Surely, I mean absolutely, it would appear on an Atlantic salmon farm long before the above dooms day prediction. Even if it was here
https://www.sfu.ca/cstudies/science/resources/1321897737.pdf
The part that you are missing, it is already here - just ask Dr. Kristy Miller. Referring to your reference - all is how one "closely" reads and understands that study. I will quote your own reference with my personal comments observations in [ ]:
“Infectious salmon anaemia (ISA) [the disease] is a major disease of Atlantic salmon, Salmo salar, caused by an orthomyxovirus (ISAV) [the virus].”
“No signs typical of ISA [the disease] and no ISAV [the virus]-related mortality occurred among any of the groups of Oncorhynchus spp. in either experiment, although ISAV [the virus] was reisolated from some fish sampled at intervals postchallenge. The results indicate that while Oncorhynchus spp. are quite resistant to ISAV [virus] relative to Atlantic salmon, the potential for ISAV [the virus] to adapt to Oncorhynchus spp. should not be ignored. [pretty clear – should not be ignored]”
“Clinical outbreaks of ISA [the disease] occur in seawater adapted Atlantic salmon reared in marine net pens [there has never been a “clinical outbreak found in the wild – THEY JUST individually - DIE]. However, ISAV [the virus] has also been identified in wild Atlantic salmon (Nylund, Kevenseth & Krossøy 1995a), sea trout, Salmo trutta L., (Raynard, Murray & Gregory 2001a) and Atlantic herring, Clupea harengus harengus L. (A. Nylund, personal communication) although no clinical signs of the disease were present [again, THEY JUST individually - DIE]. Sea trout (Nylund, Alexandersen, Løvik & Jakobsen 1994; Nylund, Alexandersen, Rolland & Jakobsen 1995b; Nylund & Jakobsen 1995; Rolland & Nylund 1998), brown trout, Salmo trutta L. (Snow, Raynard & Bruno 2001), Arctic char, Salvelinus alpinus (L.) (Snow et al. 2001), and rainbow trout (Nylund, Kvenseth, Krossøy & Hodneland 1997; Snow et al. 2001) represent possible natural reservoirs of ISAV [the virus] because the virus is able to propagate in these species without producing clinical disease, while saithe, Pollachius virens (L.), a species commonly associated with marine net pens, was shown not to be a likely reservoir (Snow, Raynard, Bruno, van Nieuwstadt, Olesen, Lovold & Wallace 2002). Recently, Kibenge et al. (2001a) reported isolation of ISAV [the virus] from farmed coho salmon, Oncorhynchus kisutch (Walbaum), in Chile. However, these clinically diseased fish exhibited markedly different pathology from typical ISA [the disease] and although the disease has been associated with an orthomyxovirus, it is reported that the disease in Chilean coho is of multifactorial [involving or dependent on a number of factors or causes. The end result is they don’t show all/or any of the clinical signs of ISA disease but they still - DIE] origin (Smith, Larenas, Contreras, Cassigoli, Venegas, Rojas, Guajardo, Troncoso & Macias 2002).”
“Here, we used a relatively severe challenge dose of ISAV delivered by intraperitoneal injection to show that Pacific salmon were considerably more resistant to ISAV compared with their Atlantic counterparts.
Although our findings suggest Pacific salmon are quite resistant to the strains we used, ISA has been reported to occur in farmed coho salmon in Chile (Kibenge et al. 2001a). However, Smith et al. (2002) have suggested that the disease associated with the orthomyxovirus recovered from Chilean coho salmon may be of multifactorial origin.”
“However, salmonids such as rainbow trout, brown trout and sea trout have been reported to be carriers of ISAV [virus], and the reisolation of ISAV [virus] from the Pacific salmon species used in these trials indicates that it would be unwise [emphasis – UNWISE] to overlook the possibility of ISAV [virus] replicating in, or establishing a carrier status among these species should they be exposed to the virus. Furthermore, the haemagglutinin gene of ISAV [virus] shows substantial diversity among isolates that may be associated with antigenic variation [see below] or recombination (Devold et al. 2001; Kibenge et al. 2001b; Cunningham, Gregory, Black, Simpson & Raynard 2002) and such variation may result in evolution of strains with differences in host range, virulence or immune response to vaccines [to ISA disease].”
Antigenic variation:
“Influenza viruses are constantly changing. They can change in two different ways.
One way they change is called “antigenic drift.” These are small changes in the genes of influenza viruses that happen continually over time as the virus replicates. These small genetic changes usually produce viruses that are pretty closely related to one another, which can be illustrated by their location close together on a phylogenetic tree. Viruses that are closely related to each other usually share the same antigenic properties and an immune system exposed to an similar virus will usually recognize it and respond. (This is sometimes called cross-protection.)
But these small genetic changes can accumulate over time and result in viruses that are antigenically different (further away on the phylogenetic tree). When this happens, the body’s immune system may not recognize those viruses.
This process works as follows: a person infected with a particular flu virus develops antibody against that virus. As antigenic changes accumulate, the antibodies created against the older viruses no longer recognize the “newer” virus, and the person can get sick again. Genetic changes that result in a virus with different antigenic properties is the main reason why people can get the flu more than one time. This is also why the flu vaccine composition must be reviewed each year, and updated as needed to keep up with evolving viruses.
The other type of change is called “antigenic shift.” Antigenic shift is an abrupt, major change in the influenza A viruses, resulting in new hemagglutinin and/or new hemagglutinin and neuraminidase proteins in influenza viruses that infect humans. Shift results in a new influenza A subtype or a virus with a hemagglutinin or a hemagglutinin and neuraminidase combination that has emerged from an animal population that is so different from the same subtype in humans that most people do not have immunity to the new (e.g. novel) virus. Such a “shift” occurred in the spring of 2009, when an H1N1 virus with a new combination of genes emerged to infect people and quickly spread, causing a pandemic. When shift happens, most people have little or no protection against the new virus.
While influenza viruses are changing by antigenic drift all the time, antigenic shift happens only occasionally. Type A viruses undergo both kinds of changes; influenza type B viruses change only by the more gradual process of antigenic drift.”