Hd. Nguyen et al., PROGRESSION OF STRIPED JACK NERVOUS NECROSIS VIRUS (SJNNV) INFECTION IN NATURALLY AND EXPERIMENTALLY INFECTED STRIPED JACK PSEUDOCARANX DENTEX LARVAE, Diseases of aquatic organisms, 24(2), 1996, pp. 99-105
The progress of infection with SJNNV (nodavirus), the causative agent
of viral nervous necrosis (VNN), was investigated by using naturally i
nfected (acute and subacute groups) and experimentally infected stripe
d jack larvae at different stages of infection. Although there were sl
ight differences in the progress of infection among the 3 groups of fi
sh examined, the general features of infection were quite similar. Nec
rosis and vacuolation of the nerve cells were first observed in the sp
inal cord, particularly in the area just above the swimbladder, later
in the brain, and then in the retina. Mortalities occurred 1 to 2 d af
ter the commencement of lytic degeneration of the cells, which resulte
d in heavy vacuolation in these nervous tissues. Virus antigens were d
etectable in the nervous tissues by the fluorescent antibody technique
(FAT) when conspicuous vacuolation appeared in the cytoplasm. Virus p
articles were detectable by electron microscopy in concurrence with th
e appearance of heavy tissue vacuolation. These results indicate that
SJNNV exhibits a tropism for nerve cells and its initial multiplicatio
n site is the spinal cord, from which the virus spreads to the brain a
nd finally to the retina. Hyperplasia was observed in the skin of 1 na
turally infected larval group (acute infection) and virus multiplicati
on was observed in these affected epithelial cells. However, the role
of skin as a portal of entry for SJNNV remains unclear.