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The progress of infection with SJNNV (nodavirus), the causative agent of viral nervous necrosis (VNN), was investigated by using naturally infected (acute and subacute groups) and experimentally infected striped jack larvae at different stages of infection. Although there were slight differences in the progress of infection among the 3 groups of fish examined, the general features of infection were quite similar. Necrosls and vacuolation of the nerve cells were first observed in the spinal cord, particularly in the area just above the swimbladder, later in the brain, and then in the retina. Mortalities occurred 1 to 2 d after the commencement of lytic degeneration of the cells, which resulted in heavy vacuolation in these nervous tissues. Virus antigens were detectable in the nervous tissues by the fluorescent antibody technique (FAT) when conspicuous vacuolation appeared in the cytoplasm. Vlrus particles were detectable by electron rnicroscopy in concurrence with the appearance of heavy tissue vacuolation. These results indicate that SJNNV exhibits a tropism for nerve cells and its Initial multiplication site is the spinal cord, from which the virus spreads to the brain and finally to the retina. Hyperplasia was observed in the skin of 1 naturally infected larval group (acute infection) and virus multiplication was observed in these affected epithelia1 cells. However, the role of skin as a portal of entry for SJNNV remains unclear

Progression of striped jack nervous necrosis virus (SJNNV) infection in naturally and experimentally infected striped jack Pseudocaranx dentex larvae