Wed, Aug 17, 2022: 5:00 PM-6:30 PM
ESA Exhibit Hall
Background/Question/MethodsEmergent pathogens remain a critical challenge for the globally expanding aquaculture sector. Infectious hematopoietic necrosis virus (IHNV) emerged in trout aquaculture in the 1970s following a host jump from sockeye salmon and has since rapidly diversified. IHNV causes acute disease and often death in all members of fish Family Salmonidae, although species vary in susceptibility. Today IHNV constitutes one of the largest disease threats to farmed rainbow trout and is OIE-reportable outside its endemic range of the Pacific Northwest region of North America. Aquaculture provides novel environmental conditions for pathogens compared to wild settings and it is possible this has uniquely shaped IHNV evolution. The system is ripe for addressing a fundamental evolutionary question: how did virulence evolve following a jump to a novel trout host? Additionally, how has virulence evolved in the ancestral salmon host? Prevailing viral evolution theory suggests that viral phenotypes may shift to reduced virulence following a host jump. We conducted a series of challenges in juvenile sockeye salmon and rainbow trout at two temperatures and two doses to quantify virulence evolution over time using a selection of 15 IHNV isolates representing two phylogenetic clades and five decades of evolution
Results/ConclusionsThis work yields several findings: first, virulence appears to be increasing among viral isolates associated with trout aquaculture. Second, IHNV isolates appear to be host-specific, where increased virulence in a novel host correlated with reduced virulence in the ancestral host. Additionally, this is the first study to investigate a temperature adaptation of IHNV. Virulence patterns were consistent across dose and temperature treatments. Increasing virulence through more recent IHNV isolates confirms previous indications that IHNV does not adhere to contemporary virulence tradeoff theory following host jumps. These data may be used to parameterize aquatic epidemiology models and provide empirical evidence that a variety of fitness tradeoffs exist for viruses. Further work may focus on relating virulence with other viral traits such as replication and transmission rates.
Results/ConclusionsThis work yields several findings: first, virulence appears to be increasing among viral isolates associated with trout aquaculture. Second, IHNV isolates appear to be host-specific, where increased virulence in a novel host correlated with reduced virulence in the ancestral host. Additionally, this is the first study to investigate a temperature adaptation of IHNV. Virulence patterns were consistent across dose and temperature treatments. Increasing virulence through more recent IHNV isolates confirms previous indications that IHNV does not adhere to contemporary virulence tradeoff theory following host jumps. These data may be used to parameterize aquatic epidemiology models and provide empirical evidence that a variety of fitness tradeoffs exist for viruses. Further work may focus on relating virulence with other viral traits such as replication and transmission rates.