Abstract
Infectious pancreatic necrosis (IPN) is a disease of great concern in aquaculture, mainly among salmonid farmers, since losses in salmonid fish—mostly very young rainbow trout (Salmo gairdnery) fry and Atlantic salmon (Salmo salar) post-smolt—frequently reach 80–90% of stocks. The virus causing the typical signs of the IPN disease in salmonids, named infectious pancreatic necrosis virus (IPNV), has also been isolated from other fish species either suffering related diseases (then named IPNV-like virus) or asymptomatic; the general term aquabirnavirus is used to encompass all these viruses. Aquabirnaviruses are non-enveloped, icosahedral bisegmented dsRNA viruses, whose genome codifies five viral proteins, three of which are structural, and one of them is an RNA-dependent RNA polymerase. Due to the great importance of the disease, there have been great efforts to find a way to predict the level of virulence of IPNV isolates. The viral genome and proteins have been the main focus of research. However, to date such a reliable magic marker has not been discovered. This review describes the processes followed for decades in the attempts to discover the viral determinants of virulence, and to help the reader understand how viral components can be involved in virulence modulation in vitro and in vivo. There is also a brief description of the disease, of host defenses, and of the molecular structure and function of the virus and its viral components.
Highlights
Infectious pancreatic necrosis (IPN) is a well-known disease originally named acute catarrhal enteritis by M’Gonigle in 1951 [1], but soon after Wood et al [2] changed its name to IPN, based on a histopathological study of brook trout (Salvelinus fontinalis) suffering an infectious disease resembling a catarrhal enteritis
A diameter ranging from 57 to 74 nm was reported in an early review by Dobos and Roberts [10], which is more in accordance with the results of a recent study by Lago et al [11], where a range of sizes between 55 and even 90 nm were visualized in different fractions of a purified IPN virus (IPNV) West Buxton type virus, the most frequently observed size being around 70 nm
If with this review we expected to find out which marker, or set of well-defined markers, could be used to predict the level of risk of a new IPNV isolate from its molecular characteristics, we must be a little disappointed
Summary
Infectious pancreatic necrosis (IPN) is a well-known disease originally named acute catarrhal enteritis by M’Gonigle in 1951 [1], but soon after Wood et al [2] changed its name to IPN, based on a histopathological study of brook trout (Salvelinus fontinalis) suffering an infectious disease resembling a catarrhal enteritis. The term IPNV is strictly used for those strains affecting salmonid fish which develop specific symptoms (see below) In those cases where the virus affects non-salmonids, with different symptoms, the term IPN is substituted by IPNV-like, and in general terms the name aquabirnaviruses is employed. Most reported episodes and isolations were initially in North America and Europe (from a large number of countries), many cases from Asian countries (including Japan, Korea, Taiwan, Iran, Turkey, and China) have been reported since the 1980s. Other areas, such as South America (Chile), Africa (Kenya), and Australia are much less represented. A brief description of the disease and the virus has been included to better understand how virulence can be modulated by the different determinants described in the literature
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