African swine fever (ASF) is a fatal infectious disease of swine caused by the African swine fever virus (ASFV). Currently, the disease is listed as a legally notifiable disease that must be reported to the World Organization for Animal Health (WOAH). The economic losses to the global pig industry have been insurmountable since the outbreak of ASF. Control and eradication of ASF are very critical during the current pandemic. Vaccination is the optimal strategy to prevent and control the ASF epidemic, but since inactivated ASFV vaccines have poor immune protection and there aren’t enough cell lines for efficient in vitro ASFV replication, an ASF vaccine with high immunoprotective potential still remains to be explored. Knowledge of the course of disease evolution, the way of virus transmission, and the breakthrough point of vaccine design will facilitate the development of an ASF vaccine. In this review, the paper aims to highlight the recent advances and breakthroughs in the epidemic and transmission of ASF, virus mutation, and the development of vaccines in recent years, focusing on future directions and trends.

We report the presence of mcr-1 in Escherichia coli and carbapenem-resistant Cronobacter sakazakii from the same diseased chicken. The mcr-1 gene linked with IS Apl1 was located on two different IncI2 plasmids, including one multidrug plasmid in E. coli , whereas fosA3-bla _NDM-9 was on an IncB/O plasmid in C. sakazakii . The development of the fosA3-bla _NDM-9 resistance region was mediated by IS 26 . The colocation of mcr-1 or bla _NDM-9 with other resistance genes will accelerate the dissemination of the two genes.

Senecavirus A (SVA), previously known as Seneca Valley virus, is classified into the genus Senecavirus in the family Picornaviridae. This virus can cause vesicular disease and epidemic transient neonatal losses in swine. Typical clinical signs include vesicular and/or ulcerative lesions on the snout, oral mucosa, coronary bands and hooves. SVA emerged in Guangdong Province of China in 2015, and thereafter gradually spread into other provinces, autonomous regions and municipalities (P.A.M.s). Nowadays more than half of the P.A.M.s have been affected by SVA, and asymptomatic infection has occurred in some areas. The phylogenetic analysis shows that China isolates are clustered into five genetic branches, implying a fast evolutionary speed since SVA emergence in 2015. This review presented current knowledge concerning SVA infection in China, including its history, epidemiology, evolutionary characteristics, diagnostics and vaccines.

N-glycosylations can regulate the adhesive function of integrins. Great variations in both the number and distribution of N-glycosylation sites are found in the 18 α and 8 β integrin subunits. Crystal structures of α_IIbβ₃ and α_Vβ₃ have resolved the precise structural location of each N-glycan site, but the structural consequences of individual N-glycan site on integrin activation remain unclear. By site-directed mutagenesis and structure-guided analyses, we dissected the function of individual N-glycan sites in β₃ integrin activation. We found that the N-glycan site, β₃-N320 at the headpiece and leg domain interface positively regulates α_IIbβ₃ but not α_Vβ₃ activation. The β₃-N559 N-glycan at the β₃-I-EGF3 and α_IIb-calf-1 domain interface, and the β₃-N654 N-glycan at the β₃-β-tail and α_IIb-calf-2 domain interface positively regulate the activation of both α_IIbβ₃ and α_Vβ₃ integrins. In contrast, removal of the β₃-N371 N-glycan near the β₃ hybrid and I-EGF3 interface, or the β₃-N452 N-glycan at the I-EGF1 domain rendered β₃ integrin more active than the wild type. We identified one unique N-glycan at the βI domain of β₁ subunit that negatively regulates α₅β₁ activation. Our study suggests that the bulky N-glycans influence the large-scale conformational rearrangement by potentially stabilizing or destabilizing the domain interfaces of integrin.

The name porcine reproductive and respiratory syndrome virus (PRRSV) NADC30-like was first coined in 2015. It originated from the NADC30 strain that was introduced into China by importing breeding pigs and has since undergone mutations or recombination, resulting in variant viruses. Following widespread outbreaks in China in recent years, these NADC30-like strains have presented major health challenges in swine production systems. Outcomes induced by PRRSV NADC30-like infection are highly variable, ranging from inapparent to severe, depending on the recombination between NADC30 and field PRRSV strains prevalent in swine farms. Vaccines and strict biosecurity measures have been explored to fight this disease; however, current PRRSV commercially modified-live virus vaccines (MLVs) have the potential to revert to virulence and only provide limited or no cross-protection efficacy against NADC30-like strains. PRRSVs will remain an ongoing challenge to the swine industry until safe and effective vaccines or antiviral reagents are developed.

Senecavirus A (SVA), also known as Seneca Valley virus, is an emerging virus that causes vesicular disease in pigs. This virus belongs to the genus Senecavirus in the family Picornaviridae. The SVA CH-LX-01-2016 was isolated from Guangdong Province of China in 2016. In this study, a recombinant SVA CH-LX-01-2016 was constructed using reverse genetics, and proven to be able to express efficiently an enhanced green fluorescent protein (eGFP) in vitro. This eGFP-tagged recombinant SVA (rSVA-eGFP) exhibited a high capacity for viral replication. Its fluorescence-tracked characteristics greatly facilitated both virus neutralization test (VNT) and antiviral assay. The rSVA-eGFP-based VNT was used to detect eight porcine serum samples, out of which four were determined to be neutralization titer-positive. Subsequently, two antiviral drugs, ribavirin and apigenin, were assayed for evaluating both effects against the rSVA-eGFP in vitro. The result showed that only the ribavirin exhibited an anti-SVA activity.