Following a request from the European Commission, the EFSA Panel on Animal Health and Welfare was asked to deliver a scientific opinion on infectious salmon anaemia (ISA). ISA is a fish disease caused by an orthomyxovirus (infectious salmon anaemia virus, ISAV) affecting Atlantic salmon, which has been responsible for high mortalities in salmon producing countries since its first detection in Norway in the mid-1980s.
This opinion reviews the available scientific evidence on the relationship between HPR0 and HPRΔ, and addresses the risk of HPRΔ ISAV emerging from HPR0 ISAV and, if relevant, indicates the risk factors for such an emergence.
Pathogenic HPRΔ ISAV variants cause a systemic infection, infecting endothelial cells of the blood circulatory system whereas HPR0 ISAV does not cause clinical disease in Atlantic salmon but causes a transient subclinical infection and replicates mainly in gills.
ISAV can be genetically differentiated on the basis of the sequence of a highly polymorphic region (HPR) of genomic segment 6 which encodes the Haemagglutinin-Esterase (HE) protein. A deletion within the HPR region (HPRΔ ISAV) is necessary for pathogenicity. ISAV without any deletions in the HPR region (Hereinafter: HPR0 ISAV) has been reported only in apparently healthy fish and has never been associated with clinical ISA disease.
HPR0 has been detected in farmed Atlantic salmon from several countries and it has also been detected in wild Atlantic salmon in the Faroe Islands and Norway. There is currently no evidence indicating that HPR0 ISAV naturally infects and replicates in species other than Atlantic salmon. The finding of HPR0 ISAV in wild Atlantic salmon indicates that a reservoir outside the farmed salmon population may exist.
ISAV isolates vary in virulence, as observed by differences in disease development and clinical signs in field outbreaks as well as in experimental trials. All ISAV isolates from ISA disease outbreaks have deletions in the HPR region with respect to the HPR0 variant. In addition, all virulent strains of ISAV have either an amino acid substitution or a short amino acid insertion immediately upstream or downstream of the putative arginine cleavage site in the fusion (F) protein.
The hypothesis that virulent HPRΔ ISAV is derived from HPR0 ISAV by deletions in the HPR of the HE molecule provides the best fit with current knowledge and epidemiological evidence. Epidemiological and historical data from solitary disease outbreaks indicate that the risk of emergence of virulent ISAV is low but not negligible.
Generic biosecurity measures such as segregation of generations, caution regarding contact points (water, equipment), sanitary handling of dead fish, cleaning and disinfection, and synchronous fallowing appear to have a good effect in terms of prevention and control of ISA.
Prior adaptive immunity provides some protection against subsequent infection with virulent ISAV. Little is known about antigenic variation in the haemagglutinin-esterase gene of ISAV and it is not possible to conclude whether this may impact population immunity. Likewise, it is not known if or to what extent prior infection with HPR0 ISAV may induce some degree of protective immunity.
The evolutionary relationship between virulent and low-virulent ISAV forms, where HPR0 mutates into a virulent form of the ISAV, appears plausible. However, no predisposing risk factors have been demonstrated or suggested to drive or increase such an evolutionary process.
Based on general virological knowledge, the risk of emergence of HPRΔ and subsequent development of disease can be expected to be related to the overall replication of HPR0 ISAV and the presence of susceptible hosts. Any factor that affects replication or host susceptibility would, therefore, also influence the risk of emergence of HPRΔ ISAV.