35-viruses-11-00706]\] deletion by genetic editing of this receptor makes pigs fully resistant to PRRSV infection. Thus, mutations in *CD163* could imply a significant change in the susceptibility of the pigs to PRRSV infection. Our results totally agree with this information in the sense that sows with the rs1107556229 variant, naturally present in nature, had a different clinical outcome when abortion was the end-point measure ([Table 5](#viruses-11-00706-t005){ref-type="table"} and [Figure 1](#viruses-11-00706-f001){ref-type="fig"}).

The next gene marker tested was a 275-bp insertion in the proximal promoter of the *MX1* gene (MX Dynamin Like GTPase 1), which enhances the transcriptional activity of this gene, mediating the humoral response to infection with PRRSV \[[@B13-viruses-11-00706]\]. As with *GBP1* and *GBP5*, *MX1* encodes a guanosine triphosphate (GTP)-metabolizing protein, whose expression is induced by interferons. MX1 has strong antiviral activity against a wide range of RNA viruses and some DNA viruses through binding and inactivation of their ribonucleocapsid. The antiviral effect of MX1 against the influenza virus has been well documented. Mice carrying the defective *MX1* gene show greater susceptibility to influenza A infection compared to mice carrying the functional protein \[[@B36-viruses-11-00706]\]. MX1 also conferred protection against the influenza A virus, classical swine fever virus, and vesicular stomatitis virus in studies performed in vitro \[[@B37-viruses-11-00706]\]. The mutation studied here was associated with higher *MX1* expression in vitro \[[@B13-viruses-11-00706]\]. In our data, this mutation showed the strongest association with a low abortion rate ([Table 5](#viruses-11-00706-t005){ref-type="table"}). The effect was completely recessive, where sows with two copies of the insertion had an abortion probability of 3% during the outbreak, while in the other sows the probability was \~25% ([Figure 1](#viruses-11-00706-f001){ref-type="fig"}). As with the favorable alleles o