Infectious pancreatic necrosis virus (IPNV) from salmonid fish enters, but does not replicate in, mammalian cells
1 Norwegian Veterinary Institute, P.O. Box 0750, Sentrum, Oslo, NO, 0106, Norway
2 Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Box 1110, Blindern, Oslo, NO, 0317, Norway
3 Department of Food Safety and Infection Biology, Norwegian School of Veterinary Science, Box 8146, Dep, Oslo, NO, 0033, Norway
Virology Journal 2012, 9:228 doi:10.1186/1743-422X-9-228Published: 5 October 2012
The aquatic birnavirus infectious pancreatic necrosis virus (IPNV) causes infectious pancreatic necrosis (IPN), a severe disease in farmed salmonid fish. IPNV has a very broad host range and infects many different species of fish as well as molluscs and crustaceans. Investigation of the host reservoir of a virus may reveal important molecular mechanisms governing the infection processes such as receptors and entry mechanisms. In the present work we have studied whether IPNV is able to infect cells with different mammalian origin.
IPNV bound in a specific manner to a membrane protein of the rabbit kidney cell line RK-13 as shown by the use of a virus overlay protein binding assay (VOPBA). Six different mammalian cell lines were inoculated with IPNV and incubated in parallels at different temperatures. At 7 days post inoculation (dpi), IPNV was detected by indirect immunofluorescent antibody test (IFAT) in all the cell lines. Confocal microscopy confirmed intracellular presence of the virus. No apparent cytopathic effect (cpe) was observed in any of the cultures, and no viral replication was demonstrated with real-time RT-PCR.
Our results show that IPNV is able to enter into a wide range of mammalian cells, and virus entry is most likely receptor mediated. We found no indication of IPNV replication in any of the mammalian cell lines tested.