Pigs are supposed to play the role of intermediate host – mixing vessel- for the reassortment of influenza A viruses of avian an human origin since their respiratory epithelium allows productive replication of the two types of viruses. Several MX proteins (IFN-induced GTPases) are known to confer an innate resistance against influenza A viruses. In laboratory mouse strains, allelic polymorphisms at the Mx1 locus affect the probability of survival after experimental influenza infection, which raises the possibility that identification of an antiviral MX isoform in pigs might allow selection programmes aimed at improving their innate resistance. Concerning the porcine Mx1 locus, three alleles coding for two distinct proteins (poMX1a and poMX1b) are known. We first investigated the distribution of the non deleted and deleted alleles and noticed an extreme allelic imbalance between the European wild boar and domestic pig populations: 100% of the wild boars genotyped were homozygous for an allele that was detected in only ~ 50 % of domestic pigs. In the latter, the "wild" allele is replaced by an allele in which a small 11-bp deletion is predicted to result in a frameshift that should yield a significantly altered MX1 protein. Secondly, in order to compare the anti- influenza capacity of both porcine MX1 proteins, specific expression vectors were constructed and transient versus stable transfections were undertaken. The replication of influenza A virus was inhibited in Vero cells expressing one or the other porcine MX proteins. These results indicate that the porcine MX1 proteins confer resistance to influenza A virus.