Competitive Endogenous RNA Network Activates Host Immune Response in SARS-CoV-2-, panH1N1 (A/California/07/2009)-, and H7N9 (A/Shanghai/1/2013)-Infected Cells

Yang, Minghui1; Li, Jin2; Deng, Shoulong3,4; Fan, Hao5; Peng, Yun1; Ye, Guoguo1; Wang, Jun1; Wei, Jinli1; Jiang, Xiao1; Xu, Zhixiang1; Qing, Ling1; Wang, Fuxiang1; Yang, Yang1; Liu, Yingxia1

2022-02-01

10.3390/cells11030487

CELLS   影响因子和分区

2073-4409

The global outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is still ongoing, as is research on the molecular mechanisms underlying cellular infection by coronaviruses, with the hope of developing therapeutic agents against this pandemic. Other important respiratory viruses such as 2009 pandemic H1N1 and H7N9 avian influenza virus (AIV), influenza A viruses, are also responsible for a possible outbreak due to their respiratory susceptibility. However, the interaction of these viruses with host cells and the regulation of post-transcriptional genes remains unclear. In this study, we detected and analyzed the comparative transcriptome profiling of SARS-CoV-2, panH1N1 (A/California/07/2009), and H7N9 (A/Shanghai/1/2013) infected cells. The results showed that the commonly upregulated genes among the three groups were mainly involved in autophagy, pertussis, and tuberculosis, which indicated that autophagy plays an important role in viral pathogenicity. There are three groups of commonly downregulated genes involved in metabolic pathways. Notably, unlike panH1N1 and H7N9, SARS-CoV-2 infection can inhibit the m-TOR pathway and activate the p53 signaling pathway, which may be responsible for unique autophagy induction and cell apoptosis. Particularly, upregulated expression of IRF1 was found in SARS-CoV-2, panH1N1, and H7N9 infection. Further analysis showed SARS-CoV-2, panH1N1, and H7N9 infection-induced upregulation of lncRNA-34087.27 could serve as a competitive endogenous RNA to stabilize IRF1 mRNA by competitively binding with miR-302b-3p. This study provides new insights into the molecular mechanisms of influenza A virus and SARS-CoV-2 infection.

SARS-CoV-2 IRF1 influenza A autophagy noncoding RNA

SCI

英语

第一 ; 通讯

Shenzhen Natural Science Foundation[JCYJ20190809152415652] ; China Postdoctoral Science Foundation[2019M660836] ; National Science and Technology Major Project["2018ZX10711001","2017ZX10103011","2018ZX09711003","2020YFC0841700"] ; Shenzhen Science and Technology Research and Development Project[202002073000001]

Cell Biology

Cell Biology

WOS:000754549600001

MDPI

Web of Science

1.Southern Univ Sci & Technol, Shenzhen Peoples Hosp 3, Shenzhen Key Lab Pathogen & Immun,Hosp 2, State Key Discipline Infect Dis,Natl Clin Res Ctr, Shenzhen 518112, Peoples R China
2.Sun Yat Sen Univ, Sch Publ Hlth Shenzhen, Shenzhen 518406, Peoples R China
3.Chinese Acad Med Sci, Inst Lab Anim Sci, NHC Key Lab Human Dis Comparat Med, Beijing 100021, Peoples R China
4.Peking Union Med Coll, Comparat Med Ctr, Beijing 100021, Peoples R China
5.Univ Chicago, Dept Med, Sect Hematol & Oncol, 5841 S Maryland Ave, Chicago, IL 60637 USA

Yang, Minghui,Li, Jin,Deng, Shoulong,et al. Competitive Endogenous RNA Network Activates Host Immune Response in SARS-CoV-2-, panH1N1 (A/California/07/2009)-, and H7N9 (A/Shanghai/1/2013)-Infected Cells[J]. CELLS,2022,11(3).

Yang, Minghui.,Li, Jin.,Deng, Shoulong.,Fan, Hao.,Peng, Yun.,...&Liu, Yingxia.(2022).Competitive Endogenous RNA Network Activates Host Immune Response in SARS-CoV-2-, panH1N1 (A/California/07/2009)-, and H7N9 (A/Shanghai/1/2013)-Infected Cells.CELLS,11(3).

Yang, Minghui,et al."Competitive Endogenous RNA Network Activates Host Immune Response in SARS-CoV-2-, panH1N1 (A/California/07/2009)-, and H7N9 (A/Shanghai/1/2013)-Infected Cells".CELLS 11.3(2022).