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猪繁殖与呼吸综合征病毒感染猪肺泡巨噬细胞的体内定量蛋白质组学分析

In vivo quantitative proteomic analysis of porcine alveolar macrophages in PRRSV-infected pigs.

作者信息

Wei Ying, Zou Chuangchao, Zeng Siying, Peng Ouyang, Hu Guangli, Huang Yihui, Xu Qiuping, Hu Fangyu, Cao Yongchang, Zhang Hao

机构信息

State Key Laboratory of Biocontrol, Life Sciences School, Sun Yat-sen University, Guangzhou, 510006, China; College of Animal Science and Technology/Luoyang Key Laboratory of Live Carrier Biomaterial and Animal Disease Prevention and Control, Henan University of Science and Technology, Luoyang, 471023, China.

State Key Laboratory of Biocontrol, Life Sciences School, Sun Yat-sen University, Guangzhou, 510006, China.

出版信息

Virol Sin. 2025 Apr;40(2):206-216. doi: 10.1016/j.virs.2025.03.002. Epub 2025 Mar 15.

DOI:10.1016/j.virs.2025.03.002
PMID:40096891
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12131027/
Abstract

Porcine reproductive and respiratory syndrome (PRRS), a highly infectious immunosuppressive disease caused by porcine reproductive and respiratory syndrome virus (PRRSV), has led to significant economic losses in the global swine industry. The complexity of preventing and controlling PRRS, compounded by the limited efficacy of current vaccines, underscores the urgent need to identify antiviral targets and develop effective therapeutics against PRRSV. From the perspective of virus-host interactions, the discovery of target molecules associated with PRRSV resistance offers a promising strategy for future disease management. In this study, we conduct a comprehensive proteomic analysis using data-independent acquisition (DIA) mode to investigate the host response throughout the acute phase of PRRSV infection. This approach provides critical insights into the regulation of host antiviral and immune pathways during acute infection, advancing our theoretical understanding of PRRSV-host interactions and host gene dynamics during this critical phase. Notably, we identified SCARB2, a major lysosomal membrane protein associated with cholesterol metabolism, as a potential regulator of PRRSV replication. These findings offer novel perspectives for the prevention and control of PRRSV, contributing to the development of targeted antiviral strategies.

摘要

猪繁殖与呼吸综合征(PRRS)是一种由猪繁殖与呼吸综合征病毒(PRRSV)引起的高度传染性免疫抑制疾病,已给全球养猪业造成重大经济损失。预防和控制PRRS的复杂性,加上当前疫苗效果有限,凸显了识别抗病毒靶点和开发针对PRRSV的有效治疗方法的迫切需求。从病毒-宿主相互作用的角度来看,发现与PRRSV抗性相关的靶分子为未来疾病管理提供了一个有前景的策略。在本研究中,我们采用数据非依赖采集(DIA)模式进行全面的蛋白质组学分析,以研究PRRSV感染急性期宿主的反应。这种方法为急性感染期间宿主抗病毒和免疫途径的调节提供了关键见解,推进了我们对这一关键阶段PRRSV-宿主相互作用和宿主基因动态的理论理解。值得注意的是,我们确定了SCARB2,一种与胆固醇代谢相关的主要溶酶体膜蛋白,作为PRRSV复制的潜在调节因子。这些发现为PRRSV的预防和控制提供了新的视角,有助于开发有针对性的抗病毒策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/23a1d6045462/figs6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/2d97d286cda5/gr1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/e863537b7615/gr5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/f2ff9ca2fe6e/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/330bf50a1225/figs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/88bbbb1660aa/figs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/9859e715c131/figs4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/41ced2891a71/figs5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/23a1d6045462/figs6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/2d97d286cda5/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/0737989e12bd/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/3c7b8cc3abbd/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/73ea4c366309/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/e863537b7615/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/3ec594bfc05f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/f2ff9ca2fe6e/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/330bf50a1225/figs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/88bbbb1660aa/figs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/9859e715c131/figs4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/41ced2891a71/figs5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2075/12131027/23a1d6045462/figs6.jpg

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Group 2 innate lymphoid cells mediate the activation of CD4 T cells and aggravate Th1/Th2 imbalance via MHC II molecules during respiratory syncytial virus infection.呼吸道合胞病毒感染时,第 2 组固有淋巴细胞通过 MHC II 分子介导 CD4 T 细胞的激活,并加重 Th1/Th2 失衡。
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