- Wang, Changli;
- Chen, Lijun;
- Chen, Yaobin;
- Jia, Wenwen;
- Cai, Xunhui;
- Liu, Yufeng;
- Ji, Fenghu;
- Xiong, Peng;
- Liang, Anyi;
- Liu, Ren;
- Guan, Yuanlin;
- Cheng, Zhongyi;
- Weng, Yejing;
- Wang, Weixin;
- Duan, Yaqi;
- Kuang, Dong;
- Xu, Sanpeng;
- Cai, Hanghang;
- Xia, Qin;
- Yang, Dehua;
- Wang, Ming-Wei;
- Yang, Xiangping;
- Zhang, Jianjun;
- Cheng, Chao;
- Liu, Liang;
- Liu, Zhongmin;
- Liang, Ren;
- Wang, Guopin;
- Li, Zhendong;
- Xia, Han;
- Xia, Tian
- Editor(s): Myers, Amanda J
Viral infections can alter host transcriptomes by manipulating host splicing machinery. Despite intensive transcriptomic studies on SARS-CoV-2, a systematic analysis of alternative splicing (AS) in severe COVID-19 patients remains largely elusive. Here we integrated proteomic and transcriptomic sequencing data to study AS changes in COVID-19 patients. We discovered that RNA splicing is among the major down-regulated proteomic signatures in COVID-19 patients. The transcriptome analysis showed that SARS-CoV-2 infection induces widespread dysregulation of transcript usage and expression, affecting blood coagulation, neutrophil activation, and cytokine production. Notably, CD74 and LRRFIP1 had increased skipping of an exon in COVID-19 patients that disrupts a functional domain, which correlated with reduced antiviral immunity. Furthermore, the dysregulation of transcripts was strongly correlated with clinical severity of COVID-19, and splice-variants may contribute to unexpected therapeutic activity. In summary, our data highlight that a better understanding of the AS landscape may aid in COVID-19 diagnosis and therapy.