A 474-base pair segment covering the hypervaible region of VP2 gene from six Korean infectious bursal disease virus(K-IBDV) isolates(K1, K2, SH/92, 225, 269, 310) and one attenuated IBDV(DAE) were amplified using RT-PCR, sequenced, and compared with published sequences for IBDV. K-IBDV isolates(K1, K2, SH/92, 225, 269) and foreigh very virulent(vv) IBDV strains had 94.93-100% amino cid sequence similarity. K-IBDV isolate 310 and other K-IBDV isolates had 84.31%-86.07% amino acid sequence similarity. Attenuated strain(DAE), like other attenuated strain, has substitution at positions 279(D to N) and 284(A to T) as well as in the serine-rich heptapeptide region. Five K-IBDV isolates except 310 isolate share unique amino acid residues at positions 222(A), 256(I), 294(I) which are not present in other standard and attenuated strains. At the two hydrophilic region, K-IBDV isolates except 310 isolate had identical amino cids comparing with Belgium vv IVDV 894VB but had four amino acid substitutions comparing with Chinese vv IBDV F9502. The SWSASGS heptapeptide is conserved in all KIBDV isolates. The sequence of K-IBDV isolate 310 was markedly different from other IBDV strains, evolving from a separate lineage than the others. By phylogenetic analysis, Five K-IBDV isolates except 310 isolate were categorized in one group with foreign vv IBDV isolates but K-IBDV isolate 310 was categorized ina separate group which was differentiated form other compared IBDV strains.

Brain, spleen, and selected lymph nodes from sheep with clinical signs of scrapie were analyzed for presence of proteinase K-resistant protein (PrP-res). Diagnosis of scrapie on the basis of detection of PrP-res was compared with diagnosis on the basis of histologic evaluation of the brain from clinically affected or exposed sheep. Proteinase K-resistant protein was found in every brain that was histologically positive for scrapie, and in addition, was found in the brain of several clinically positive sheep that were not diagnosed as scrapie-positive by histologic evaluation. Proteinase K-resistant protein was also found in 87% of the spleens and lymph nodes from sheep that had PrP-res detected in brain homogenates. Therefore, analysis of sheep brain, spleen, or lymph nodes for PrP-res provided a diagnostic approach that was superior to histologic examination alone for detection of naturally scrapie agent-infected sheep.

Rabbit hemorrhagic disease is a highly acute and fatal viral disease caused by rabbit hemorrhagic disease virus (RHDV). Since first outbreak in Korea 1987, RHDV has been continually affected in the country, but the pattern of outbreak seem to be changed. In this study, to understand the pathogenesis of the new RHDVa serotype, we therefore carried out to inoculate RHDVa to rabbits, and to examine the sequential histopathologic changes and viral distribution. Macroscopically, various sized dark red or white spots or appearance were observed in the liver, lung, kidney uterus and ureter. In euhanized rabbits, significant pathologic findings such as infiltration of heterophils and mononuclear cells were observed at 24 hours after inoculation (HAI), and these were sequentially extended periportal to centrilobular area. However, in dead rabbits, severe hepatic degeneration and/or necrosis with relatively weak inflammatory responses were observed. RHDV antigens began to detect in liver, spleen, and lung from 12 HAI by PCR. Immunohistochemically, RHDV positive cells were seen in only liver from 24 HAI, and the degree of immunogen reactivity was stronger in dead rabbits than in euthanized ones. In conclusion, RHDVa caused the subacute or chronic infection accompanying low mortality and moderate to severe inflammatory reaction in rabbits, suggesting the possibility that RHD could become endemic.

The present study was carried out to investigate the pathogenicity and pathogenesis of wild rats(Rattus norvegicus), trapped in nature, intranasally infected Aujeszky's disease virus(ADV/NYJ-1-87) by histopathology, immunohistochemistry and in situ hybridization(ISH). Fifteen rats inoculated intranasally were roughened haircoat, anorexia, listlessness, and depression second day after inoculation, and three rats died in 66-72 hours. Eight rats showed severe pruritus at the fact that was accompanied by frequent face-washing movements of the forelegs, and then became violent and spasmodic for and hour or until they died. Four rats slowly recovered after showing mild clinical signs of the disease. Microscopic lesions in infected rats were characterized by meningitis, perivascular round cell infiltration, focal gliosis, and neuronal degeneration and necrosis. And intranuclear inclusion bodies were frequently detected in the cerebral cortex and medulla. Positive reaction to ADV by immunohistochemistry and ISH were detected in the following areas:trigemimal ganglion, brain, tonsil, nasal mucosa, spleen, lung and liver. The result has suggested that ADV intranasally infected in wild rats is followed by replication in epithelial cells of nasal mucosa and tonsil, then invade local lymph nodes by way of the lymphatics. It is also believed that the virus invades bipolar olfactory cells and trigerminal ganglion, and then spread into central nervous system.