Betaine was found to alleviate inflammation in different studies. Here, newly hatched broilers were randomly divided into control and betaine consumptive groups, who had access to normal drinking water and water with betaine at a dose of 1000 mg/L, respectively. At the age of two weeks, the boilers were intraperitoneally treated with LPS. The protective effects of betaine against LPS-induced skeletal muscle inflammation were studied. Betaine attenuated the LPS-induced overexpression of IL-6 significantly in the leg muscle. Furthermore, LPS lowered the expression of TLR4 and TLR2 but increased the expression of MyD88. Betaine eliminated the effect of LPS on the expression of TLR4 but not TLR2 and MyD88. LPS also increased the expression of Tet methylcytosine dioxygenase 2 (Tet2), and this effect was also eliminated by betaine consumption. MeDIP-qPCR analysis showed that the methylation level in the promoter region of IL-6 was decreased by LPS treatment, whilst betaine cannot prevent this effect. On the contrary, LPS significantly increase the methylation level in the promoter region of TLR4, which was decreased by the consumption of betaine. Our findings suggest that betaine can alleviate LPS-induced muscle inflammation in chicken, and the regulation of aberrant DNA methylation might be a possible mechanism.

African swine fever (ASF) is a highly contagious disease caused by African swine fever virus (ASFV), affecting domestic and wild boars. The polyprotein pp220 of ASFV is responsible for producing the major structural proteins p150, p37, p14, p34, and p5 via proteolytic processing. The p34 protein is the main component of the ASFV core shell. However, the immunologic properties of the p34 protein in vitro and in vivo remain unclear. The results showed that the recombinant p34 protein expressed in prokaryotes and eukaryotes could react with convalescent swine sera to ASFV, suggesting that p34 is an immunogenic protein. Significantly, anti-p34 antibodies were found to inhibit the replication of ASFV in target cells. Furthermore, rabbits immunized with the recombinant C-strain of classical swine fever virus containing p34 produced both anti-p34 humoral and cellular immune responses. In addition, the p34 protein could induce a cell-mediated immune response, and a T-cell epitope on the p34 protein was identified using immunoinformatics and enzyme-linked immunospot (ELIspot) assay. Our study demonstrates that the p34 protein is a novel antigen of ASFV with protective potential.

Porcine epidemic diarrhea virus (PEDV) is an important pathogen in swine, causing severe economic losses to the global swine industry. As a coronavirus, PEDV is prone to mutations and recombination. Therefore, characterizing circulating strains is essential for disease control. In this study, a PEDV strain (GD1) was isolated from diarrheic piglets in Guangdong Province, China, and identified by RT-PCR and immunofluorescence. Pathogenicity was evaluated in piglet challenge experiment. The results showed that GD1 strain could be stably passaged in Vero cells, forming syncytia. Phylogenetic analysis based on the complete genome and spike (S) gene both placed GD1 strain within the GIIc genotype. Amino acid sequence alignment of the S protein revealed multiple amino acid mutations in the neutralizing epitopes COE, SE16, and SS6 of GD1 strain compared with the classical vaccine strain CV777. Recombination analysis suggested that GD1 may be a novel recombination strain originating from strains SD2021 and GDS28, with the recombination breakpoint located in the ORF1a region. Pathogenicity assessment demonstrated that GD1 is highly virulent, inducing severe watery diarrhea and vomiting in newborn piglets within 24 h post-inoculation, and causing histopathological lesions characterized by intestinal villous atrophy and shedding. Immunohistochemistry confirmed that PEDV antigen was predominantly distributed in the villous epithelial cells of the small intestine. The successful isolation and characterization of the GD1 strain provide important viral resources for further research on the genetic evolution of PEDV and the development of matched vaccines.