RT Journal
A1 Wang, Yanqun
A1 Li, Jie
A1 Zhang, Lu
A1 Sun, Hai-Xi
A1 Zhang, Zhaoyong
A1 Xu, Jinjin
A1 Xu, Yonghao
A1 Lin, Yu
A1 Zhu, Airu
A1 Luo, Yuxue
A1 Zhou, Haibo
A1 Wu, Yan
A1 Lin, Shanwen
A1 Sun, Yuzhe
A1 Xiao, Fei
A1 Chen, Ruiying
A1 Wen, Liyan
A1 Chen, Wei
A1 Li, Fang
A1 Ou, Rijing
A1 Zhang, Yanjun
A1 Kuo, Tingyou
A1 Li, Yuming
A1 Li, Lingguo
A1 Sun, Jing
A1 Sun, Kun
A1 Zhuang, Zhen
A1 Lu, Haorong
A1 Chen, Zhao
A1 Mai, Guoqiang
A1 Zhuo, Jianfen
A1 Qian, Puyi
A1 Chen, Jiayu
A1 Yang, Huanming
A1 Wang, Jian
A1 Xu, Xun
A1 Zhong, Nanshan
A1 Zhao, Jingxian
A1 Li, Junhua
A1 Zhao, Jincun
A1 Jin, Xin
T1 Plasma cell-free RNA characteristics in COVID-19 patients
JF Genome Research 
JO Genome Research 
YR 2022 
FD February 01 
VO 32 
IS 2 
SP 228 
OP 241 
DO 10.1101/gr.276175.121 
UL http://genome.cshlp.org/content/32/2/228.abstract 
AB 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.