19 patients and healthy donors, which accounts for the potential core mechanism of cytokine storm syndromes; the tRNA pools change significantly between the COVID-19 and healthy group, leading to the accumulation of SARS-CoV-2 biased codons, which facilitate SARS-CoV-2 replication. Finally, several pneumonia-related microorganisms were detected in the plasma of COVID-19 patients, raising the possibility of simultaneously monitoring immune response regulation and microbial communities using cfRNA analysis. This study fills the knowledge gap in the plasma cfRNA landscape of COVID-19 patients and offers insight into the potential mechanisms of cfRNAs to explain COVID-19 pathogenesis.}, 
URL = {http://genome.cshlp.org/content/32/2/228.abstract}, 
eprint = {http://genome.cshlp.org/content/32/2/228.full.pdf+html}, 
journal = {Genome Research} 
}