Charlie
Well-Known Member
part 3
4. Relevant risk factors for emergence of HPRΔ (ToR 2b)
There is an evolutionary relationship between virulent and low-virulence forms of ISAV, whereby HPR0 possibly through several steps mutates into a virulent form of the ISAV. However, no predisposing risk factors have been demonstrated or suggested to drive or increase such an evolutionary process. Hence, there is a lack of knowledge on specific risk factors for HPRΔ emergence from HPR0. The available evidence on transmission within populations and spread between populations and control thereof is almost entirely based on studies of HPRΔ (ISAV); however, the observations from the Faroe Islands and Norway have provided some insight into the dynamics of HPR0.
4.2. HPRdelta emergence from endemic HPR0 infection
Fish susceptibility to virulent viruses may be modulated by acquired immunity. HE is a major antigen of ISAV and contributes to stimulating a protective immune response (see Section 2.4). Previous infections with ISAV, like vaccination with attenuated viruses, may induce a level of protection against subsequent infections with the same or other ISAV variants. The possibility that a subclinical infection with HPR0 might prevent or mitigate subsequent infections with virulent variants has not been investigated.
Industrialised farming of salmon is exposed to a range of environmental challenges, such as high density, low physical activity, water with periodically suboptimal oxygen levels and changing temperatures, intensive feeding and growth rate, and handling. Such exposures may be regarded as chronic or temporary stress inducers, harming their defence mechanisms and aggravating disease outbreak dynamics, as well as potentially influencing the evolution and replication ability of the infectious agents themselves. Moreover, high-density farming increases the number of possible infectious contacts whereby an infection and disease in a single salmon can become a communicable disease in an industrialised high-density setting.
CONCLUSIONS AND RECOMMENDATIONS
GENERAL CONCLUSIONS
Atlantic salmon is the only species in which the disease ISA has been observed naturally.
ISAV can be genetically differentiated on the basis of the sequence of an HPR of genomic segment 6 which encodes the HE protein.
Initial reports of findings of ISAV before 2002 did not distinguish between HPR0 and HPRΔ, making interpretation of older findings more difficult in the light of current knowledge.
A single observation of HPR0 ISAV in wild Atlantic salmon indicates that the virus may exist outside the farmed salmon population.
TOR 1 THE CAPABILITY OF HPR0 ISAV TO CAUSE CLINICAL DISEASE.
HPR0 ISAV does not cause clinical disease in Atlantic salmon.
It is known that HPR0 ISAV causes a transient subclinical infection and replicates mainly in gills.
There is currently no evidence indicating that HPR0 ISAV leads to natural infection and replication in fish species other than Atlantic salmon.
TOR 2 THE RISK OF HPR-DELETED ISA EMERGING FROM HPR0 ISA AND, IF RELEVANT, INDICATING FACTORS FOR SUCH AN EMERGENCE.
2a Risk of HPRΔ emerging from HPR0
All virulent ISAV have deletions in the HPR region of the HE gene and they have either an insertion or the Q266L mutation in the F gene. Transitional viruses having only one of the HE or F mutations have not been found.
The most plausible hypothesis is that virulent ISAV (HPRΔ) is derived from HPR0 ISAV.
The close association between genetic relatedness and the spatio-temporal distance of virus strains in solitary outbreaks further supports the hypothesis that virulent ISAV evolve from HPR0-ISAV.
Epidemiological and historical data from solitary disease outbreaks indicate that the risk of emergence of virulent ISAV is low but not negligible.
2b Risk factors
There is a lack of knowledge on risk factors for HPRΔ emergence from HPR0.
The risk of emergence of HPRΔ ISAV and subsequent development of disease can be expected to be related to the overall replication rate 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.
RECOMMENDATION
Baseline monitoring is needed to estimate the prevalence of ISAV HPR0 in farmed Atlantic salmon and wild fish in proximity to farming facilities.
The whole opinion can be found here:
http://www.efsa.europa.eu/en/efsajournal/doc/2971.pdf
BTW... I actually read every word of what I post! Hell... sometimes I actually write them!
4. Relevant risk factors for emergence of HPRΔ (ToR 2b)
There is an evolutionary relationship between virulent and low-virulence forms of ISAV, whereby HPR0 possibly through several steps mutates into a virulent form of the ISAV. However, no predisposing risk factors have been demonstrated or suggested to drive or increase such an evolutionary process. Hence, there is a lack of knowledge on specific risk factors for HPRΔ emergence from HPR0. The available evidence on transmission within populations and spread between populations and control thereof is almost entirely based on studies of HPRΔ (ISAV); however, the observations from the Faroe Islands and Norway have provided some insight into the dynamics of HPR0.
4.2. HPRdelta emergence from endemic HPR0 infection
Fish susceptibility to virulent viruses may be modulated by acquired immunity. HE is a major antigen of ISAV and contributes to stimulating a protective immune response (see Section 2.4). Previous infections with ISAV, like vaccination with attenuated viruses, may induce a level of protection against subsequent infections with the same or other ISAV variants. The possibility that a subclinical infection with HPR0 might prevent or mitigate subsequent infections with virulent variants has not been investigated.
Industrialised farming of salmon is exposed to a range of environmental challenges, such as high density, low physical activity, water with periodically suboptimal oxygen levels and changing temperatures, intensive feeding and growth rate, and handling. Such exposures may be regarded as chronic or temporary stress inducers, harming their defence mechanisms and aggravating disease outbreak dynamics, as well as potentially influencing the evolution and replication ability of the infectious agents themselves. Moreover, high-density farming increases the number of possible infectious contacts whereby an infection and disease in a single salmon can become a communicable disease in an industrialised high-density setting.
CONCLUSIONS AND RECOMMENDATIONS
GENERAL CONCLUSIONS
Atlantic salmon is the only species in which the disease ISA has been observed naturally.
ISAV can be genetically differentiated on the basis of the sequence of an HPR of genomic segment 6 which encodes the HE protein.
Initial reports of findings of ISAV before 2002 did not distinguish between HPR0 and HPRΔ, making interpretation of older findings more difficult in the light of current knowledge.
A single observation of HPR0 ISAV in wild Atlantic salmon indicates that the virus may exist outside the farmed salmon population.
TOR 1 THE CAPABILITY OF HPR0 ISAV TO CAUSE CLINICAL DISEASE.
HPR0 ISAV does not cause clinical disease in Atlantic salmon.
It is known that HPR0 ISAV causes a transient subclinical infection and replicates mainly in gills.
There is currently no evidence indicating that HPR0 ISAV leads to natural infection and replication in fish species other than Atlantic salmon.
TOR 2 THE RISK OF HPR-DELETED ISA EMERGING FROM HPR0 ISA AND, IF RELEVANT, INDICATING FACTORS FOR SUCH AN EMERGENCE.
2a Risk of HPRΔ emerging from HPR0
All virulent ISAV have deletions in the HPR region of the HE gene and they have either an insertion or the Q266L mutation in the F gene. Transitional viruses having only one of the HE or F mutations have not been found.
The most plausible hypothesis is that virulent ISAV (HPRΔ) is derived from HPR0 ISAV.
The close association between genetic relatedness and the spatio-temporal distance of virus strains in solitary outbreaks further supports the hypothesis that virulent ISAV evolve from HPR0-ISAV.
Epidemiological and historical data from solitary disease outbreaks indicate that the risk of emergence of virulent ISAV is low but not negligible.
2b Risk factors
There is a lack of knowledge on risk factors for HPRΔ emergence from HPR0.
The risk of emergence of HPRΔ ISAV and subsequent development of disease can be expected to be related to the overall replication rate 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.
RECOMMENDATION
Baseline monitoring is needed to estimate the prevalence of ISAV HPR0 in farmed Atlantic salmon and wild fish in proximity to farming facilities.
The whole opinion can be found here:
http://www.efsa.europa.eu/en/efsajournal/doc/2971.pdf
BTW... I actually read every word of what I post! Hell... sometimes I actually write them!
