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, 2010; Martenot et al., 2011, 2013). It has been postulated that the variant OsHV-1 ��var is more virulent than the reference strain (OsHV-1) and could be the etiological agent of juvenile mortalities (Segarra et al., 2010; Martenot et al., 2011, 2013; Schikorski et al., 2011a,b). However, these assumptions are speculative (to the authors�� knowledge, no published data has formally demonstrated that the pathogenicity of OsHV-1 ��var is higher than that of OsHV-1) and await further confirmations. In particular, recent technological improvments in the procedures used to detect the viral DNA load in animal tissues now offer an opportunity revisiting these assumptions. The real-time PCR-based assays recently developed and now widely used as detection tools have been shown to be at least two orders of magnitude more sensitive than earlier quantitative PCR assays (Arzul et al., 2002; Pepin et al., 2008; Martenot et al., 2010). Hence, the determination of the viral DNA quantity in archived samples (collected before 2008) using the older and newer protocols should be performed to verify that the increase of mortality correlates with an increase in virus prevalence. Therefore, it is yet to be determined if the increase in juvenile oyster mortalities since 2008 corresponds to a new disease or to a worsening summer mortality syndrome, emphasizing the need to continue investigating the diversity and functioning of all oyster disease agents. This is particularly important for oyster farming because the only regulation implemented to help the oyster industry to date is based on the hypothesis that juvenile mortalities are due to the emergence of a new disease connected to OsHV-1 ��var. The European Union Regulation (175/2010), implemented in March of 2010, suggests that when the presence of OsHV-1 ��var is detected, disease control measures should be implemented, including the establishment of a containment area to restrict the movement of C. gigas oysters. Thus, demonstrating that the herpes virus is a marker of the disease and/or the unique etiological agent requires further investigations. Previous research efforts have mainly focused on the viral hypothesis and knowledge on the role of bacteria remains limited. We recently investigated the oyster disease ecology of microdiverse Vibrio genotypes using a new field-based approach (Lemire et al., 2014). We took advantage of recently developed specific-pathogen-free (SPF) juveniles of C. gigas, which become naturally infected when placed in an estuarine CASK environment (Petton et al., 2013). We showed that the onset of disease in oysters is associated with progressive replacement of diverse and benign colonizers by members of a non-clonal but phylogenetically coherent virulent population of Vibrio crassostreae.