Walleye epidermal hyperplasia virus 1
| Walleye epidermal hyperplasia virus | |
|---|---|
| Virus classification | |
| Group: | Group VI (ssRNA-RT) |
| Order: | Unassigned |
| Family: | Retroviridae |
| Subfamily: | Orthoretrovirinae |
| Genus: | Epsilonretrovirus |
| Species | |
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Walleye epidermal hyperplasia virus is a retrovirus classified under, Epsilonretroviruses, a recent genus addition to the family of Retroviridae. There are three genome sequenced and identified exogenous retroviruses of this genus which include two known types (WEHV-1 and WEHV-2) associated with walleye epidermal hyperplasia disease. Both viral types are confirmed to be the causative agents of the neoplastic condition in the freshwater fish species, the North American Walleye (Stizostedion vitreum). The specific association of retroviral infection with proliferative lesions in fish is based on the presence of retrovirus-like particles (observed via electron microscopy) and reverse transcriptase activity (using reverse transcriptase polymerase chain reaction techniques) from neoplastic tissue. Although both virus types have been observed in lesions of diseased fish, each cell of the infected tissue is host to a specific virus. Transmission studies have also shown that WEHV-2 has been the more proliferative agent of the condition as compared to WEHV-1.
Phylogenetic analysis of the three confirmed Epsilonretroviruses shows they are related. After cloning techniques, sequence analysis determined that WEHV-1 and WEHV-2 are similar in size and share 95% amino acid identity in the pol region of reverse transcriptase. This finding suggests that they are different strains of the same virus or likely distinct species. The two types of WEHV also share over 80% of their amino acid sequence with the third member of the epsilonretrovirus genus. Included in this analysis was the observation of a homologous genomic organization in all three Epsilonretroviruses.
Walleye epidermal hyperplasia lesions are characteristically broad, flat, translucent plaques that range in size (2–50 mm in diameter). Lesions are most often observed in sexually mature fish although transmission studies have shown that fingerling fish can be infected using cell-free virus components extracted from lesions. Multiple growths are also known to coalesce into larger lesions. Seasonal observations of the fish by scientists and sportsmen show a high incidence of the condition during the late fall, winter, and early spring months. Mortality in the host fish is hypothesized to be less related to the virus and more to secondary infections that invade necrotic tissue. These viruses have evolved a means to maintain a fine balance between its own proliferation and leaving behind a fit and reproductive host.
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