Swine fever virus (CSFV) E2 glycoprotein is a major inducer of neutralizing antibodies and protective immunity in pigs. E2 mediate virus adsorption to the cells in the object, and contains the genetic determinants associated with the pathogenic virus. Between CSFV E2 is also related to the pestivirus which are the bovine viral diarrhea virus (BVDV) and border disease of CSFV Virus (BDV) a monoclonal antibody that is used to differentiate that is recognized by the monoclonal antibody (mAb) WH303, residues 829 to 837 It includes the epitope (TAVSPTTLR) distinct. In this study, we used an infectious clone of a pathogenic CSFV Brescia isolates (BICv) in order to gradually mutant WH303 the mAb epitopes of CSFV E2 homologous to the amino acid sequence (TSFNMDTLA) of BVDV strain NADL E2. The virus mutants T1v (TSFSPTTLR), T2v (TSFNPTTLR), T3v (TSFNMTTLR), while showing the in vitro growth characteristics similar to those of the parent BICv, mutants T4v (TSFNMDTLR) and T5v (TSFNMDTLA) obtained is compared to the maternal BICv when it exhibited a significant reduction in plaque size and reduction of the 10-fold in virus yield. Chemical reactivity of immune cells and WH303 were lost only T3v, T4v and T5v. Interestingly, WH303 gradual mutation of the epitope naetneunde that the additional impact on the virus attenuated in pigs, mutants T1v, T2v or T3v is gradually weak, but was induced fatal CSF invariably, T4v only mild and transient clinical induced diseases, T5v did not induce disease. Pigs infected with T4v or T5v showed a significant reduction in the amygdala, lymph drainage, reduced viral replication in the spleen and kidneys, and viruses emissions. After all, animals infected with T5v were protected from clinical disease immunity when tested in three days or 21 days after T5v virulent Brescia virus inoculation. These results indicate that these genes in the crystal and the position of amino acid residues 830 to 834 of E2 in the pathogenicity of CSFV in pigs eng
