Also known as the black bullhead virus, it is phylogenetically similar to IcHV-1. Distinction between the two species is reliant on the places of detection and the severity of clinical signs. IcHV-2 has been experimentally observed to result in more severe clinical signs in channel catfish than IcHV1.[2]
Background
IcHV-2 was first observed in 1994 after two mass mortality events occurred in two different catfish farms in Italy, resulting in severe economic loss.[3]
As observed in experimental trials, there is a higher mortality rate in channel catfish when exposed to IcHV-2 than in trials and previous background studies where channel catfish were exposed to IcHV-1.[2] It is also shown that through syncytialcytopathic effect, both strains of Ictalurid herpesvirus are homologous to the syncytia produced.[3]
Genome
Next-generation sequencing performed on IcHV2 revealed its complete genome to be 142,925 bp, along with 77 (predicted) protein-coding regions with 12 open reading frames (ORFs) where these ORFs are seen to be homologous with every other Alloherpesvirus sequenced.[4] High synteny between IcHV1 and IcHV2 was also observed.
Diagnosis
Detection of IcHV-2 uses quantitative PCR (qPCR) for any potential carriers or for checking for isolates. While IcHV-2 was detected in all organs, the virus was seen the highest in the kidney and spleen; meanwhile, liver and gill concentrations were much lower.[5]
Other uses of qPCR can help detect IcHV-2 in latently infected carrier fish.[5] This helps reduce the risk of potentially relocating the virus and introducing it into new aquaculture and whether or not high morbidity rates are from IcHV-2 or another pathogen.
Pathology
Clinical signs of IcHV-2 include disoriented swimming or instances where they dwell at the surface of the pond bank.[3] Other signs include scattered hemorrhages and kidney tissue death.[4]
IcHV2 propagation control is a highly researched topic due to it showing much more intensive mortality rates in channel catfish than IcHV-1. The high mortality rate is due to the fact that IcHV-2 propagation and viral transmission has an optimal temperature of 24°C, which is relatively lower than IcHV-1.[4] Furthermore, overcrowded pens contribute to the transmission of the virus.
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