Abstract

BackgroundAfrican swine fever virus (ASFV) is a highly lethal virus that can infect porcine alveolar macrophages (PAMs). Since ASFV, China has dealt with a heavy blow to the pig industry. However, the effect of infection of ASFV strains isolated from China on PAM transcription level is not yet clarified.MethodsIn this study, RNA sequencing (RNA-seq) was used to detect the differential expression of genes in PAMs at different time points after ASFV-CN/GS/2018 infection. The fluorescent quantitative polymerase chain reaction (qPCR) method was used to confirm the altered expression of related genes in PAMs infected with ASFV.ResultsA total of 1154 differentially expressed genes were identified after ASFV-CN/GS/2018 infection, of which 816 were upregulated, and 338 were downregulated. GO and KEGG analysis showed that these genes were dynamically enriched in various biological processes, including innate immune response, inflammatory response, chemokines, and apoptosis. Furthermore, qPCR verified that the DEAD box polypeptide 58 (DDX58), Interferon-induced helicase C domain-containing protein 1 (IFIH1), Toll-like receptor 3 (TLR3), and TLR7 of PAMs were upregulated after ASFV infection, while TLR4 and TLR6 had a significant downward trend during ASFV infection. The expression of some factors related to antiviral and inflammation was altered significantly after ASFV infection, among which interferon-induced protein with tetratricopeptide repeats 1 (IFIT1), IFIT2, Interleukin-6 (IL-6) were upregulated, and Ewing’s tumor-associated antigen 1 homolog (ETAA1) and Prosaposin receptor GPR37 (GPR37) were downregulated. In addition, we discovered that ASFV infection is involved in the regulation of chemokine expression in PAMs, and the chemokines, such as C-X-C motif chemokine 8 (CXCL8) and CXCL10, were upregulated after infection. However, the expression of chemokine receptor C-X-C chemokine receptor type 2 (CXCR2) is downregulated. Also, that the transcriptional levels of pro-apoptotic and anti-apoptotic factors changed after infection.ConclusionsAfter ASFV-CN/GS/2018 infection, the expression of some antiviral and inflammatory factors in PAMs changed significantly. The ASFV infection may activates the RLR and TLR signaling pathways. In addition, ASFV infection is involved in regulating of chemokine expression in PAMs and host cell apoptosis.

Highlights

  • African swine fever virus (ASFV) is a highly lethal virus that can infect porcine alveolar macrophages (PAMs)

  • Combined with the data of RNA sequencing (RNA-seq), the transcription level of cytokines related to apoptosis was verified, and we found that ISG12 (A) (Fig. 7A), Tumor necrosis factor ligand superfamily member 10 (TNFSF10) (Fig. 7B), GADD45B (Fig. 7C), which promotes apoptosis, and Interferon alpha-inducible protein 6 (IFI6) (Fig. 7D), which negatively regulates apoptosis, were upregulated after ASFV infection

  • Extensive transcriptome and related experimental studies have shown that ASFV-CN/GS/2018 infection leads to leads to changes of Pattern recognition receptors (PRR) transcription in some RLR and TLR signaling pathways, as well as the significant changes of transcriptional of some anti-viral and inflammatory factors

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Summary

Introduction

African swine fever virus (ASFV) is a highly lethal virus that can infect porcine alveolar macrophages (PAMs). African swine fever (ASF) is an acute, febrile, highly contagious, and fatal animal infectious disease caused by ASF virus (ASFV) [1, 2], a large double-stranded DNA virus. ASFV is the only member of the Afarviridae family and the only known insect-borne DNA virus that affects mammals [4,5,6]. It infects breeds of domestic pigs, African and Eurasian wild boars, and blunt ticks [7, 8]. The experimental vaccine was produced by a natural, cell culture attenuated, or genetically modified ASFV, no effective vaccine has yet been produced

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