|| Checking for direct PDF access through Ovid
Early innate gene expression was monitored in yellow perch exposed to VHSV-IVb.VHSV exposure fails to induce robust Mx expression in the head kidney and spleen.Virus accumulation in the head kidney and spleen and overall mortality is high.Mx gene activation is correlated to VHSV accumulation in the liver.SAA and IL-1β activation is correlated to VHSV accumulation in all three tissues.The recently discovered strain of viral hemorrhagic septicemia virus, VHSV-IVb, represents an example of the introduction of an extremely pathogenic rhabdovirus capable of infecting a wide variety of new fish species in a new host-environment. The goal of the present study was to delineate the expression kinetics of key genes in the innate immune response relative to the very early stages of VHSV-IVb infection using the yellow perch (Perca flavescens) as a model. Administration of VHSV-IVb by IP-injection into juvenile yellow perch resulted in 84% cumulative mortality, indicating their high susceptibility to this disease. In fish sampled in the very early stages of infection, a significant up-regulation of Mx gene expression in the liver, as well as IL-1β and SAA activation in the head kidney, spleen, and liver was directly correlated to viral load. The potential down-regulation of Mx in the hematopoietic tissues, head kidney and spleen, may represent a strategy utilized by the virus to increase replication.