RISS 검색 - 국내학술지논문 상세보기

다국어 초록 (Multilingual Abstract)

Swine enteritis in all ages is caused by porcine epidemic diarrhea virus (PEDV), transmissible gastroenteritis virus (TGE), rotavirus, Eimeria spp. etc., and is often fatal among neonatal piglets. This study aimed to compare the pathogenicity and nucleotide sequence of ORF3 between wild-type porcine epidemic diarrhea virus (wt-PEDV) and cell culture-adapted PEDV (ca-PEDV). A total of 30 colostrum- deprived piglets that were 1 day old were inoculated with either wt-PEDV or ca-PEDV to compare the villus height and crypt depth (VH/CD) ratio, amount of viral nucleic acid in jejunum, and open reading frame (ORF) 3 nucleotide sequence via immunofluorescence labeling of viral antigen and western blot analysis. Mean jejunal villus height and crypt depth (VH/CD) ratio in piglets infected orally with Korean strain of PEDV were 6.8 ± 0.8, 7.0 ± 0.8, 8.2 ± 1.0, 8.0 ± 1.3, and 7.9 ± 1.1 in uninfected control piglets; 7.2 ± 1.2, 5.2 ± 1.4, 2.7 ± 0.3, 1.4 ± 0.2, and 1.5 ± 0.1 in wt-PEDV-infected piglets; and 7.6 ± 1.8, 3.2 ± 0.4, 2.2 ± 0.3, 1.3 ± 0.3, and 1.1 ± 0.2 in ca-PEDV-infected piglets at 12, 24, 36, 48, and 60 h post inoculation. Conclusively, the mean VH/CD ratio for wt-PEDV piglets was significantly different from that of ca-PEDV piglets at 24, 36, and 60 h post inoculation. The in situ hybridization (ISH) positive results in piglets orally infected with the Korean strain of PEDV in jejunal villus were 4.0 ± 0.8, 10.3 ± 0.5, 7.3 ± 0.5, 7.0 ± 0.8, and 5.3 ± 0.5 in ca-PEDV-infected piglets; and 4.3 ± 0.9, 16.7 ± 1.2, 9.3 ± 0.5, 9.0 ± 0.8, and 5.7 ± 0.9 in wt-PEDV-infected piglets. Conclusively, a significant difference was observed in each group. A greater amount of PEDV nucleic acid was detected in the jejunal tissues (P < 0.05) of the ca-PEDV-inoculated piglets than in those of the wt-PEDV-infected piglets at 24, 36, and 60 h post-inoculation. The nucleotide sequences of wt-PEDV and ca-PEDV were nearly identical (98.7% homology); nucleotide substitutions were noted in ORF3 that caused some amino acid changes. Statistically significant differences were observed in the pathogenicity of ca-PEDV compared with its parental wt-PEDV; ORF3 nucleotide changes were identified in ca-PEDV that possibly influenced PEDV pathogenicity

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