Modulation of Host Antiviral Innate Immunity by African Swine Fever Virus: A Review

He, Wen-Rui; Yuan, Jin; Ma, Yuhe; Zhao, Cheng-Yan; Yang, Zhongyuan; Zhang, Yuhang; Han, Shichong; Wan, Bo; Zhang, Gaiping

doi:10.3390/ani12212935

Cited by 15 publications

(19 citation statements)

References 87 publications

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“…Recent studies have demonstrated that several ASFV-encoded proteins targeting cGAS-STING pathway can inhibit IFN-I production in diverse manners ( Table 1 ) [ 25 ]. In this pathway, cyclic GMP-AMP synthase (cGAS), which was previously identified to be a cytosolic DNA sensor, can directly recognize and bind to the non-self ASFV DNA [ 37 ].…”

Section: Suppression Of Ifn-i Production and Ifn-induced Antiviral Re...mentioning

confidence: 99%

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Antagonisms of ASFV towards Host Defense Mechanisms: Knowledge Gaps in Viral Immune Evasion and Pathogenesis

Zhu

Deng³

et al. 2023

Viruses

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African swine fever (ASF) causes high morbidity and mortality of both domestic pigs and wild boars and severely impacts the swine industry worldwide. ASF virus (ASFV), the etiologic agent of ASF epidemics, mainly infects myeloid cells in swine mononuclear phagocyte system (MPS), including blood-circulating monocytes, tissue-resident macrophages, and dendritic cells (DCs). Since their significant roles in bridging host innate and adaptive immunity, these cells provide ASFV with favorable targets to manipulate and block their antiviral activities, leading to immune escape and immunosuppression. To date, vaccines are still being regarded as the most promising measure to prevent and control ASF outbreaks. However, ASF vaccine development is delayed and limited by existing knowledge gaps in viral immune evasion, pathogenesis, etc. Recent studies have revealed that ASFV can employ diverse strategies to interrupt the host defense mechanisms via abundant self-encoded proteins. Thus, this review mainly focuses on the antagonisms of ASFV-encoded proteins towards IFN-I production, IFN-induced antiviral response, NLRP3 inflammasome activation, and GSDMD-mediated pyroptosis. Additionally, we also make a brief discussion concerning the potential challenges in future development of ASF vaccine.

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Section: Suppression Of Ifn-i Production and Ifn-induced Antiviral Re...mentioning

confidence: 99%

“…To date, a few articles have already highlighted the negative impact of plentiful ASFV proteins on antiviral immune response [ 25 , 26 , 27 ]. However, several ASFV immunosuppressive proteins (e.g., pE184L, pD345L, pD117L) and novel immune evasion mechanisms have not been summarized.…”

Section: Introductionmentioning

confidence: 99%

Antagonisms of ASFV towards Host Defense Mechanisms: Knowledge Gaps in Viral Immune Evasion and Pathogenesis

Zhu

Deng³

et al. 2023

Viruses

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“…As resistance to ASFV is known to correlate with a robust IFN response [ 5 ], the virus is predicted to have evolved a number of counter-strategies to inhibit the IFN response, a prediction that has been verified [ 6 ]. Therefore, deletion of virus genes inhibiting induction and/or impact of IFN is a logical choice for the construction of such an attenuated gene deletion virus vaccine.…”

Section: Introductionmentioning

confidence: 99%

I329L: A Dual Action Viral Antagonist of TLR Activation Encoded by the African Swine Fever Virus (ASFV)

Correia

Moura

Ventura

et al. 2023

Viruses

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The African Swine Fever Virus (ASFV) is an economically important, large DNA virus which causes a highly contagious and frequently fatal disease in domestic pigs. Due to the acute nature of the infection and the complexity of the protective porcine anti-ASFV response, there is no accepted vaccine in use. As resistance to ASFV is known to correlate with a robust IFN response, the virus is predicted to have evolved strategies to inhibit innate immunity by modulating the IFN response. The deletion of virus host evasion gene(s) inhibiting IFN is a logical solution to develop an attenuated virus vaccine. One such candidate, the ASFV ORF I329L gene, is highly conserved in pathogenic and non-pathogenic virus isolates and in this study we confirm and extend the conclusion that it has evolved for the inhibition of innate immunity initiated through Toll-like receptors (TLRs). Specifically, the ASFV I329L extracellular (ECD) and intracellular (ICD) domains inhibit TLR signalling by two entirely different mechanisms. Bioinformatics modelling suggests that the ECD inhibits several TLR signalling pathways through a short sequence homologous to the conserved TLR dimerization domain, here termed the putative dimerization domain (PDD). Remarkably, both full length and PDD constructs of I329L were demonstrated to inhibit activation, not only of TLR3, but also TLR4, TLR5, TLR8 and TLR9. Additionally, the demonstration of a weak association of I329L with TLR3 is consistent with the formation of a non-signalling I329L-TLR3 heterodimer, perhaps mediated through the PDD of I329L. Finally, the ICD associates with TRIF, thereby impacting on both TLR3 and TLR4 signalling. Thus, I329L offers potential as a general inhibitor of TLR responses and is a rational candidate for construction and testing of an I329L deletion mutant vaccine.

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“…African swine fever (ASF) is an acute, febrile, and hemorrhagic disease in domestic and wild pigs that is caused by the African swine fever virus (ASFV). ASFV is a large-diameter icosahedral DNA virus, and the genome is a linear 170–190 kb double-stranded DNA [ 1 ]encoding 150–200 viral proteins, including 68 structural proteins and more than 100 non-structural proteins [ 2 ]; however, the functions of most proteins are still unknown [ 3 , 4 ]. ASF was first reported in Kenya in 1921 [ 5 ], and it subsequently became endemic in most of sub-Saharan Africa and Sardinia [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

“…ASFV spread outside Africa to the Iberian Peninsula, initially to Portugal in 1957 and 1960, and subsequently to Europe and Latin America, then it was eradicated from all Western Europe except Sardinia by 1995 [ 7 ]. In 2007, ASF caused a serious outbreaks in Georgia, subsequently spreading to other adjacent countries of Europe, including Ukraine and Russia [ 1 , 8 ]. In 2018, the first outbreak of ASF was reported in Liaoning, China [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Identification of Potential miRNA-mRNA Regulatory Network Associated with Regulating Immunity and Metabolism in Pigs Induced by ASFV Infection

Pang

Chen

Cui³

et al. 2023

Animals

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African swine fever (ASF) is a devastating infectious disease in domestic pigs caused by African swine fever virus (ASFV) with a mortality rate of about 100%. However, the understanding of the interaction between ASFV and host is still not clear. In this study, the expression differences and functional analysis of microRNA (miRNA) in porcine peripheral blood lymphocytes of ASFV infected pigs and healthy pigs were compared based on Illumina high-throughput sequencing, then the GO and KEGG signal pathways were analyzed. The miRNA related to immunity and inflammation were screened, and the regulatory network of miRNA-mRNA was drawn. A total of 70 differentially expressed miRNAs were found (p ≤ 0.05). Of these, 45 were upregulated and 25 were downregulated in ASFV-infected pigs vs. healthy pigs. A total of 8179 mRNA genes targeted by these 70 differentially expressed miRNA were predicted, of which 1447 mRNA genes were targeted by ssc-miR-2320-5p. Five differentially expressed miRNA were validated by RT-qPCR, which were consistent with the RNA-Seq results. The GO analysis revealed that a total of 30 gene functions were significantly enriched, including 7 molecular functions (MF), 13 cellular components (CC), and 10 biological processes (BP). The KEGG enrichment analysis revealed that the differentially expressed genes were significantly enriched in pathways related to immunity, inflammation, and various metabolic processes, in which a total of two downregulated miRNAs after infection and eight upregulated miRNAs related to immunity and inflammation were screened in ASFV-infected pigs vs. healthy pigs. The network of miRNA-mRNA showed that the mRNA target genes were strongly regulated by ssc-miR-214, ssc-miR-199b-3p, and ssc-miR-199a-3p. The mRNA target genes were enriched into the MAPK signaling pathway, Toll-like receptor signaling pathway, TNF signaling pathway, and IL-17 signaling pathway by using a KEGG enrichment analysis. Therefore, ASFV could regulate immunity and metabolism-related pathways in infected pigs by inducing differential expression of miRNAs. These results provided a new basis for further elucidating the interactions between ASFV and the host as well as the immunity regulation mechanisms of ASFV, which will be conducive to better controlling ASF.

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Modulation of Host Antiviral Innate Immunity by African Swine Fever Virus: A Review

Cited by 15 publications

References 87 publications

Antagonisms of ASFV towards Host Defense Mechanisms: Knowledge Gaps in Viral Immune Evasion and Pathogenesis

Antagonisms of ASFV towards Host Defense Mechanisms: Knowledge Gaps in Viral Immune Evasion and Pathogenesis

I329L: A Dual Action Viral Antagonist of TLR Activation Encoded by the African Swine Fever Virus (ASFV)

Identification of Potential miRNA-mRNA Regulatory Network Associated with Regulating Immunity and Metabolism in Pigs Induced by ASFV Infection

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