The objective of this study was to identify genetic host components of resistance or tolerance to PRRSv. Three trials of ~200 barrows were infected with PRRSv at ~3 weeks of age. Weekly piglet weights, up to 42 days post infection (dpi), were used to evaluate weight gain (WG). Viral load (VL) was quantified as area under the curve of log transformed viral qRT-PCR levels in serum, up to 21 dpi. Piglets were genotyped using the SNP60 Beadchip. A genome wide association study of VL, using Bayesian methods in GenSel, revealed regions on Sus Scrofa chromosome 4 (SSC4) and SSCX that explained a considerable amount of variation; the SSC4 region also affected WG. ASREML was used to further explore the impact of both regions and their interaction. The SSC4 region appeared dominant, with the heterozygote estimated to decrease VL by 0.66 phenotypic standard deviations (sd), and increase WG by 2.5 kg, or 0.57 sd. The favorable SSCX allele was estimated to decrease VL by 0.84 sd, and increase WG by 2.3 kg, or 0.53 sd. The interaction between the two regions was not significant (P>0.2). Several candidate genes were identified in each region. These results show that it may be possible to select pigs for resistance to PRRSv. This work was supported by the National Pork Board, USDA NIFA PRRS CAP Award 2008-55620-19132, USDA ARS, NRSP-8 swine and bioinformatics coordination projects, and breeding companies that provided pigs. EW is a Fellow supported by USDA NIFA National Needs grant # 2010-38420-20328.