The research herein is an extension of the PRRS Host Genetics Consortium (PHGC), which is a national effort to identify genomic markers and host response pathways in response to PRRSV infection. The typical trial includes 200 pigs that are followed through 42 days post-infection (dpi) of PRRSV, with blood (serum and RNA tempus), oral fluids, and weights collected for phenotypic analysis. DNA recovered from each pig is then genotyped using the Porcine SNP60 Bead chip. The pigs in the PHGC model have shown wide variation in weight gain, with some pigs gaining weight at a relatively normal rate, while others failed to thrive during the 42 day infection period. Furthermore, weight gain following PRRSV infection was moderately heritable (0.3) and a substantial proportion of the genetic variation in weight gain following challenge was mapped to chromosome 4 (SSC 4), indicating a role for host genetics. Therefore, this research paper took advantage of two PHGC trials 13 and 14, and investigated the individual digestibility of dry matter and energy in the face of PRRSV infection. Total tract feces was collected and pooled from individual infected (n=376) pigs during peak virus load (9-14 dpi). Total tract apparent digestibility coefficients on 122 pigs were then used to estimate genetic parameters and to perform a genome-wide association study. This novel study is the first to provide genetic parameters for digestibility traits in PRRSV infected pigs. Heritability estimates were low to moderate. Digestibility was not phenotypically correlated with weight gain and viral load, but their genetic correlation was moderate, indicating that some of the same genes may control these traits. Several QTL for digestibility were identified, jointly explaining over 8% of the genetic variance in dry matter and energy digestibility. Many of these regions have been previously associated with growth or feed intake related traits and harbor genes that are involved in important mechanisms related to energy and nutrient usage. Albeit small, this data set allowed us to identify one SNP controlling variation in digestibility of dry matter and energy, and provided further information on the effect of the WUR SNP on PRRSV infected pigs.