he genetics of the female (host genetics). For instance, there is interbreed and intrabreed variation in humoral and cell-mediated immune responses, both of which are activated following exposure to the virus (reviewed in References \[[@B4-viruses-11-00706]\] and \[[@B5-viruses-11-00706]\]). The heritability of most of these responses is moderate or high \[[@B5-viruses-11-00706]\]. All of this supports the hypothesis that animals exposed to the same pathogen in the same environmental conditions will develop different immune responses. Lewis et al. \[[@B6-viruses-11-00706]\] showed that there was a genetic component to PRRSV resilience in sows, as indicated by the greater heritability of dead and mummified piglets observed during the epidemic phase of the disease compared to the healthy phase.

A small number of genetic markers have been studied in relation to the respiratory \[[@B7-viruses-11-00706],[@B8-viruses-11-00706],[@B9-viruses-11-00706]\] and reproductive \[[@B3-viruses-11-00706],[@B10-viruses-11-00706]\] phases of PRRSV or the in vitro responses to PRRSV cell infection \[[@B11-viruses-11-00706],[@B12-viruses-11-00706],[@B13-viruses-11-00706],[@B14-viruses-11-00706]\]. However, none have been assessed to date in relation to the incidence of abortion during a PRRSV outbreak. With this in mind, the objective of the present study was to use data from two resource populations to analyze the association between six previously reported PRRSV immune response markers and the likelihood of abortion in production sows ([Table 1](#viruses-11-00706-t001){ref-type="table"}). In an effort to identify new potential markers associated with the incidence of abortion, we also described sequence variants in the *HDAC6* (histone deacetylase 6) gene given its involvement in controlling PRRSV replication \[[@B15-viruses-11-00706]\]. This gene has been partially sequenced, and two polymorphisms have been studied in relation to the abortion rate.

2. Materials and Methods {#sec2-viruses-11-00706}
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2.1. P