Pacific oyster Crassostrea gigas suffers from chronic or sporadic mortality outbreaks worldwide, resulting from infectious diseases and/or physiological disorders triggered by environmental factors. Since 2008, ostreid herpesvirus OsHV-1 μVar has been identified as the main agent responsible for mass mortality of juvenile oysters in Europe. Previous studies of genome-wide expression profiling have provided candidate genes that potentially contribute to genetically-based resistance to summer mortality. To assess their value in determining resistance to the juvenile mass mortality that has occurred in France since 2008, we analyzed the expression of 17 candidate genes in an experimental infection by OsHV-1 μVar, and in an in vivo field experiment. Individual quantification of mRNA levels of 10 out of the 17 targeted genes revealed significant variation, of which 7 genes were showed differences between conditions that created significant differences in mortality, and 6 depended on the number of OsHV-1 genome copies individually quantified in mantle tissue. Complex SOD metalloenzymes known to be part of the antioxidant defense strategies may at least partly determine susceptibility or resistance to OsHV-1-associated mortality. Furthermore, inhibitor 2 of NF-κB, termed CgIκB2, exhibited highly significant variation of mRNA levels depending on OsHV-1 load in both experiments, suggesting its implication in the antiviral immune response of C. gigas. Our results suggest that CgIκB2 expression would make a good starting point for further functional research and that it could be used in marker-assisted selection.