Background African 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. Methods In 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. Results A 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. Conclusions After 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.

The porcine reproductive and respiratory syndrome virus (PRRSV) is the pathogen causing epidemics of porcine reproductive and respiratory syndrome (PRRS), and is present in every major swine-farming country in the world. Previous studies have demonstrated that PRRSV infection leads to a range of consequences, such as persistent infection, secondary infection, and co-infection, and is common among pigs in the field. In recent years, coinfection of PRRSV and other porcine pathogens has occurred often, making it more difficult to define and diagnose PRRSV-related diseases. The study of coinfections may be extremely suitable for the current prevention and control in the field. However, there is a limited understanding of coinfection. Therefore, in this review, we have focused on the epidemiology of PRRSV coinfection with other pathogens in swine, both in vivo and in vitro.

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Z-conformation nucleic acid binding protein 1 (ZBP1), a powerful innate immune sensor, has been identified as the important signaling initiation factor in innate immune response and the multiple inflammatory cell death known as PANoptosis. The initiation of ZBP1 signaling requires recognition of left-handed double-helix Z-nucleic acid (includes Z-DNA and Z-RNA) and subsequent signaling transduction depends on the interaction between ZBP1 and its adapter proteins, such as TANK-binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), receptor-interacting serine/threonine-protein kinase 1 (RIPK1), and RIPK3. ZBP1 activated innate immunity, including type-I interferon (IFN-I) response and NF-κB signaling, constitutes an important line of defense against pathogenic infection. In addition, ZBP1-mediated PANoptosis is a double-edged sword in anti-infection, auto-inflammatory diseases, and tumor immunity. ZBP1-mediated PANoptosis is beneficial for eliminating infected cells and tumor cells, but abnormal or excessive PANoptosis can lead to a strong inflammatory response that is harmful to the host. Thus, pathogens and host have each developed multiplex tactics targeting ZBP1 signaling to maintain strong virulence or immune homeostasis. In this paper, we reviewed the mechanisms of ZBP1 signaling, the effects of ZBP1 signaling on host immunity and pathogen infection, and various antagonistic strategies of host and pathogen against ZBP1. We also discuss existent gaps regarding ZBP1 signaling and forecast potential directions for future research.

African swine fever virus (ASFV) is prevalent in many countries and is a contagious and lethal virus that infects pigs, posing a threat to the global pig industry and public health. The interaction between the virus and the host is key to unlocking the mystery behind viral pathogenesis. A comprehensive understanding of the viral and host protein interaction may provide clues for developing new antiviral strategies. Here, we show a network of ASFV MGF360-9L protein interactions in porcine kidney (PK-15) cells. Overall, 268 proteins that interact with MGF360-9L are identified using immunoprecipitation and liquid chromatography–mass spectrometry (LC-MS). Accordingly, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted, and the protein–protein interaction (PPI) network was created. It was speculated that the cellular proteins interacting with MGF360-9L are involved in protein binding, metabolism, and the innate immune response. Proteasome subunit alpha type (PSMA3), 26S protease regulatory subunit 4 (PSMC1), autophagy and beclin 1 regulator 1 (AMBRA1), and DEAD-box helicase 20 (DDX20) could interact with MGF360-9L in vitro. PSMA3 and PSMC1 overexpression significantly promoted ASFV replication, and MGF360-9L maintained the transcriptional level of PSMA3 and PSMC1. Here, we show the interaction between ASFV MGF360-9L and cellular proteins and elucidate the virus–host interaction network, which effectively provides useful protein-related information that can enable further study of the potential mechanism and pathogenesis of ASFV infection.

African swine fever (ASF) is an infectious disease characterized by hemorrhagic fever, highly pathogenic, and severe mortality in domestic pigs caused by the ASF virus (ASFV). ASFV is a large DNA virus and primarily infects porcine monocyte macrophages. The interaction between ASFV and host macrophages is the major reason for gross pathological lesions caused by ASFV. Necroptosis is an inflammatory programmed cell death and plays an important immune role during virus infection. However, whether and how ASFV induces macrophage necroptosis and what effect of necroptosis signaling on host immunity and ASFV infection remains unknown. This study uncovered that ASFV activates the necroptosis signaling in the spleen, lung, liver, and kidney from ASFV-infected pigs. And macrophage necroptosis also was induced by ASFV infection in vitro. Further evidence showed that the macrophage necroptosis is independent of TNF-α-RIPK1 or TLR-TRIF pathway but depends on Z-DNA binding protein 1 (ZBP1). ASFV infection upregulates the expression of ZBP1 and RIPK3 to consist of the ZBP1-RIPK3-MLKL necrosome and further activates macrophage necroptosis. Subsequently, the Z-DNA signals were further confirmed to be present and colocalized with ZBP1 in the cytoplasm and nucleus of ASFV-infected cells. Moreover, ZBP1-mediated macrophage necroptosis caused the extracellular release of proinflammatory cytokines TNF-α and IL-1β induced by ASFV infection. Finally, we demonstrated that ZBP1-mediated necroptosis signaling significantly inhibits ASFV replication in host macrophages. Our findings uncovered a novel mechanism by which ASFV induces macrophage necroptosis by facilitating Z-DNA accumulation and ZBP1 necrosome assembly, providing significant insights into the pathogenesis of ASFV infection.

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African swine fever (ASF) is a contagious and lethal hemorrhagic disease in pigs; its spread results in huge economic losses to the global pig industry. ASF virus (ASFV) is a large double-stranded DNA virus encoding >150 open reading frames. Among them, ASFV-encoded D1133L was predicted to be a helicase but its specific function remains unknown. Since virus-host protein interactions are key to understanding viral protein function, we used co-immunoprecipitation combined with liquid chromatography-mass spectrometry to investigate D1133L. This study describes the interaction network of ASFV D1133L protein in porcine kidney PK-15 cells. Overall, 1,471 host proteins that potentially interact with D1133L are identified. Based on these host proteins, a protein–protein network was constructed. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses showed that cellular D1133L-interacted proteins are involved in the ribosome, spliceosome, RNA transport, oxidative phosphorylation, proteasome, and DNA replication. Vimentin (VIM), tripartite motif-containing protein 21 (TRIM21), and Tu translation elongation factor (TUFM) were confirmed to interact with D1133L in vitro. VIM or TRIM21 overexpression significantly promoted ASFV replication, but TUFM overexpression significantly inhibited ASFV replication. These results help elucidate the specific functions of D1133L and the potential mechanisms underlying ASFV replication.