rus t o rNVI15-DVP5 is deficient in VP5 expression. In the present report, the role of VP5 in apoptosis was assessed both in vitro and in vivo, using pancreatic necrosis (IPN). Outbreaks are typically seen at fry start feeding, and shortly after sea transfer of smolts. As survivors continue to harbo...
| Other Authors: | |
|---|---|
| Format: | Text |
| Language: | English |
| Subjects: | |
| Online Access: | http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.555.4653 http://www.ncku.edu.tw/~biotech/teacher/Jiann-Ruey Hong/13.pdf |
| Summary: | rus t o rNVI15-DVP5 is deficient in VP5 expression. In the present report, the role of VP5 in apoptosis was assessed both in vitro and in vivo, using pancreatic necrosis (IPN). Outbreaks are typically seen at fry start feeding, and shortly after sea transfer of smolts. As survivors continue to harbor virus in their bodies for long periods, presumably in head kidney macrophages (Reno et al., 1978; Mangunwiryo and Aguis, 1988; Johansen and Virology 342 (2005) 1the recombinant IPNV strains. Apoptosis was observed in hepatocytes of Atlantic salmon post-smolts challenged with all three VP5 mutant viruses. Using a double-labeling technique to detect apoptotic cells and IPNV antigens, we found that viral antigen and apoptotic cells co-distributed. In addition, numerous double-positive cells were seen. The recombinant viruses also induced apoptosis in infected cell cultures, and the morphology and membrane integrity of infected cells at different time points was similar. In summary, these results indicate that IPNV induces apoptosis in infected cell cultures and in fish, independent of VP5 expression. However, substitutions of putative functionally important amino acids in the BH2 domain of VP5 of IPNV–Sp strains were identified, which might influence the anti-apoptosis effect of the protein, and partly explain the apparent absence of this specific function. |
|---|