Research Progress of Disease Resistance breeding in Pigs

The goal of high yield usually leads to a decrease in pig resistance. At the same time, pig farm diseases, especially viral infectious diseases, are a serious threat to the health of pigs. Although vaccination played an important role in prevention and treatment, the epidemic of infectious diseases could not be completely controlled and eliminated. In the long run, using genetic methods to improve the resistance of pigs to pathogens, carrying out disease-resistant breeding has the effect of curing the root causes. In the 1930s, some scholars reported that there were differences in the sensitivity of different chicken breeds to Marek's disease, and systematically studied the disease resistance of pigs or other livestock and poultry in the following period of time. With the development of immunology and biological products, most infectious diseases have been effectively controlled through vaccination, so that disease resistance has been neglected. Since the 1980s, with the development of molecular biology and genetic engineering technology, it has not only provided a new idea for disease resistance, but also made people pay more attention to the research of disease resistance breeding.

1 genetic basis of disease resistance pathogens will encounter three defense mechanisms in the process of infection, namely, epithelial defense mechanism, non-specific defense mechanism and specific defense mechanism. When individuals are infected by pathogens, they will mobilize these three defense mechanisms to resist. The disease of pigs depends on the interaction between infection and defense function, and pigs with stronger defense function show natural resistance to disease. According to the different genetic basis, disease resistance can be divided into special disease resistance and general disease resistance. Special disease resistance refers to the resistance of pigs to a specific disease or pathogen, which is mainly controlled by one major gene locus and can also be affected by other loci (including regulators) and environmental factors. The existing research results show that the inherent mechanism of special disease resistance lies in the existence or lack of a seed molecule or its variant in the host, which has the following functions:

① determines allogeneic recognition and specific allogeneic reaction in

② determines the special adhesion of pathogens.

After entering the human body, ③ pathogen proliferates in the body, which determines whether it can cause the host disease or not. The general disease resistance is not limited to a certain pathogen, it is affected by multiple genes and environment, and the difference of antigenicity of pathogens has little or no effect on the general disease resistance. This resistance reflects the overall defense function of the body against disease. For example, the MHC of chickens is related to the resistance and sensitivity of Marek's disease, coccidiosis and Ross's sarcoma.

1.1MHC and disease resistance major histocompatibility complex (MajorHlstocompatibllltycomplex,MHC) is a group of genes closely related to disease resistance and immune response. It encodes cell surface specific proteins and exists in all higher animals. MHC encodes three types of genes, which are closely linked to form haplotypes on autosomal chromosomes and show autosomal codominant inheritance. Porcine MHC (named SLA) is located on porcine chromosome 7 (Warner,1987), including type 1 and Ⅱ type genes, in which type 1 gene has a very strong polymorphism. SLA complex is closely related to immune response, ROthS. Hild et al. (1984) confirmed that the immune response of five American pig breeds to Pasteurella bronchosepticum was under the control of SLA. Mallard et al. (1989) found that individuals with SLA genotypes dd, dg and SS were strong responders to sheep erythrocytes, hen protein lysozyme and synthetic peptide (TMAE G)-Amurl in NIH pigs. In terms of disease resistance, Tissot. Et al. (1989) found that hereditary cutaneous malignant melanoma was associated with SLA complex. Renard et al. (1985) found that the pre-weaning mortality caused by diarrhea was related to the haplotype of SLA. In addition, different haplotypes of SLA had different types of resistance to parasites (Lunney et al., 1988). Warner (1991) completely listed the association with disease and the binding and function of SLA complex, which was updated by Lunney et al. (1998) and Valman et al. (1998).

1.2 the special resistance of major genes for disease resistance is controlled by major genes for specific resistance to certain diseases or pathogens. The identification of such specific resistance genes is of great significance to disease resistance breeding. Not only major gene selection and disease resistance breeding can be carried out directly, but also transgenic animals can be further cultivated. The receptor genes of porcine Escherichia coli K88 and F18 were clearly studied. Diarrhea in newborn piglets is caused by the attachment of the cell surface antigen of strain K88 to the corresponding receptors on the surface of intestinal mucosal epithelial cells. The bacteria conjugates with the receptors and proliferates massively, releasing enterotoxin and causing diarrhea. Piglets lacking K88 receptors can resist K88 attachment and thus resist diarrhea (Sellwood,1975). The K88 receptor gene is located on porcine chromosome 13 (Rothschild,1992). Whether its receptor is controlled by a pair of alleles S and s, the receptor (S) is completely dominant to the non-receptor (s), which is Mendelian inheritance. The frequency of K88 positive pigs is very high in all countries in the world. For example, Australian K88 positive pigs account for 88% of the studied Landrace and Landrace pig populations (Sondgrasss et al. 1981), while the frequency of K88 receptor in Chinese native pigs is very low and has natural disease resistance (Chappuls,1984). Bertschinser (1983) found that piglet edema disease before and after weaning was caused by the combination of F18 strain with cell surface receptor to release enterotoxin. Piglets lacking F18 normal receptor can resist diarrhea and edema disease. F18 receptor gene is located on porcine chromosome 6 and is closely linked to blood group inhibitor S, erythrocyte enzyme system and halothane gene. The receptor gene that can bind to F18 adhesin is a sensitive gene, which is dominant inheritance, otherwise it is resistance gene, that is, recessive inheritance (Vogeli et al., 1992). Vogeli (1997) also used candidate gene method and linkage analysis to study that the a (1.2) fucosyltransferase gene FUTI and FUTZ located in the 6qll region could be used as a candidate gene to control F18 adhesion. In addition, major genes related to disease resistance and E.COltF4 receptor genes located in the 13q31 region are also associated with diarrhea in pigs.

1.3 the relationship between disease resistance, immune response and production traits there is still a lack of experimental evidence on the relationship between disease resistance, immune response and production performance, and the results are different. Vander et al. (1983) chose high productivity to increase susceptibility to Marek's disease, while Lamont et al. (1989) found that there was a negative correlation between Marek's disease and egg production performance. In pigs, Meeker et al. (1987) found that the growth rate was negatively correlated with the immune response after vaccination with commercial Pasteurella bronchial septicemia vaccine or pseudorabies virus vaccine, and pigs with intestinal K88 receptor grew faster and had better feed utilization (Edfors et al., 1986). Porcine SLA is linked to a variety of production traits (Warne et al., 1991 × Lunney, et al. 1998). These results are positively correlated with the relationship between SLA and growth, dorsal and reproductive traits, so SLA gene should be the preferred gene for disease resistance breeding in the future. Mallard et al. (1998) found that H line reached the market weight 10 days earlier than L line in the high immune response (H strain) and low immune response (L line) strains formed by 8 generations selection.

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