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ILDR1 promotes influenza A virus replication through binding to PLSCR1

文献类型: 外文期刊

作者: Liu, Yueyue 1 ; Lin, Shuqian 1 ; Xie, Yunhui 1 ; Zhao, Lu 1 ; Du, Haibo 2 ; Yang, Shifa 1 ; Yin, Bin 1 ; Li, Guiming 1 ; Zhao, Zengcheng 1 ; Huang, Zhongli 1 ; Xu, Zhigang 2 ; Wu, Jiaqiang 1 ;

作者机构: 1.Shandong Acad Agr Sci, Inst Poultry Sci, Shandong Prov Anim & Poultry Green Hlth Prod Crea, Jinan 250100, Shandong, Peoples R China

2.Shandong Univ, Sch Life Sci, Shandong Prov Key Lab Anim Cells & Dev Biol, Qingdao 266237, Shandong, Peoples R China

3.Shandong Normal Univ, Shandong Prov Collaborat Innovat Ctr Cell Biol, Jinan 250014, Shandong, Peoples R China

4.Shandong Normal Univ, Coll Life Sci, Key Lab Anim Resistant Biol Shandong, Jinan 250014, Shandong, Peoples R China

期刊名称:SCIENTIFIC REPORTS ( 影响因子:4.996; 五年影响因子:5.516 )

ISSN: 2045-2322

年卷期: 2022 年 12 卷 1 期

页码:

收录情况: SCI

摘要: As a natural antiviral regulator, phospholipid scramblase 1 (PLSCR1) has been shown to inhibit influenza virus replication in infected cells through interacting with NP of influenza A virus (IAV). But its antiviral function as well as the underlying regulatory mechanism has not been examined in vivo. In the present work, we show that PLSCR1 expression is decreased in H1N1 SIV-infected mice, and Plscr1(-/-) mice are more susceptible to H1N1 SIV infection. By performing yeast two-hybrid screening, we identified immunoglobulin-like domain-containing receptor 1 (ILDR1) as a novel PLSCR1-binding partner. ILDR1 is highly expressed in the lungs, and its expression level is increased after virus infection. Interestingly, ILDR1 could not directly interact with virus NP protein, but could combine with PLSCR1 competitively. Our data indicates that there is a previously unidentified PLSCR1-ILDR1-NP regulatory pathway playing a vital role in limiting IAV infection, which provides novel insights into IAV-host interactions.

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