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在猪瘟病毒感染下，SERINC5 和 IFITM1/2/3 的相互作用调节自噬-凋亡-免疫网络。

Interaction of SERINC5 and IFITM1/2/3 regulates the autophagy-apoptosis-immune network under CSFV infection.

机构信息

College of Veterinary Medicine, South China Agricultural University, Guangzhou, China.

Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, China.

出版信息

Virulence. 2022 Dec;13(1):1720-1740. doi: 10.1080/21505594.2022.2127241.

DOI:10.1080/21505594.2022.2127241
PMID:36205528
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9553151/
Abstract

The host restriction factor serine incorporator 5 (SERINC5) plays a key role in inhibiting viral activity and has been shown to inhibit classical swine fever virus (CSFV) infection. However, the action of SERINC5 in the interaction between host cells and CSFV remains poorly understood. This study found that SERINC5 represses CSFV-induced autophagy through MAPK1/3-mTOR and AKT-mTOR signalling pathways. Further research showed that SERINC5 promotes apoptosis by repressing autophagy. Likewise, it was demonstrated that SERINC5 interacting proteins IFITM1/2/3 inhibit CSFV replication and regulate autophagy in a lysosomal-associated membrane protein LAMP1-dependent manner. In addition, IFITM1/2/3 interference promotes the NF-κB signalling pathway for potential immunoregulation by inhibiting autophagy. Finally, the functional silencing of IFITM1/2/3 genes was demonstrated to enhance the inhibitory effect of SERINC5 on autophagy. Taken together, These data uncover a novel mechanism through SERINC5 and its interacting proteins IFITM1/2/3, which mediates CSFV replication, and provides new avenues for controlling CSFV.

摘要

宿主限制因子丝氨酸掺入因子 5（SERINC5）在抑制病毒活性方面发挥着关键作用，并且已被证明可以抑制古典猪瘟病毒（CSFV）感染。然而，SERINC5 在宿主细胞与 CSFV 相互作用中的作用仍知之甚少。本研究发现 SERINC5 通过 MAPK1/3-mTOR 和 AKT-mTOR 信号通路抑制 CSFV 诱导的自噬。进一步的研究表明，SERINC5 通过抑制自噬来促进细胞凋亡。同样，研究表明 SERINC5 相互作用蛋白 IFITM1/2/3 通过溶酶体相关膜蛋白 LAMP1 依赖性方式抑制 CSFV 复制并调节自噬。此外，IFITM1/2/3 的干扰通过抑制自噬促进了 NF-κB 信号通路的潜在免疫调节作用。最后，功能沉默 IFITM1/2/3 基因被证明可以增强 SERINC5 对自噬的抑制作用。总之，这些数据揭示了一种通过 SERINC5 及其相互作用蛋白 IFITM1/2/3 介导 CSFV 复制的新机制，并为控制 CSFV 提供了新的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/55414828af2e/KVIR_A_2127241_F0011_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/d92bc7ac2870/KVIR_A_2127241_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/a71a538ce2fa/KVIR_A_2127241_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/12eeeb1899e8/KVIR_A_2127241_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/17467d49c672/KVIR_A_2127241_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/ceb8e00d0b73/KVIR_A_2127241_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/54d8ba1a1d76/KVIR_A_2127241_F0006_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/b76ad6682464/KVIR_A_2127241_F0007_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/0686664e44ab/KVIR_A_2127241_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/f92b41ddc8d9/KVIR_A_2127241_F0009_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/76e0ca4b6c4a/KVIR_A_2127241_F0010_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/55414828af2e/KVIR_A_2127241_F0011_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/d92bc7ac2870/KVIR_A_2127241_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/a71a538ce2fa/KVIR_A_2127241_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/12eeeb1899e8/KVIR_A_2127241_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/17467d49c672/KVIR_A_2127241_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/ceb8e00d0b73/KVIR_A_2127241_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/54d8ba1a1d76/KVIR_A_2127241_F0006_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/b76ad6682464/KVIR_A_2127241_F0007_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/0686664e44ab/KVIR_A_2127241_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/f92b41ddc8d9/KVIR_A_2127241_F0009_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/76e0ca4b6c4a/KVIR_A_2127241_F0010_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1348/9553151/55414828af2e/KVIR_A_2127241_F0011_B.jpg

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J Neuroimmunol. 2021 Jun 15;355:577567. doi: 10.1016/j.jneuroim.2021.577567. Epub 2021 Apr 2.
2
A Critical Review about Different Vaccines against Classical Swine Fever Virus and Their Repercussions in Endemic Regions.关于针对猪瘟病毒的不同疫苗及其在流行地区影响的批判性综述。
Vaccines (Basel). 2021 Feb 15;9(2):154. doi: 10.3390/vaccines9020154.
3
Front Cell Infect Microbiol. 2025 Jan 20;14:1516806. doi: 10.3389/fcimb.2024.1516806. eCollection 2024.
4
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5
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4
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5
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