SUSCEPTIBILITY AND HUMORAL RESPONSE OF BROWN TROUT X LAKE TROUT HYBRIDS TO INFECTIOUS HEMATOPOIETIC NECROSIS VIRUS - A MODEL FOR EXAMINING DISEASE RESISTANCE MECHANISMS

A model system for examining resistance mechanisms of interspecific hy brids to a viral disease was designed and tested. Diploid rainbow trou t Oncorhynchus mykiss and heat-induced triploid brown trout Salmo trut ta female X lake trout Salvelinus namaycush male hybrids (or brake tro ut) were evaluated for susceptibility and humoral response to infectio us hematopoietic necrosis virus (IHNV). The triploid hybrids exposed t o waterborne virus had a cumulative mortality of 2% (1/49) compared to 53% (27/51) in the pure species diploid rainbow trout. Virus neutrali zation activity was not detected in serum obtained from control fish, however, all serum pools from surviving rainbow trout exposed to water borne IHNV had antibody titers significantly higher (P < 0.05) than po oled sera from brake trout. This suggested that the IHNV resistance of the hybrids occurred at the cellular level that minimized infection a nd internalization of the virus. To determine if resistance was a func tion of external epithelial cell attachment and entry, susceptibility was also evaluated to intraperitoneally injected virus. Mortality was also significantly less (P < 0.001) in hybrid trout (mean weight, 10.2 and 26.2 g) injected with IHNV compared to rainbow trout (mean weight , 22.3 and 90.0 g). The decrease in mortality was associated with a st rong humoral response where 70% of the surviving triploid hybrids had antibody titers greater than or equal to 640. Necrosis of the renal an d splenic interstitial hematopoietic tissue of rainbow trout was typic al of lesions due to IHNV infection, however, the lesions in the hybri ds were less extensive and severe. The decreased severity and extent o f the lesions correlated with the decreased mortality and high antibod y titers demonstrated in the hybrid trout as compared to the matched g roup of rainbow trout. These results suggest that more than one host f actor can affect resistance to IHNV.