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The spread of African swine fever virus (ASFV) caused huge economic costs, so early detection is particularly important. Here, we established a fluorescence biosensor based on carbon nanodots (CNDs) and loop-mediated isothermal amplification (LAMP) to ultra-sensitively detect ASFV. LAMP with high efficiency produced a large amount of pyro phosphoric acid and caused pH change in a short time. CNDs with strong light stability had a large fluorescence response at the emission wavelength of 585.5 nm to small pH change by the excitation wavelength of 550 nm. The biosensor realized \"turn-off-on\" mode for ASFV detection with the detection limit as low as 15.21 copies [mu]L.sup.-1. In addition, the biosensor had high accuracy in the actual sample assay. Therefore, the biosensor achieved rapid, sensitive, low-cost, and simple detection for ASFV. Moreover, the biosensor broadened the detection pathway of LAMP as a tool with great development prospect. Graphical abstract

African swine fever virus (ASFV) genotype II is endemic to Vietnam. We detected recombinant ASFV genotypes I and II (rASFV I/II) strains in domestic pigs from 6 northern provinces in Vietnam. The introduction of rASFV I/II strains could complicate ongoing ASFV control measures in the region.

In order to observe the dosage-effect of recombinant pig interleukin-6 gene and CpG motifs on the immune responses of swine to vaccine, a novel recombinant eukaryotic VPIL6C plasmid was packed with chitosan nanoparticles (CNP) prepared by ionic cross linkage, which contains pig interleukin-6 gene and immunostimulatory sequence consisted of 11 CpG motifs. CNP-VRIL6C was then utilized to inoculate 30-day-old piglets intramuscularly at the dosage of 0.5, 1.0 and 1.5 mg/per capita, respectively. Meanwhile, the piglets were injected with attenuated classical Hog cholera vaccine and designated as A1, A2 and A3 group. The blood was weekly collected from the piglets after vaccination to detect the changes of immunoglobulins, specific antibody, interleukins, IFN-γ and immune cells. The results were found that compared to those of the control piglets injected with VR1020-CNP, the content of IgG, IgA and IgM, specific antibodies, IL-2, IL-6 and IFN-γ significantly increased in the sera from the treated three groups from 14 to 70 days after vaccination ( P < 0.05); the number of T H, T C and CD3 + positive T cells raised obviously in the blood of VPIL6C treated piglets ( P < 0.05). Also the above immune indexes of A1 group were significantly lower to different extent in comparison with those of A2 and A3 group from 14 to 56 days post inoculation ( P > 0.05). Moreover, the lymphocytes also remarkably elevated in the treated groups ( P < 0.05). These indicate that VPIL6C entrapped with CNP is a novel effective adjuvant to boost the humoral and cellular immunity of pig to Hog cholera, implying it's potentiality to enhance the resistance of pig against infectious diseases.

In 2007 African swine fever (ASF) arrived at a Black Sea harbour in Georgia and in 2014 the infection reached the European Union (EU), where it still expands its territory. ASF is a fatal viral disease affecting domestic pigs and wild boar of all ages with clinical presentations ranging from per-acute to chronic disease, including apparently asymptomatic courses. Until the detection of the first case inside the EU, infections in the current epidemic were mainly seen among pig farms with generally low biosecurity, and with incidental spill over to the wild boar population. In the EU, however, the infection survived locally in the wild boar population independently from outbreaks in domestic pigs, with a steady and low prevalence. Apart from the wild boar population and the habitat, the current epidemic recognizes humans as the main responsible for both long distance transmission and virus introduction in the domestic pig farms. This underlines the importance to include social science when planning ASF-prevention, −control, or -eradication measures. Based on experiences, knowledge and data gained from the current epidemic this review highlights some recent developments in the epidemiological understanding of ASF, especially concerning the role of wild boar and their habitats in ASF epidemiology. In this regard, the qualities of three epidemiological traits: contagiousity, tenacity, and case fatality rate, and their impact on ASF persistence and transmission are especially discussed.

Porcine circovirus 2 (PCV2) is the etiological agent that causes porcine circovirus diseases and porcine circovirus-associated diseases (PCVD/PCVAD), which are present in every major swine-producing country in the world. PCV2 infections may downregulate the host immune system and enhance the infection and replication of other pathogens. However, the exact mechanisms of PCVD/PCVAD are currently unknown. To date, many studies have reported that several cofactors, such as other swine viruses or bacteria, vaccination failure, and stress or crowding, in combination with PCV2, lead to PCVD/PCVAD. Among these cofactors, co-infection of PCV2 with other viruses, such as porcine reproductive and respiratory syndrome virus, porcine parvovirus, swine influenza virus and classical swine fever virus have been widely studied for decades. In this review, we focus on the current state of knowledge regarding swine co-infection with different PCV2 genotypes or strains, as well as with PCV2 and other swine viruses.

The multigene family genes (MGFs) in the left variable region (LVR) of the African swine fever virus (ASFV) genome have been reported to be involved in viral replication in primary porcine alveolar macrophages (PAMs) and virulence in pigs. However, the exact functions of key MGFs in the LVR that regulate the replication and virulence of ASFV remain unclear. In this study, we identified the MGF300-2R gene to be critical for viral replication in PAMs by deleting different sets of MGFs in the LVR from the highly virulent strain ASFV HLJ/18 (ASFV-WT). The ASFV mutant lacking the MGF300-2R gene (Del2R) showed a 1-log reduction in viral titer, and induced higher IL-1[beta] and TNF-[alpha] production in PAMs than did ASFV-WT. Mechanistically, the MGF300-2R protein was found to interact with and degrade IKK[alpha] and IKK[beta] via the selective autophagy pathway. Furthermore, we showed that MGF300-2R promoted the K27-linked polyubiquitination of IKK[alpha] and IKK[beta], which subsequently served as a recognition signal for the cargo receptor TOLLIP-mediated selective autophagic degradation. Importantly, Del2R exhibited a significant reduction in both replication and virulence compared with ASFV-WT in pigs, likely due to the increased IL-1[beta] and TNF-[alpha], indicating that MGF300-2R is a virulence determinant. These findings reveal that MGF300-2R suppresses host innate immune responses by mediating the degradation of IKK[alpha] and IKK[beta], which provides clues to paving the way for the rational design of live attenuated vaccines to control ASF.

The type I interferon (IFN-I) signaling pathway is an important part of the innate immune response and plays a vital role in controlling and eliminating pathogens. African swine fever virus (ASFV) encodes various proteins to evade the host’s natural immunity. However, the molecular mechanism by which the ASFV-encoded proteins inhibit interferon production remains poorly understood. In the present study, ASFV MGF360-11L inhibited cGAS, STING, TBK1, IKKε, IRF7 and IRF3-5D mediated activation of the IFN-β and ISRE promoters, accompanied by decreases in IFN-β, ISG15 and ISG56 mRNA expression. ASFV MGF360-11L interacted with TBK1 and IRF7, degrading TBK1 and IRF7 through the cysteine, ubiquitin–proteasome and autophagy pathways. Moreover, ASFV MGF360-11L also inhibited the phosphorylation of TBK1 and IRF3 stimulated by cGAS-STING overexpression. Truncation mutation analysis revealed that aa 167-353 of ASFV MGF360-11L could inhibit cGAS-STING-mediated activation of the IFN-β and ISRE promoters. Finally, the results indicated that ASFV MGF360-11L plays a significant role in inhibiting IL-1β, IL-6 and IFN-β production in PAM cells (PAMs) infected with ASFV. In short, these results demonstrated that ASFV MGF360-11L was involved in regulating IFN-I expression by negatively regulating the cGAS signaling pathway. In summary, this study preliminarily clarified the molecular mechanism by which the ASFV MGF360-11L protein antagonizes IFN-I-mediated antiviral activity, which will help to provide new strategies for the treatment and prevention of ASF.

African swine fever is a growing threat to the livestock industry. We examined data indicating that in most countries in Asia, most notified events were related to farm outbreaks; meanwhile, only a few wild boar cases were reported. We hypothesize the virus circulates unnoticed in wild boar populations in Asia.

Classical swine fever virus (CSFV) is the etiological agent of classical swine fever, a highly contagious disease that causes significant economic losses to the swine industry. Systemic prophylactic immunization with the live attenuated vaccine, the C-strain vaccine, is one of the effective measures for CSF control. However, one of the limitations of the C-strain vaccine is that the field strains-infected animals cannot be differentiated from the C-strain vaccinated herds by serological tests (DIVA). This constraint hampers the practical usage of the C-strain vaccine to eradicate the CSF in China. In the current study, a novel CSF modified live marker vaccine candidate was constructed based on the attenuation of the prevalent 2.1 genotype strain by the deletion of two virulence associated functional residues in the CSFV Eʳⁿˢ, H79, and C171. Meanwhile, four residues S14, G22, E24, and E25 were identified specifically for the 6B8 mAb binding to the CSFV E2 as the novel conformational epitope. Then four substitutions of S14K, G22A, E24R, and G25D were further incorporated in the double deletion construct as a negative serological marker. Finally, the double-deletion marker MLV candidate GD18-ddErnHC-KARD was rescued, and its safety and efficacy profiles were evaluated in piglets. The safety study results indicated that the candidate did not induce fever, clinical signs, or pathological lesions with a high dose of 10⁵.⁰ TCID₅₀, and in addition, no virus shedding was detected until 21 days post-inoculation. Meanwhile, the efficacy study results demonstrated that at a low dose of 10³.⁰ TCID₅₀, it conferred complete clinical protection and no virus shedding was detected after the challenge with a highly virulent Shimen strain. Importantly, the infected animals were differentiated using the accompanied DIVA ELISA. These results constitute a proof-of-concept for rationally designing a CSF antigenically marked modified live vaccine candidate.