Although vaccination-based immune prevention plays an important role in controlling viral infections in animals, in recent years, with the rise of intensive farming and changes in farming conditions, some ancient infectious diseases have re-emerged and also occurred. Some new viral infections; some viruses have antigenic drift, and some super-virulent strains have appeared; in newborn animals, maternal antibodies interfere with the vaccine effect; attenuated vaccines also have the risk of virulence . Therefore, people are exploring new epidemic prevention methods, screening and breeding disease-resistant animal strains, which is an important research field.  In 1982, Palmiter et al. transferred the rat growth hormone gene into the chromosome of mice through transgenic technology, which not only made the gene expressable and could be inherited to the offspring, but its expression products showed obvious growth-promoting effects, and the cultivation was obtained in the world. *Example "Super Mouse". This technology opens up a new way for animal breeding research. At the same time, people use the principles and techniques of genetic engineering to not only isolate or synthesize DNA or cDNA such as IFN, interleukin and other cytokines with antiviral and immunomodulatory effects, but also to find the reverse of transcription and translation of viral genes. A class of small RNAs such as RNA and Ribozyme. These DNA, c DNA or RNA expression plasmids can not only be inserted into the chromosomal DNA of the cell and expressed, but also the transformed cells can obtain antiviral and the like. Therefore, domestic and foreign scholars have put forward the idea of ​​genetic engineering disease-resistant breeding in the early 1980s, and conducted in-depth exploration and research. Chen et al. (1988) introduced a fusion gene of mMT1 and human IFNβ1 into mouse germline to obtain transgenic mice. The serum of mice contains human IFNβ1 and can be protected in vitro. WISH cells are protected from vesicular stomatitis virus. The mouse footpads were inoculated with 850 PFU of pseudorabies virus. After 6 days, all non-transgenic individuals died, while the transgenic individuals (A7 5) died only one day after 9 days of inoculation. In another (B9) transgenic mouse, 25% of the individuals remained healthy for several months after receiving the virus, and they were propagated for 6 generations, and a transgenic mouse clone was established. Other researchers at home and abroad have also carried out similar research work in mice and rabbits, and obtained satisfactory results. Lindenmann et al. (1964) found that mice with a chromosomal dominant Mx allele had natural resistance to influenza A and B viruses, and later found that the Mx gene is present in almost all eukaryotes, only to In the form of a sex allele, this gene (Mx1) in mouse is located on chromosome 16 and can be expressed under the induction of IFN, double-stranded RNA and virus. Aebi et al. (1989) demonstrated that Mx1 protein is closely related to the inhibition of influenza virus replication in cultured cells. Parlovic et al. (1990) found that human MxA and rat Mx1 proteins not only have anti-influenza activity on cells, but also inhibit vesicular stomatitis virus replication. Garber used chicken full-length cDNA of mouse Mx1 protein to transfect chicken embryo fibroblasts, and the transformed cells inhibited the replication of chicken influenza viruses A/Turkey/Wisconsin/68 and A/Turkey/Massachussetts/65. Arnheiter et al. (1990) introduced a full-length cDNA containing the promoter of this gene into mouse fertilized eggs, and obtained transgenic mice. The 979-series mice were highly reactive, regardless of the dose of influenza virus infected, and the anti-infection efficiency. Both are between 63 and 69%. The non-reactive line (1009), like the litter non-transgenic individuals, died after challenge. The 964 line is a low-response line. Transgenic mice do not die when challenged with high-dose (50 000 LD50) influenza virus, but not at low doses (5-50 LD50), but with simultaneous injection of IFN and small doses of virus. You can avoid death. This indicates that the level of Mx protein expression is induced by viral dose or IFN level and directly affects its ability to resist infection by virus. Therefore, the Mx1 protein must be brought to a protective level before the challenge. It has been reported that anti-influenza virus transgenic pigs cultivated with this gene have also been successful. However, the specific mechanism of antiviral Mx1 protein remains to be elucidated.  Antisense RNAzui was first discovered in prokaryotes, which in a naturally occurring manner, through base pairing, specifically binds to mRNA and prevents mRNA translation. It is a gene expression regulator present in prokaryotes. Some such small RNA molecules have also been found in eukaryotic cells, and the function of antisense RNA to inhibit or shut down mR NA translation in eukaryotic cells has been confirmed by gene transfer technology. They bind to mRNA to form a dimer that disrupts the normal translation process of mRNA. The anti-sense nucleic acid assay for inhibiting viral replication has not only achieved great success on cultured cells, but also antisense inhibition of certain viruses in animals. Han et al. (1991) reverse-inserted the proviral packaging sequence (ψ) of Moloney murine leukemia virus (M-MuLV) downstream of the transcriptional regulatory region of the lymphocyte promoter/regulator of M-MuLV LTR or the syncytial virus In the early early regi on, the antisense expression sequence for preventing viral RNA packaging into the capsid is introduced into the mouse fertilized egg on NIH-3T3 cells, and no M-MuLV challenge is performed on the day of birth of the mouse. As soon as leukemia occurred, 31% of the normal mice in the control were sick. Ernst et al. (1991) successfully established transgenic rabbits using the antisense expression plasmid of human type 5 adenovirus (Ad5). Anti-adenoviral activity was titrated by primary kidney cell culture of transgenic rabbits, and 2 of the 5 transgenic rabbits tested showed significant Ad5 resistance. The genetic engineering laboratory of the Agriculture and Animal Husbandry University also uses antisense suppression technology to study the breeding of anti-swine fever virus. The antisense cDNA of classical swine fever virus synthesized by chemical synthesis and reverse transcription was transformed into PK-15 cells, and a cell line resistant to swine fever virus was screened. It can be seen that the application of antisense RNA for disease resistance breeding is a valuable field of exploration. Ribozyme is a natural small RNA molecule, which is called ribozyme. This small RNA molecule functions to catalyze an RNA cleavage reaction and can specifically cleave RNA in sequence. Studies have shown that Ribozyme mainly consists of a three-part structure, one is to recognize the A-binding portion of GUX (X=C, A) on the substrate RNA, and the second is a highly conserved sequence of 13 nucleotides. In the B-part of the helical secondary structure, the three pairs of bases in the helix can be changed, and the terminal RN A loop can be broken. Therefore, the Ribozyme can be divided into two halves. The third part is complementary to the target RNA sequence on both sides. Part C, which allows Ribozyme to specifically bind to the substrate, allowing the reaction gene to be precisely located, the sequence of which is determined by the nucleotide sequence of the substrate R NA . From this point of view, the thiol complementary region of the two parts A and C determines the specificity of the Ribozyme cleavage reaction; the B part is the active site of the Ribozyme, which determines the cleavage activity of the Ribozyme. Therefore, as long as the RNA sequence of a certain virus is known, the corresponding antiviral Ribozyme can be designed and synthesized, and the above method can be used for breeding of the transgenic animal.ç ”ç©¶ Research on the cultivation of transgenic animals with other anti-virus related genes has also made some progress. However, antiviral infection breeding is a vast bioengineering. As far as current technology is concerned, it is not very difficult to breed a new individual against a specific virus infection, but to cultivate a stable and excellent biological trait while at the same time Groups that do not affect other biological traits of this population will also need to work for years or even decades. 
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