Abstract: A mammalian cell having a mismatch repair-deficient phenotype is provided, where one or both alleles of a gene essential for mismatch repair, such as an Msh gene, are inactivated. Using this cell in a gene knock-out methodology advantageously allows efficient homologous recombination, even when the DNA sequences of the donor and recipient sequences diverge by significantly more than 0.6%.

Abstract: A mammalian cell having a mismatch repair-deficient phenotype is provided, where one or both alleles of a gene essential for mismatch repair, such as an Msh gene, are inactivated. Using this cell in a gene knock-out methodology advantageously allows efficient homologous recombination, even when the DNA sequences of the donor and recipient sequences diverge by significantly more than 0.6%.

Abstract: A mammalian cell having a mismatch repair-deficient phenotype is provided, where one or both alleles of a gene essential for mismatch repair, such as an Msh gene, are inactivated. Using this cell in a gene knock-out methodology advantageously allows efficient homologous recombination, even when the DNA sequences of the donor and recipient sequences diverge by significantly more than 0.6%.

Abstract: The invention relates to a pseudorabies virus (PRV) not found in nature and having a genome containing a mutation in the protein kinase gene region and/or in the 28K gene region. The mutation is e.g. a nucleic acid substitution, deletion, insertion or inversion, or a combination thereof. The mutations are introduced, by genetic engineering techniques, into the genome of a naturally occuring PRV, preferably NIA-3. Insertions may be nucleic acid sequences encoding antigenic polypeptides characteristic of a pathogen found in pigs. The invention also relates to vaccines containing a pseudorabies virus according to the invention, and to a process for preparing such vaccines.