ArticlePathogens (Basel, Switzerland)2022
Transcriptome Profiling in Swine Macrophages Infected with African Swine Fever Virus (ASFV) Uncovers the Complex and Close Relationship with Host.
Article in Pathogens (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Advances in understanding the dual roles of testicular immune responses: From immune privilege to inflammation.Seminars in immunopathology · 2026Review
- Single-Cell Atlas of Spleen Remodeling Reveals Macrophage Subset-Driven ASFV Pathogenesis.Biology · 2025Article
- Diversities of African swine fever virus host-virus dynamics revealed by single-cell profiling.Journal of virology · 2025Article
- Transcriptome profiles of organ tissues from pigs experimentally infected with African swine fever virus in early phase of infection.Emerging microbes & infections · 2024Article
- Genome-wide characterization of structure variations in the Xiang pig for genetic resistance to African swine fever.Virulence · 2024Article
- Fangchinoline Inhibits African Swine Fever Virus Replication by Suppressing the AKT/mTOR/NF-κB Signaling Pathway in Porcine Alveolar Macrophages.International journal of molecular sciences · 2024Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
African swine fever virus (ASFV) is a pathogen to cause devastating and economically significant diseases in domestic and feral swine. ASFV mainly infects macrophages and monocytes and regulates its replication process by affecting the content of cytokines in the infected cells. There is a limited understanding of host gene expression and differential profiles before and after ASFV infection in susceptible cells. In this study, RNA-seq technology was used to analyze the transcriptomic change in PAMs infected with ASFV at different time points (0 h, 12 h, 24 h). As a result, a total of 2748, 1570, and 560 genes were enriched in group V12 h vs. MOCK, V24 h vs. MOCK, and V24 h vs. V12 h, respectively. These DEGs (differentially expressed genes) in each group were mainly concentrated in the KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways related to innate immunization and inflammation, including the NF-κB signaling pathway, Toll-like receptor signaling pathway, TNF signaling pathway, IL-17 signaling pathway, cytokine-cytokine receptor interaction, and chemokine signaling pathway. Furthermore, the increased levels of IL-1β, TNF-α, IKKβ, CXCL2, and TRAF2 and decreased level of IκBα were validated through the qPCR method. These results suggested that ASFV infection can activate the NF-κB signaling pathway in the early stage. In general, this study provides a theoretical basis for further understanding the pathogenesis and immune escape mechanism of ASFV.
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Registered trials
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