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猪圆环病毒调节猪气管上皮细胞和猪肺泡巨噬细胞中的猪流感病毒复制。

Porcine Circovirus Modulates Swine Influenza Virus Replication in Pig Tracheal Epithelial Cells and Porcine Alveolar Macrophages.

机构信息

Swine and Poultry Infectious Diseases Research Center (CRIPA-FRQ), Faculté de Médecine Vétérinaire, Université de Montréal, Saint-Hyacinthe, QC J2S 2M2, Canada.

Molecular Diagnostic Laboratory, Centre de Diagnostic Vétérinaire de l'Université de Montréal (CDVUM), Saint-Hyacinthe, QC J2S 2M2, Canada.

出版信息

Viruses. 2023 May 20;15(5):1207. doi: 10.3390/v15051207.

DOI:10.3390/v15051207
PMID:37243291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10222781/
Abstract

The pathogenesis of porcine circovirus type 2b (PCV2b) and swine influenza A virus (SwIV) during co-infection in swine respiratory cells is poorly understood. To elucidate the impact of PCV2b/SwIV co-infection, newborn porcine tracheal epithelial cells (NPTr) and immortalized porcine alveolar macrophages (iPAM 3D4/21) were co-infected with PCV2b and SwIV (H1N1 or H3N2 genotype). Viral replication, cell viability and cytokine mRNA expression were determined and compared between single-infected and co-infected cells. Finally, 3'mRNA sequencing was performed to identify the modulation of gene expression and cellular pathways in co-infected cells. It was found that PCV2b significantly decreased or improved SwIV replication in co-infected NPTr and iPAM 3D4/21 cells, respectively, compared to single-infected cells. Interestingly, PCV2b/SwIV co-infection synergistically up-regulated IFN expression in NPTr cells, whereas in iPAM 3D4/21 cells, PCV2b impaired the SwIV IFN induced response, both correlating with SwIV replication modulation. RNA-sequencing analyses revealed that the modulation of gene expression and enriched cellular pathways during PCV2b/SwIV H1N1 co-infection is regulated in a cell-type-dependent manner. This study revealed different outcomes of PCV2b/SwIV co-infection in porcine epithelial cells and macrophages and provides new insights on porcine viral co-infections pathogenesis.

摘要

猪圆环病毒 2 型(PCV2b)和猪流感 A 病毒(SwIV)在猪呼吸道细胞中共同感染的发病机制尚不清楚。为了阐明 PCV2b/SwIV 共同感染的影响,本研究使用新生猪气管上皮细胞(NPTr)和永生化猪肺泡巨噬细胞(iPAM 3D4/21)对 PCV2b 和 SwIV(H1N1 或 H3N2 基因型)进行了共感染。测定了病毒复制、细胞活力和细胞因子 mRNA 表达,并比较了单感染和共感染细胞之间的差异。最后,进行了 3'mRNA 测序,以鉴定共感染细胞中基因表达和细胞通路的调控。结果发现,与单感染细胞相比,PCV2b 显著降低或改善了共感染 NPTr 和 iPAM 3D4/21 细胞中的 SwIV 复制。有趣的是,PCV2b/SwIV 共感染在 NPTr 细胞中协同上调 IFN 表达,而在 iPAM 3D4/21 细胞中,PCV2b 损害了 SwIV IFN 诱导的反应,这两种情况都与 SwIV 复制的调控有关。RNA-seq 分析表明,PCV2b/SwIV H1N1 共感染过程中基因表达的调控和富集的细胞通路在细胞类型依赖性方式下发生。本研究揭示了 PCV2b/SwIV 在猪上皮细胞和巨噬细胞中共同感染的不同结果,并为猪病毒共感染的发病机制提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8e/10222781/c2a3df3f906b/viruses-15-01207-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8e/10222781/e51e9d9cfe5b/viruses-15-01207-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8e/10222781/c2a3df3f906b/viruses-15-01207-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8e/10222781/cb35da10c7eb/viruses-15-01207-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8e/10222781/f70dd723240e/viruses-15-01207-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8e/10222781/0df098016b53/viruses-15-01207-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8e/10222781/e51e9d9cfe5b/viruses-15-01207-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8e/10222781/c2a3df3f906b/viruses-15-01207-g007.jpg

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